Secondary hypertension

Last updated

Secondary hypertension
Other namesInessential hypertension
Specialty Cardiology, nephrology   OOjs UI icon edit-ltr-progressive.svg

Secondary hypertension (or, less commonly, inessential hypertension) is a type of hypertension which by definition is caused by an identifiable underlying primary cause. It is much less common than the other type, called essential hypertension, affecting only 5-10% of hypertensive patients. It has many different causes including endocrine diseases, kidney diseases, and tumors. It also can be a side effect of many medications.

Contents

Types

Kidney

Renovascular hypertension

It has two main causes: fibromuscular dysplasia and atherosclerosis of the renal artery resulting in stenosis.[ citation needed ]

Kidney

Other well known causes include diseases of the kidney. This includes diseases such as polycystic kidney disease which is a cystic genetic disorder of the kidneys, PKD, which is characterized by the presence of multiple cysts (hence, "polycystic") in both kidneys, can also damage the liver, pancreas, and rarely, the heart and brain. [1] [2] [3] [4] It can be autosomal dominant or autosomal recessive, with the autosomal dominant form being more common and characterized by progressive cyst development and bilaterally enlarged kidneys with multiple cysts, with concurrent development of hypertension, chronic kidney disease and kidney pain. [5] Or chronic glomerulonephritis which is a disease characterized by inflammation of the glomeruli, or small blood vessels in the kidneys. [6] [7] [8]

Hypertension can also be produced by diseases of the renal arteries supplying the kidney. This is known as renovascular hypertension; it is thought that decreased perfusion of renal tissue due to stenosis of a main or branch renal artery activates the renin–angiotensin system. [9] [10] [11]

Also, some renal tumors can cause hypertension. The differential diagnosis of a renal tumor in a young patient with hypertension includes juxtaglomerular cell tumor, Wilms' tumor, and renal cell carcinoma, all of which may produce renin. [12]

Hypertension secondary to other renal disorders

Here, however, increased CO cannot solve the structural problems causing renal artery hypotension, with the result that CO remains chronically elevated.[ citation needed ]

Hypertension secondary to endocrine disorders

Adrenal

A variety of adrenal cortical abnormalities can cause hypertension, In primary aldosteronism there is a clear relationship between the aldosterone-induced sodium retention and the hypertension. [14]

Congenital adrenal hyperplasia, a group of autosomal recessive disorders of the enzymes responsible for steroid hormone production, can lead to secondary hypertension by creating atypically high levels of mineralocorticoid steroid hormones. These mineralocorticoids cross-react with the aldosterone receptor, activating it and raising blood pressure.[ citation needed ]

Yet another related disorder causing hypertension is glucocorticoid remediable aldosteronism, which is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient, causing of primary hyperaldosteronism, the Gene mutated will result in an aldosterone synthase that is ACTH-sensitive, which is normally not. [22] [23] [24] [25] [26] GRA appears to be the most common monogenic form of human hypertension. [27]

Compare these effects to those seen in Conn's disease, an adrenocortical tumor which causes excess release of aldosterone, [28] that leads to hypertension. [29] [30] [31]

Another adrenal related cause is Cushing's syndrome which is a disorder caused by high levels of cortisol. Cortisol is a hormone secreted by the cortex of the adrenal glands. Cushing's syndrome can be caused by taking glucocorticoid drugs, or by tumors that produce cortisol or adrenocorticotropic hormone (ACTH). [32] More than 80% of patients with Cushing's syndrome develop hypertension., [33] which is accompanied by distinct symptoms of the syndrome, such as central obesity, lipodystrophy, moon face, sweating, hirsutism and anxiety. [34]

Neuroendocrine tumors are also a well known cause of secondary hypertension. Pheochromocytoma [35] (most often located in the adrenal medulla) increases secretion of catecholamines such as epinephrine and norepinephrine, causing excessive stimulation of adrenergic receptors, which results in peripheral vasoconstriction and cardiac stimulation. This diagnosis is confirmed by demonstrating increased urinary excretion of epinephrine and norepinephrine and/or their metabolites (vanillylmandelic acid).[ citation needed ]

