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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diuretics act primarily by blocking reabsorption of sodium at four major sites in the nephron. Clinically useful agents that block sodium reabsorption effectively in the proximal tubule are lacking. Furosemide (Lasix), ethacrynic acid (Edecrin), and possibly organomercurial agents are effective in the ascending limb of Henle's loop. Thiazides are the major agents acting in the early distal tubule. In the late distal tubule and collecting duct, spironolactone (Aldactone) and triamterene (Dyrenium) are useful, especially in combination with diuretics which act more proximally. In treating edematous states, initial therapy with thiazides is effective in most patients who do not exhibit moderate or severe renal insufficiency, severe hyperaldosteronism with excessive distal reabsorption of sodium in exchange for potassium, or excessive sodium reabsorption in the proximal tubule or ascending limb. Nonedematous states in which diuretic therapy is useful include hypertension, hypercalcemia, hypercalciuria, diabetes insipidus, and acute renal failure.
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PMID:Diuretic agents. Mechanisms of action and clinical uses. 126 95

The syndrome of primary aldosteronism is caused either by an aldosterone-producing adenoma or by idiopathic bilateral adrenal hyperplasia. Hypokalemic hypertension is the leading symptome of the disease. Diagnosis is by the combination of abnormally high and non-suppressible aldosterone values with undetectable or low renin values unresponsive to postural changes or salt restriction. Patients with aldosterone-producing adenoma normally show a fall in plasma aldosterone in response to posture and ACTH-dependent circadian rhythm of aldosterone, whereas bilateral hyperplasia is characterized by postural increases in plasma aldosterone and an ACTH-independent diurnal aldosterone rhythm. These creteria serve to differentiate between adenoma and hyperplasia. An aldosterone-producing adenoma can be localized by veinography, determination of aldosterone concentration in both adrenal veins and by 131I-cholesterol scintigraphy. In our hands the determination of aldosterone in blood from both adrenal veins is the most efficient procedure. In interpreting the results, however, rhythmic and sudden changes in adrenal hormone secretion should be considered. In cases where no adrenal venous blood is obtained, 131I-cholesterol scintigraphy may be used to localize adenoma. In patients with aldosterone-producing adenomas unilateral adrenalectomy should be performed, whereas patients with idiopathic bilateral hyperplasia should receive antihypertensive therapy. As rare instances of primary aldosteronism, a case of aldosterone-producing carcinoma of the adrenal cortex and a case of presumably unilateral adrenal hyperplasia are reported.
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PMID:[Primary aldosteronism]. 126 63

In a 31-year old woman with a six year history of headache and hypertension a diagnosis of primary aldosteronism was made on the basis of urine samples containing 45 mug/day of aldosterone. The preoperative systemic blood pressure was 240 mm Hg systolic and 120 mm Hg diastolic. The serum potassium level was 2.6 mEq/L and other laboratory findings were within normal limits. The patient was to undergo operation. Pre-medication consisted of oral pentobarbitone, intramuscular pethidine and atropine. For induction of anaesthesia, enflurane 2.0-2.5% maximum was given with O2 (21/min) and N2O (61/min); no intravenous agents were used. Suxamethonium chloride 40 mg was administered to facilitate endotracheal intubation. Anaesthesia was maintained with enflurane 1.5-2.0% with 50% N2O and O2. Tubocurarine 27 mg was given for muscle relaxation. When the tumour was manipulated, systemic arterial blood pressure was elevated again to 190 mm Hg systolic and 120 mm Hg diastolic. After removal of the tumour, the arterial pressure and heart rate were stable and recovery from anaesthesia was without circulatory or respiratory complications. Plasma aldosterone levels reached a maximum when the tumour was manipulated and fell to normal levels on the second post-operative day. Cortisol levels were not altered markedly even when the tumour was handled. These data imply that adrenocortical response to enflurane anaesthesia as jadged by plasma aldosterone levels would be different from that as estimated by plasma cortisol levels.
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PMID:Enflurane anaesthesia for removal of aldosterone producing adenoma. 126 18

L-Arginine, the precursor of endothelium-derived relaxing factor (EDRF)/nitric oxide (NO), was administered intravenously in five patients with essential hypertension, one with renovascular hypertension, one with primary aldosteronism, and one with Cushing's syndrome. During the administration, the mean arterial pressure decreased concomitantly with an elevation of cardiac output and a fall in total peripheral resistance in all cases. Indicators of NO release in vivo such as plasma concentrations of L-citrulline and urinary excretion of nitrite/nitrate increased simultaneously during the administration. These results suggest that exogenous L-arginine can produce a vasodilatory effect via stimulating NO release in hypertensives.
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PMID:L-arginine as an antihypertensive agent. 128 68

