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

The possible pathogenetic mechanisms underlying arterial hypertension with low activity of renin in blood plasma are discussed. The peculiarities of some of its forms marked by normal or increased blood plasma aldosterone content are considered. Criteria for distinguishing a subgroup of patients with hypertensive disease marked by low blood plasma renin activity and for the differentiation of patients with primary and secondary hyperaldosteronism are substantiated.
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PMID:[Pathogenesis of arterial hypertension with a low renin activity in the blood plasma]. 36 65

Kallikrein excreted with the urine appears to be formed in the kidney. The kallikrein-kinin system in the kidney is localized in the distal nephron from the juxtaglomerular apparatus to the collecting duct. It has been shown that intrarenal infusion of kinins produces an increase in renal blood flow as well as diuresis and natriuresis. Part of the effect of kinins appears to be mediated by the release of prostaglandins. However, the precise role of the renal kallikrein-kinin system in sodium and volume homeostasis and in blood pressure regulation still remains to be determined. Mineralocorticoids as well as the diuretics furosemide, bumetanide and bendroflumethiazide increase, spironolactone decreases kallikrein excretion. Urinary kallikrein has been shown to increase acid-as well as cryoactivation of prorenin in vitro. It is unclear as yet, however, whether the renal kallikrein-kinin system takes part in converting inactive prorenin into active renin in vivo. There are reports on subnormal, normal as well as increased kallikrein excretion in spontaneously hypertensive rats. In rats susceptible to the hypertensive effect of salt a substantially decreased excretion of kallikrein has been observed. Kallikrein excretion has been described to be increased in primary aldosteronism and to be reduced in a proportion of patients with established essential hypertension. In patients with labile hypertension, however, kallikrein excretion appears to be normal suggesting that decreased urinary kallikrein in essential hypertension is a consequence rather than a cause of hypertension. The renal kallikrein-kinin system does not appear to play a primary role in the pathogenesis of hypertension.
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PMID:[Renal kallikrein-kinin system and control of blood pressure (author's transl)]. 39 77

We describe the natural recovery from the aggravated hypertension, hypokalemia and suppression of the renin-aldosterone axis after the glycyrrhizin discontinuation in two mild hypertensive women aged 71 and 68 years, who had been administered 273 to 546 mg glycyrrhizin daily for 1.5 and 6 months, respectively, for the treatment of liver disease. About one month after the glycyrrhizin discontinuation, acceleration of hypertension, hypokalemia and suppression of the renin-aldosterone system still continued in both patients. At this stage, sodium restriction resulted in the normalization of blood pressure with weight loss and the subsequent sodium repletion produced a rapid increase in blood pressure to hypertensive levels observed before sodium restriction, with weight gain. Plasma renin activity and plasma aldosterone were low and did not respond to sodium restriction. Inappropriately excessive amounts of potassium were also excreted in the presence of hypokalemia. About one and a half months later, the improvements of aggravated hypertension, hypokalemia and suppressed renin-aldosterone system gradually occurred in both patients. Sodium restriction performed about three months later in case 2 no longer produced the changes in blood pressure and body weight. Plasma renin activity and plasma aldosterone responded subnormally to sodium restriction. These results demonstrate that both patients had a prolongation of the syndrome resembling primary aldosteronism except the low plasma aldosterone level about one month after the glycyrrhizin discontinuation. The possible mechanisms by which this prolongation was caused are discussed.
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PMID:Prolonged pseudoaldosteronism induced by glycyrrhizin. 39 3

The recognition of secondary causes of hypertension, such as renovascular disease and aldosteronism, can be enhanced by stimulation and suppression of the 2 limbs of the renin angiotensin system. Normal values have been established in unstimulated and stimulated conditions. Saline infusion suppresses plasma aldosterone normally. Patients with proved adenomas do no suppress renin and are outside the well established ranges of normal suppression. Likewise, furosemide will stimulate renin release. Patients with proved aldosteronism are outside the normal ranges of plasma renin activity. These maneuvers also are useful in discriminating renovascular hypertension, particularly when achieving differential renal venous collections under stimulated conditions (after furosemide and tilting). By stressing this system (with furosemide stimulation or saline suppression) one can discriminate better secondary hypertension by the failure to respond normally.
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PMID:Evaluation of patients for secondary hypertension. 39 53