Other secondary hypertension

Medication side effects

Certain medications, including NSAIDs (ibuprofen/Motrin) and steroids can cause hypertension. [41] [42] [43] [44] [45] Other medications include estrogens (such as those found in oral contraceptives with high estrogenic activity), certain antidepressants (such as venlafaxine), buspirone, carbamazepine, bromocriptine, clozapine, and cyclosporine. [39] High blood pressure that is associated with the sudden withdrawal of various antihypertensive medications is called rebound hypertension. [46] [47] [48] [49] [50] [51] [52] The increases in blood pressure may result in blood pressures greater than when the medication was initiated. Depending on the severity of the increase in blood pressure, rebound hypertension may result in a hypertensive emergency. Rebound hypertension is avoided by gradually reducing the dose (also known as "dose tapering"), thereby giving the body enough time to adjust to reduction in dose. Medications commonly associated with rebound hypertension include centrally-acting antihypertensive agents, such as clonidine [53] and methyl-dopa. [52]

Other herbal or "natural products" which have been associated with hypertension include Ephedra, St John's wort, and licorice. [39]

Pregnancy

Few women of childbearing age have high blood pressure, up to 11% develop hypertension of pregnancy. [54] While generally benign, it may herald three complications of pregnancy: pre-eclampsia, HELLP syndrome and eclampsia. Follow-up and control with medication is therefore often necessary. [55] [56]

Sleep disturbances

Another common and under-recognized cause of hypertension is sleep apnea, [57] [58] which is often best treated with nocturnal nasal continuous positive airway pressure (CPAP), but other approaches include the mandibular advancement splint (MAS), UPPP, tonsillectomy, adenoidectomy, septoplasty, or weight loss. Another cause is an exceptionally rare neurological disease called Binswanger's disease, causing dementia; it is a rare form of multi-infarct dementia, and is one of the neurological syndromes associated with hypertension. [59]

Arsenic exposure

Because of the ubiquity of arsenic in ground water supplies and its effect on cardiovascular health, low dose arsenic poisoning should be inferred as a part of the pathogenesis of idiopathic hypertension. Idiopathic and essential are both somewhat synonymous with primary hypertension. Arsenic exposure has also many of the same signs of primary hypertension such as headache, somnolence, [60] confusion, proteinuria, [61] visual disturbances, and nausea and vomiting. [62]

Potassium deficiency

Due to the role of intracellular potassium in regulation of cellular pressures related to sodium, establishing potassium balance has been shown to reverse hypertension. [63]

Diagnosis

The ABCDE mnemonic can be used to help determine a secondary cause of hypertension.

Related Research Articles

<span class="mw-page-title-main">Adrenal gland</span> Endocrine gland

The adrenal glands are endocrine glands that produce a variety of hormones including adrenaline and the steroids aldosterone and cortisol. They are found above the kidneys. Each gland has an outer cortex which produces steroid hormones and an inner medulla. The adrenal cortex itself is divided into three main zones: the zona glomerulosa, the zona fasciculata and the zona reticularis.

<span class="mw-page-title-main">Adrenal cortex</span> Cortex of the adrenal gland

The adrenal cortex is the outer region and also the largest part of the adrenal gland. It is divided into three separate zones: zona glomerulosa, zona fasciculata and zona reticularis. Each zone is responsible for producing specific hormones. It is also a secondary site of androgen synthesis.

<span class="mw-page-title-main">Aldosterone</span> Mineralocorticoid steroid hormone

Aldosterone is the main mineralocorticoid steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland. It is essential for sodium conservation in the kidney, salivary glands, sweat glands, and colon. It plays a central role in the homeostatic regulation of blood pressure, plasma sodium (Na+), and potassium (K+) levels. It does so primarily by acting on the mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron. It influences the reabsorption of sodium and excretion of potassium (from and into the tubular fluids, respectively) of the kidney, thereby indirectly influencing water retention or loss, blood pressure, and blood volume. When dysregulated, aldosterone is pathogenic and contributes to the development and progression of cardiovascular and kidney disease. Aldosterone has exactly the opposite function of the atrial natriuretic hormone secreted by the heart.

<span class="mw-page-title-main">Primary aldosteronism</span> Medical condition

Primary aldosteronism (PA), also known as primary hyperaldosteronism or Conn's syndrome, refers to the excess production of the hormone aldosterone from the adrenal glands, resulting in low renin levels and high blood pressure. This abnormality is caused by hyperplasia or tumors. Many experience fatigue, potassium deficiency and high blood pressure which may cause poor vision, confusion or headaches. Symptoms may also include: muscular aches and weakness, muscle spasms, low back and flank pain from the kidneys, trembling, tingling sensations, dizziness/vertigo, nocturia and excessive urination. Complications include cardiovascular disease such as stroke, myocardial infarction, kidney failure and abnormal heart rhythms.