Angiotensin-converting enzyme (ACE) inhibitors act by lowering the level of angiotensin II. The therapeutic benefits of these drugs and their potential side-effects therefore result from suppression of the physiological effects of angiotensin II. It is rational to prescribe an ACE inhibitor when the renin-angiotensin system is activated, as in renin-dependent essential hypertension, malignant hypertension and hypertension associated with heart failure. The beneficial effects of ACE inhibitor must be weighed against the special risks of renovascular hypertension: risk of renal artery thrombosis in case of unilateral stenosis and risk of renal failure if the stenosis is bilateral or affects a solitary kidney. In some situations the renin-angiotensin system is not directly involved in hypertension but may play a local haemodynamic role, as in some cases of primary or diabetic nephropathy. In such case the ACE inhibitors are thought to exert a protective effect. ACE inhibitors were reputed to be less effective in the elderly than in younger patients, but we now know that they can be prescribed with equal success in both instances to reduce peripheral resistance and improve regional blood flow as well as arterial compliance. Finally, ACE inhibitors can be prescribed, albeit with limited effectiveness, when the renin-angiotensin system is not activated, as in low renin hypertension and idiopathic hyperaldosteronism due to adrenal hyperplasia. They are ineffective in case of Conn's adenoma and contra-indicated in pregnant women.
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PMID:[For which hypertensive patient should angiotensin-converting enzyme inhibitor be prescribed or forbidden?]. 129 38

In this work we describe a case of Conn's syndrome caused by a suprarenal adenoma in a sixty-one year female. The patient had come to our observation because of severe hypertension and hypokalemia. Primary aldosteronism resulting from the secretion of excessive amounts of aldosterone caused by autonomous hyperfunction of the adrenal cortex usually by a solitary adenoma. In most series of unselected patients, it is found in fewer than 0.5% of hypertensives. In our study we demonstrated the circadian changes of arterial blood pressure but we failed to demonstrate the presence of hypertrophic cardiomyopathy as recently emphasized in the literature. Regardless of its rarity, primary aldosteronism is a fascinating disease, protean in its manifestations, logical in its pathophysiology.
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PMID:[Arterial hypertension secondary to Conn's disease: an infrequent pathology in nephrology. Report of a clinical case]. 130 Apr 65

Left ventricular hypertrophy is a major risk factor associated with the appearance of adverse cardiovascular events. A distortion in myocardial structure, mediated by an abnormal accumulation of fibrillar collagen within the adventitia of intramyocardial coronary arteries and neighbouring interstitial spaces, alters the electrical and mechanical behaviour of the myocardium. The mechanisms responsible for the regulation of cardiac myocyte growth and collagen accumulation are therefore of considerable interest. Herein we review results of in vivo studies conducted in the authors' laboratory that addressed these issues in various experimental models. The findings indicate that in arterial hypertension myocardial hypertrophy is related to ventricular systolic pressure work. Myocardial fibrosis, on the other hand, is not related to haemodynamic workload, but rather the presence of mineralocorticoid excess relative to sodium intake and excretion. Accordingly, fibrosis can appear in both the hypertensive left and non-hypertensive right ventricles. Pharmacological probes, administered in variable doses, were used to further test and support this hypothesis. In both primary and secondary hyperaldosteronism, it was possible to prevent the pathological structural remodelling of the myocardium with an aldosterone receptor antagonist, while in unilateral renal ischaemia ACE inhibition was similarly cardioprotective. Other studies demonstrated that it was feasible to regress the fibrous tissue response and normalise diastolic stiffness. This concept of cardioreparation suggests that heart failure due to this type of structural remodelling may be reversible.
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PMID:Regulatory mechanisms of myocardial hypertrophy and fibrosis: results of in vivo studies. 130 Dec 54

Patients with glucocorticoid-remediable aldosteronism (GRA) from 12 kindreds possess chimaeric gene duplications arising from unequal crossing-over, fusing regulatory sequences of steroid 11 beta-hydroxylase to coding sequences of aldosterone synthase. These chimaeric genes are specific for GRA and explain the biochemistry, physiology and genetics of this form of hypertension. Sites of crossing over range from intron 2 to intron 4. Most mutations have arisen independently from either sister or non-sister chromatid exchange between these genes, which are only 45 kilobases apart. The possibility of a susceptibility allele for GRA of Irish origin is suggested. These findings indicate the utility of a direct genetic test for this disorder.
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PMID:Hereditary hypertension caused by chimaeric gene duplications and ectopic expression of aldosterone synthase. 130 53

Twenty-eight patients with primary aldosteronism were treated from 1974 to 1990. The serum potassium concentration was higher than normal level in all patients with the exception of one whose serum potassium concentration was normal. All of 14 tested patients had low renin values. The plasma aldosterone concentration was higher than standard value in all of 5 patients, and the A/PRA ratio was more than 400. Spironolactone administered preoperatively could not only normalize serum potassium concentration level and blood pressure, but also predict postoperative prognosis of hypertension. Only 37.5% of adenomas were detected by retroperitoneal pneumography with tomography in the early period. 80.0% of adenomas were found by B-ultrasonography, and 92.8% by CT after 1982. The operation was done through abdominal incision because of indefinite localization of adenoma before 1982, and the operation was performed through lumbar incision because of definite localization of adenoma after 1982.
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PMID:[Diagnosis and treatment of primary aldosteronism]. 130 99

A case of primary aldosteronism treated with spironolactone therapy has been followed up for 24 years. This is probably the longest case of spironolactone therapy for primary aldosteronism that has ever been reported. Long-term treatment with spironolactone controlled the hypertension and prevented hypokalemic alkalosis in this patient, without any deleterious effects on steroid biosynthesis. Based on data obtained during dose reduction and subsequent withdrawal of spironolactone, it is suggested that the suppressed plasma renin activity associated with adenoma-induced aldosteronism develops prior to hypokalemia and hypertension.
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PMID:Twenty-four year spironolactone therapy in an aged patient with aldosterone-producing adenoma. 131 94


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