<span class="mw-page-title-main">Mineralocorticoid</span> Group of corticosteroids

Mineralocorticoids are a class of corticosteroids, which in turn are a class of steroid hormones. Mineralocorticoids are produced in the adrenal cortex and influence salt and water balances. The primary mineralocorticoid is aldosterone.

<span class="mw-page-title-main">Adrenal insufficiency</span> Medical condition

Adrenal insufficiency is a condition in which the adrenal glands do not produce adequate amounts of steroid hormones. The adrenal glands—also referred to as the adrenal cortex—normally secrete glucocorticoids, mineralocorticoids, and androgens. These hormones are important in regulating blood pressure, electrolytes, and metabolism as a whole. Deficiency of these hormones leads to symptoms ranging from abdominal pain, vomiting, muscle weakness and fatigue, low blood pressure, depression, mood and personality changes to organ failure and shock. Adrenal crisis may occur if a person having adrenal insufficiency experiences stresses, such as an accident, injury, surgery, or severe infection; this is a life-threatening medical condition resulting from severe deficiency of cortisol in the body. Death may quickly follow.

<span class="mw-page-title-main">Renal artery stenosis</span> Medical condition

Renal artery stenosis (RAS) is the narrowing of one or both of the renal arteries, most often caused by atherosclerosis or fibromuscular dysplasia. This narrowing of the renal artery can impede blood flow to the target kidney, resulting in renovascular hypertension – a secondary type of high blood pressure. Possible complications of renal artery stenosis are chronic kidney disease and coronary artery disease.

<span class="mw-page-title-main">Hypoaldosteronism</span> Medical condition

Hypoaldosteronism is an endocrinological disorder characterized by decreased levels of the hormone aldosterone. Similarly, isolated hypoaldosteronism is the condition of having lowered aldosterone without corresponding changes in cortisol.

11β-Hydroxysteroid dehydrogenase enzymes catalyze the conversion of inert 11 keto-products (cortisone) to active cortisol, or vice versa, thus regulating the access of glucocorticoids to the steroid receptors.

<span class="mw-page-title-main">Hyperaldosteronism</span> Hormonal disorder

Hyperaldosteronism is a medical condition wherein too much aldosterone is produced by the adrenal glands, which can lead to lowered levels of potassium in the blood (hypokalemia) and increased hydrogen ion excretion (alkalosis).

<span class="mw-page-title-main">Adrenalectomy</span> Surgical removal of adrenal glands

Adrenalectomy is the surgical removal of one or both adrenal glands. It is usually done to remove tumors of the adrenal glands that are producing excess hormones or is large in size. Adrenalectomy can also be done to remove a cancerous tumor of the adrenal glands, or cancer that has spread from another location, such as the kidney or lung. Adrenalectomy is not performed on those who have severe coagulopathy or whose heart and lungs are too weak to undergo surgery. The procedure can be performed using an open incision (laparotomy) or minimally invasive laparoscopic or robot-assisted techniques. Minimally invasive techniques are increasingly the gold standard of care due to shorter length of stay in the hospital, lower blood loss, and similar complication rates.

<span class="mw-page-title-main">Apparent mineralocorticoid excess syndrome</span> Medical condition

Apparent mineralocorticoid excess is an autosomal recessive disorder causing hypertension, hypernatremia and hypokalemia. It results from mutations in the HSD11B2 gene, which encodes the kidney isozyme of 11β-hydroxysteroid dehydrogenase type 2. In an unaffected individual, this isozyme inactivates circulating cortisol to the less active metabolite cortisone. The inactivating mutation leads to elevated local concentrations of cortisol in the aldosterone sensitive tissues like the kidney. Cortisol at high concentrations can cross-react and activate the mineralocorticoid receptor due to the non-selectivity of the receptor, leading to aldosterone-like effects in the kidney. This is what causes the hypokalemia, hypertension, and hypernatremia associated with the syndrome. Patients often present with severe hypertension and end-organ changes associated with it like left ventricular hypertrophy, retinal, renal and neurological vascular changes along with growth retardation and failure to thrive. In serum both aldosterone and renin levels are low.

<span class="mw-page-title-main">Mineralocorticoid receptor antagonist</span> Drug class

A mineralocorticoid receptor antagonist or aldosterone antagonist, is a diuretic drug which antagonizes the action of aldosterone at mineralocorticoid receptors. This group of drugs is often used as adjunctive therapy, in combination with other drugs, for the management of chronic heart failure. Spironolactone, the first member of the class, is also used in the management of hyperaldosteronism and female hirsutism. Most antimineralocorticoids, including spironolactone, are steroidal spirolactones. Finerenone is a nonsteroidal antimineralocorticoid.

<span class="mw-page-title-main">Liddle's syndrome</span> Medical condition

Liddle's syndrome, also called Liddle syndrome, is a genetic disorder inherited in an autosomal dominant manner that is characterized by early, and frequently severe, high blood pressure associated with low plasma renin activity, metabolic alkalosis, low blood potassium, and normal to low levels of aldosterone. Liddle syndrome involves abnormal kidney function, with excess reabsorption of sodium and loss of potassium from the renal tubule, and is treated with a combination of low sodium diet and potassium-sparing diuretics. It is extremely rare, with fewer than 30 pedigrees or isolated cases having been reported worldwide as of 2008.

Pseudohyperaldosteronism is a medical condition which mimics the effects of elevated aldosterone (hyperaldosteronism) by presenting with high blood pressure (hypertension), low blood potassium levels (hypokalemia), metabolic alkalosis, and low levels of plasma renin activity (PRA). However, unlike hyperaldosteronism, this conditions exhibits low or normal levels of aldosterone in the blood. Causes include genetic disorders, acquired conditions, metabolic disorders, and dietary imbalances including excessive consumption of licorice. Confirmatory diagnosis depends on the specific root cause and may involve blood tests, urine tests, or genetic testing; however, all forms of this condition exhibit abnormally low concentrations of both plasma renin activity (PRA) and plasma aldosterone concentration (PAC) which differentiates this group of conditions from other forms of secondary hypertension. Treatment is tailored to the specific cause and focuses on symptom control, blood pressure management, and avoidance of triggers.

<span class="mw-page-title-main">11-Deoxycorticosterone</span> Chemical compound

11-Deoxycorticosterone (DOC), or simply deoxycorticosterone, also known as 21-hydroxyprogesterone, as well as desoxycortone (INN), deoxycortone, and cortexone, is a steroid hormone produced by the adrenal gland that possesses mineralocorticoid activity and acts as a precursor to aldosterone. It is an active (Na+-retaining) mineralocorticoid. As its names indicate, 11-deoxycorticosterone can be understood as the 21-hydroxy-variant of progesterone or as the 11-deoxy-variant of corticosterone.

<span class="mw-page-title-main">Aldosterone synthase</span> Protein-coding gene in the species Homo sapiens

Aldosterone synthase, also called steroid 18-hydroxylase, corticosterone 18-monooxygenase or P450C18, is a steroid hydroxylase cytochrome P450 enzyme involved in the biosynthesis of the mineralocorticoid aldosterone and other steroids. The enzyme catalyzes sequential hydroxylations of the steroid angular methyl group at C18 after initial 11β-hydroxylation. It is encoded by the CYP11B2 gene in humans.

<span class="mw-page-title-main">11-Deoxycortisol</span> Chemical compound

11-Deoxycortisol, also known as cortodoxone (INN), cortexolone as well as 17α,21-dihydroxyprogesterone or 17α,21-dihydroxypregn-4-ene-3,20-dione, is an endogenous glucocorticoid steroid hormone, and a metabolic intermediate towards cortisol. It was first described by Tadeusz Reichstein in 1938 as Substance S, thus has also been referred to as Reichstein's Substance S or Compound S.

Glucocorticoid remediable aldosteronism also describable as aldosterone synthase hyperactivity, is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient.

Familial hyperaldosteronism is a group of inherited conditions in which the adrenal glands, which are small glands located on top of each kidney, produce too much of the hormone aldosterone. Excess aldosterone causes the kidneys to retain more salt than normal, which in turn increases the body's fluid levels and causes high blood pressure. People with familial hyperaldosteronism may develop severe high blood pressure, often early in life. Without treatment, hypertension increases the risk of strokes, heart attacks, and kidney failure. There are other forms of hyperaldosteronism that are not inherited.

References

  1. ↑ Ecder T, Schrier RW (April 2009). "Cardiovascular abnormalities in autosomal-dominant polycystic kidney disease". Nature Reviews Nephrology . 5 (4): 221–28. doi:10.1038/nrneph.2009.13. PMC   2720315 . PMID   19322187.
  2. ↑ Gross P (May 2008). "Polycystic kidney disease: will it become treatable?". Polskie Archiwum Medycyny Wewnȩtrznej . 118 (5): 298–301. PMID   18619180 . Retrieved 19 June 2009.
  3. ↑ Masoumi A, Reed-Gitomer B, Kelleher C, Schrier RW (2007). "Potential pharmacological interventions in polycystic kidney disease". Drugs . 67 (17): 2495–510. doi:10.2165/00003495-200767170-00004. PMID   18034588. S2CID   7041761.
  4. ↑ Chapman AB (May 2007). "Autosomal dominant polycystic kidney disease: time for a change?". Journal of the American Society of Nephrology . 18 (5): 1399–407. doi: 10.1681/ASN.2007020155 . PMID   17429048 . Retrieved 19 June 2009.
  5. ↑ Chapman AB (July 2008). "Approaches to testing new treatments in autosomal dominant polycystic kidney disease: insights from the CRISP and HALT-PKD studies". Clinical Journal of the American Society of Nephrology . 3 (4): 1197–204. doi: 10.2215/CJN.00060108 . PMID   18579674 . Retrieved 19 June 2009.
  6. ↑ Berthoux FC, Mohey H, Afiani A (January 2008). "Natural history of primary IgA nephropathy". Seminars in Nephrology . 28 (1): 4–9. doi:10.1016/j.semnephrol.2007.10.001. PMID   18222341 . Retrieved 19 June 2009.
  7. ↑ D'Cruz D (February 2009). "Renal manifestations of the antiphospholipid syndrome". Current Rheumatology Reports . 11 (1): 52–60. doi:10.1007/s11926-009-0008-2. PMID   19171112. S2CID   23082656.
  8. ↑ Licht C, Fremeaux-Bacchi V (February 2009). "Hereditary and acquired complement dysregulation in membranoproliferative glomerulonephritis". Thrombosis and Haemostasis . 101 (2): 271–78. doi:10.1160/th08-09-0575. PMID   19190809. S2CID   1436800 . Retrieved 19 June 2009.
  9. ↑ Textor SC (May 2009). "Current Approaches to Renovascular Hypertension". The Medical Clinics of North America . 93 (3): 717–32, Table of Contents. doi:10.1016/j.mcna.2009.02.012. PMC   2752469 . PMID   19427501 . Retrieved 19 June 2009.
  10. ↑ Voiculescu A, Rump LC (January 2009). "[Hypertension in patients with renal artery stenosis]". Der Internist (in German). 50 (1): 42–50. doi:10.1007/s00108-008-2198-5. PMID   19096816.
  11. ↑ Kendrick J, Chonchol M (October 2008). "Renal artery stenosis and chronic ischemic nephropathy: epidemiology and diagnosis". Advances in Chronic Kidney Disease . 15 (4): 355–62. doi:10.1053/j.ackd.2008.07.004. PMID   18805381.
  12. ↑ Méndez GP, Klock C, Nosé V (December 2008). "Juxtaglomerular Cell Tumor of the Kidney: Case Report and Differential Diagnosis With Emphasis on Pathologic and Cytopathologic Features". Int. J. Surg. Pathol. 19 (1): 93–98. doi:10.1177/1066896908329413. PMID   19098017. S2CID   38702564.
  13. ↑ Samuel J Mann (2003). "Neurogenic essential hypertension revisited: the case for increased clinical and research attention". American Journal of Hypertension . 16 (10): 881–88. doi: 10.1016/S0895-7061(03)00978-6 . PMID   14553971.
  14. ↑ Giacchetti G, Turchi F, Boscaro M, Ronconi V (April 2009). "Management of primary aldosteronism: its complications and their outcomes after treatment". Current Vascular Pharmacology . 7 (2): 244–49. doi:10.2174/157016109787455716. PMID   19356005.
  15. ↑ "C-17 Hydroxylase Deficiency: Practice Essentials, Pathophysiology, Epidemiology". Medscape. February 2018.
  16. ↑ Bailey MA, Paterson JM, Hadoke PW, et al. (January 2008). "A Switch in the Mechanism of Hypertension in the Syndrome of Apparent Mineralocorticoid Excess". Journal of the American Society of Nephrology . 19 (1): 47–58. doi:10.1681/ASN.2007040401. PMC   2391031 . PMID   18032795.
  17. ↑ Vantyghem MC, Marcelli-Tourvieille S, Defrance F, Wemeau JL (October 2007). "11beta-hydroxysteroide dehydrogenases. Recent advances". Annales d'endocrinologie (in French). 68 (5): 349–56. doi:10.1016/j.ando.2007.02.003. PMID   17368420.
  18. ↑ Atanasov AG, Ignatova ID, Nashev LG, et al. (April 2007). "Impaired protein stability of 11beta-hydroxysteroid dehydrogenase type 2: a novel mechanism of apparent mineralocorticoid excess". Journal of the American Society of Nephrology . 18 (4): 1262–70. doi: 10.1681/ASN.2006111235 . PMID   17314322 . Retrieved 19 June 2009.
  19. 1 2 Johns C (January 2009). "Glycyrrhizic acid toxicity caused by consumption of licorice candy cigars". Canadian Journal of Emergency Medical Care . 11 (1): 94–96. doi: 10.1017/s1481803500010988 . PMID   19166646.
  20. ↑ Sontia B, Mooney J, Gaudet L, Touyz RM (February 2008). "Pseudohyperaldosteronism, liquorice, and hypertension". Journal of Clinical Hypertension . 10 (2): 153–57. doi:10.1111/j.1751-7176.2008.07470.x. PMC   8109973 . PMID   18256580. S2CID   20098685.
  21. ↑ Whitworth, Judith (December 2015). "Cardiovascular Consequences of Cortisol Excess". Vasc Health Risk Manag. 1 (4): 291–99. doi: 10.2147/vhrm.2005.1.4.291 . PMC   1993964 . PMID   17315601.
  22. ↑ Escher G (April 2009). "Hyperaldosteronism in pregnancy". Therapeutic Advances in Cardiovascular Disease . 3 (2): 123–32. doi: 10.1177/1753944708100180 . PMID   19171690.
  23. ↑ Sukor N, Mulatero P, Gordon RD, et al. (August 2008). "Further evidence for linkage of familial hyperaldosteronism type II at chromosome 7p22 in Italian as well as Australian and South American families". Journal of Hypertension . 26 (8): 1577–82. doi:10.1097/HJH.0b013e3283028352. PMID   18622235. S2CID   46607812.
  24. ↑ Omura M, Nishikawa T (May 2006). "[Glucocorticoid remediable aldosteronism]". Nippon Rinsho (in Japanese). Suppl 1: 628–34. PMID   16776234.
  25. ↑ Luft FC (October 2003). "Mendelian Forms of Human Hypertension and Mechanisms of Disease". Clinical Medicine & Research . 1 (4): 291–300. doi:10.3121/cmr.1.4.291. PMC   1069058 . PMID   15931322.
  26. ↑ Nicod J, Dick B, Frey FJ, Ferrari P (February 2004). "Mutation analysis of CYP11B1 and CYP11B2 in patients with increased 18-hydroxycortisol production". Molecular and Cellular Endocrinology . 214 (1–2): 167–74. doi:10.1016/j.mce.2003.10.056. PMID   15062555. S2CID   617448.
  27. ↑ McMahon GT, Dluhy RG (2004). "Glucocorticoid-remediable aldosteronism". Cardiology in Review . 12 (1): 44–48. doi:10.1097/01.crd.0000096417.42861.ce. PMID   14667264. S2CID   2813697.
  28. ↑ Ziaja J, Cholewa K, Mazurek U, Cierpka L (2008). "[Molecular basics of aldosterone and cortisol synthesis in normal adrenals and adrenocortical adenomas]". Endokrynologia Polska (in Polish). 59 (4): 330–39. PMID   18777504.
  29. ↑ Astegiano M, Bresso F, Demarchi B, et al. (March 2005). "Association between Crohn's disease and Conn's syndrome. A report of two cases". Panminerva Medica . 47 (1): 61–4. PMID   15985978.
  30. ↑ Pereira RM, Michalkiewicz E, Sandrini F, et al. (October 2004). "[Childhood adrenocortical tumors]". Arquivos Brasileiros de Endocrinologia e Metabologia (in Portuguese). 48 (5): 651–58. doi: 10.1590/S0004-27302004000500010 . PMID   15761535.
  31. ↑ Kievit J, Haak HR (March 2000). "Diagnosis and treatment of adrenal incidentaloma. A cost-effectiveness analysis". Endocrinology and Metabolism Clinics of North America . 29 (1): 69–90, viii–ix. doi:10.1016/S0889-8529(05)70117-1. PMID   10732265.
  32. ↑ Kumar, Abbas, Fausto. Robbins and Cotran Pathologic Basis of Disease, 7th ed. Elsevier-Saunders; New York, 2005.
  33. ↑ Dodt C, Wellhöner JP, Schütt M, Sayk F (January 2009). "[Glucocorticoids and hypertension]". Der Internist (in German). 50 (1): 36–41. doi:10.1007/s00108-008-2197-6. PMID   19096817. S2CID   35266216.
  34. ↑ Yudofsky, Stuart C.; Robert E. Hales (2007). The American Psychiatric Publishing Textbook of Neuropsychiatry and Behavioral Neurosciences (5th ed.). American Psychiatric Pub, Inc. ISBN   978-1-58562-239-9.
  35. ↑ Kassim TA, Clarke DD, Mai VQ, Clyde PW, Mohamed Shakir KM (December 2008). "Catecholamine-induced cardiomyopathy". Endocrine Practice . 14 (9): 1137–49. doi:10.4158/ep.14.9.1137. PMID   19158054 . Retrieved 19 June 2009.
  36. 1 2 Rivasi, G; Menale, S; Turrin, G; Coscarelli, A; Giordano, A; Ungar, A (October 2022). "The Effects of Pain and Analgesic Medications on Blood Pressure". Current Hypertension Reports. 24 (10): 385–394. doi:10.1007/s11906-022-01205-5. PMC   9509303 . PMID   35704141.
  37. ↑ Calvi, A; Fischetti, I; Verzicco, I; Belvederi Murri, M; Zanetidou, S; Volpi, R; Coghi, P; Tedeschi, S; Amore, M; Cabassi, A (2021). "Antidepressant Drugs Effects on Blood Pressure". Frontiers in Cardiovascular Medicine. 8: 704281. doi: 10.3389/fcvm.2021.704281 . PMC   8370473 . PMID   34414219.
  38. ↑ Salerno, SM; Jackson, JL; Berbano, EP (8–22 August 2005). "Effect of oral pseudoephedrine on blood pressure and heart rate: a meta-analysis". Archives of Internal Medicine. 165 (15): 1686–94. doi:10.1001/archinte.165.15.1686. PMID   16087815.
  39. 1 2 3 Chobanian AV, et al. (2003). "The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report". JAMA . 289 (19): 2560–72. doi:10.1001/jama.289.19.2560. PMID   12748199.
  40. ↑ Varon J, Marik PE (2008). "Perioperative hypertension management". Vasc Health Risk Manag. 4 (3): 615–27. doi: 10.2147/VHRM.S2471 . PMC   2515421 . PMID   18827911.
  41. ↑ Simone Rossi, ed. (2006). Australian medicines handbook 2006. Adelaide: Australian Medicines Handbook Pty Ltd. ISBN   978-0-9757919-2-9.[ page needed ]
  42. ↑ White WB (May 2009). "Defining the problem of treating the patient with hypertension and arthritis pain". The American Journal of Medicine . 122 (5 Suppl): S3–9. doi:10.1016/j.amjmed.2009.03.002. PMID   19393824.
  43. ↑ Mackenzie IS, Rutherford D, MacDonald TM (2008). "Nitric oxide and cardiovascular effects: new insights in the role of nitric oxide for the management of osteoarthritis". Arthritis Research & Therapy . 10 (Suppl 2): S3. doi: 10.1186/ar2464 . PMC   2582806 . PMID   19007428.
  44. ↑ Berenbaum F (2008). "New horizons and perspectives in the treatment of osteoarthritis". Arthritis Research & Therapy . 10 (Suppl 2): S1. doi: 10.1186/ar2462 . PMC   2582808 . PMID   19007426.
  45. ↑ Akinbamowo AO, Salzberg DJ, Weir MR (October 2008). "Renal consequences of prostaglandin inhibition in heart failure". Heart Failure Clinics . 4 (4): 505–10. doi:10.1016/j.hfc.2008.03.002. PMID   18760760.
  46. ↑ Lowenstein J (January 1980). "Drugs five years later: clonidine". Annals of Internal Medicine . 92 (1): 74–77. doi:10.7326/0003-4819-92-1-74. PMID   6101302.
  47. ↑ Robertson JI (January 1997). "Risk factors and drugs in the treatment of hypertension". Journal of Hypertension Supplement . 15 (1): S43–6. doi:10.1097/00004872-199715011-00006. PMID   9050985. S2CID   28804593.
  48. ↑ Schachter M (August 1999). "Moxonidine: a review of safety and tolerability after seven years of clinical experience". Journal of Hypertension Supplement . 17 (3): S37–9. PMID   10489097.
  49. ↑ Schäfer SG, Kaan EC, Christen MO, Löw-Kröger A, Mest HJ, Molderings GJ (July 1995). "Why imidazoline receptor modulator in the treatment of hypertension?". Annals of the New York Academy of Sciences . 763 (1): 659–72. Bibcode:1995NYASA.763..659S. doi:10.1111/j.1749-6632.1995.tb32460.x. PMID   7677385. S2CID   9634310.
  50. ↑ Larsen R, Kleinschmidt S (April 1995). "[Controlled hypotension]". Der Anaesthesist (in German). 44 (4): 291–308. doi:10.1007/s001010050157. PMID   7785759. S2CID   46283051.
  51. ↑ Scholtysik G (March 1986). "Animal pharmacology of guanfacine". The American Journal of Cardiology . 57 (9): 13E–17E. doi:10.1016/0002-9149(86)90717-4. PMID   3006469.
  52. 1 2 Myers MG (January 1977). "New drugs in hypertension". Canadian Medical Association Journal . 116 (2): 173–76. PMC   1879000 . PMID   343894.
  53. ↑ van Zwieten PA, Thoolen MJ, Timmermans PB (1984). "The hypotensive activity and side effects of methyldopa, clonidine, and guanfacine". Hypertension. 6 (5 Pt 2): II28–33. doi: 10.1161/01.hyp.6.5_pt_2.ii28 . PMID   6094346.
  54. ↑ Kang A, Struben H (November 2008). "[Pre-eclampsia screening in first and second trimester]". Therapeutische Umschau (in German). 65 (11): 663–66. doi:10.1024/0040-5930.65.11.663. PMID   18979429.
  55. ↑ Marik PE (March 2009). "Hypertensive disorders of pregnancy". Postgraduate Medicine . 121 (2): 69–76. doi:10.3810/pgm.2009.03.1978. PMID   19332964. S2CID   207564356 . Retrieved 18 June 2009.
  56. ↑ Mounier-Vehier C, Delsart P (April 2009). "[Pregnancy-related hypertension: a cardiovascular risk situation]". Presse Médicale (in French). 38 (4): 600–08. doi:10.1016/j.lpm.2008.11.018. PMID   19250798 . Retrieved 18 June 2009.
  57. ↑ Pack AI, Gislason T (2009). "Obstructive sleep apnea and cardiovascular disease: a perspective and future directions". Progress in Cardiovascular Diseases . 51 (5): 434–51. doi:10.1016/j.pcad.2009.01.002. PMID   19249449.
  58. ↑ Silverberg DS, Iaina A, Oksenberg A (January 2002). "Treating Obstructive Sleep Apnea Improves Essential Hypertension and Quality of Life". American Family Physician. 65 (2): 229–36. PMID   11820487.
  59. ↑ Tomimoto H, Ihara M, Takahashi R, Fukuyama H (November 2008). "[Functional imaging in Binswanger's disease]". Rinsho Shinkeigaku (in Japanese). 48 (11): 947–50. doi: 10.5692/clinicalneurol.48.947 . PMID   19198127.
  60. ↑ Arsenic trioxide drugs dot com
  61. ↑ atsdr-medical management guidelines for arsenic trioxide
  62. ↑ Arsenic Author: Frances M Dyro, MD, Chief of the Neuromuscular Section, Associate Professor, Department of Neurology, New York Medical College, Westchester Medical Center
  63. ↑ Addison WL (March 1928). "The Use of Sodium Chloride, Potassium Chloride, Sodium Bromide, and Potassium Bromide in Cases of Arterial Hypertension which are Amenable to Potassium Chloride". Can Med Assoc J. 18 (3): 281–85. PMC   1710082 . PMID   20316740.
  64. ↑ Williams B, et al. (2006). "Secondary Hypertension". Hypertension Etiology & Classification - Secondary Hypertension. Armenian Medical Network. Retrieved 2 December 2007.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.