Plasma concentrations of vasopressin and plasma renin activity were measured every 30 min for 24 h in 5 normal active humans, in 1 normal woman confined to bed (except for brief periods up to the bathroom), in 2 active patients with primary aldosteronism and in 1 patient with low-renin hypertension. Plasma vasopressin varied markedly over the day and night in a pattern suggesting episodic secretion of the hormone in the normal subjects. Assumption of upright posture was accompanied by a rise in plasma levels from undetectable to 20--50 pg/ml. Episodic secretion, however, also occurred during bed rest and sleep. In contrast, patients with primary aldosteronism and low-renin hypertension had plasma vasopressin levels considerably lower than the normals, and their profiles of plasma concentration lacked the peaks seen in normals. In the normals, although vasopressin and renin secretion often coincided, only 2 of 6 studies showed a significant correlation between the plasma levels of the two hormones. This study, therefore, shows that vasopressin is secreted periodically in normal humans, that upright posture is an important modulator of secretory activity and that the renin-angiotensin system may or may not influence the pattern of secretion. In addition, it underlines the necessity of recumbency in establishing the existence of a circadian rhythm of plasma vasopressin levels.
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PMID:Plasma vasopressin variation and renin activity in normal active humans. 46 6

A case of muscle weakness with hypertension is presented. The patient had symptoms of depression. Diagnosis of hyperaldosteronism was suspected because of a low serum potassium and confirmed by discovery of an adrenal adenoma. The role of hypokalemia in mental disturbances is reviewed. Emphasis is placed on possible metabolic etiologies when mood changes, muscle paresis and hypertension coexist.
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PMID:Hyperaldosteronism (Conn's disease) presenting as depression. 46 62

During a protocol study for the evaluation of patients with primary aldosteronism, a variety of diagnostic studies were employed in an attempt to identify patients with primary aldosteronism and to differentiate patients with adrenal adenoma from patients with idiopathic adrenal hyperplasia. In this study, we are able to demonstrate the utility of (1) absent postural increase in plasma aldosterone concentration, (2) adrenal scanning and (3) normalization of blood pressure with spironolactone therapy in identifying patients with primary aldosterone excess who have an adrenal adenoma, surgical removal of which results in eliminating their hypertension.
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PMID:Identification and differentiation of surgically correctable hypertension due to primary aldosteronism. 47 85

The behaviour of the renin-angiotensin-aldosterone system was evaluated in 16 acromegalic patients, of whom 7 were hypertensive. The patients were studied in basal conditions, after suppression with 9alpha-fluorohydrocortisone, and after stimulation with furosemide. Baseline and after furosemide PRA were significantly lower in acromegalic hypertensive patients than in the normotensive group. Mean urinary aldosterone excretion was found at the upper limits of the normal range; it was occasionally elevated, but the values were not satistically different in the two groups. There was a suppression after 9 alpha fluorohydrocortisone in both groups, though it did not reached the 50%. These data show that there is a disorder of the renin-angiotensin-aldosterone system in acromegalic subjects. This defective regulation is sometimes similar to that present in primary aldosteronism. In fact in two patients a typical phlebographic and scintigraphic picture of primary aldosteronism has been found; surgery, performed in both patients, revealed a large cortical adenoma in one case and a macronodular hyperplasia in the second case. However, the relationship between this adrenal abnormalities and hypertension in acromegaly are not yet completely clarified.
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PMID:Plasma renin activity and urinary aldosterone in acromegaly. 48 12

The authors discuss a reported case of primary aldosteronism, which is relatively uncommon within hypertensive population. The diagnosis of primary aldosteronism must be suggested by the presence of the association of arterial hypertension and hypokaliemia, which nevertheless is not pathognomonic. It is emphasized the significance of the detection of this syndrome on account of the correction following surgical removal of the adenoma of the adrenal cortex. Two attacks of paroxismal hypertension, which are atypical in primary aldosteronism, had been observed in the reported case; however, apart from these exceptions, arterial hypertension has resulted generally constant and of moderate degree, as well as the majority of the others descriptions. The personal experience confirms the need to determine plasma levels of renin and aldosterone before the therapeutic or diagnostic use of spironolactone.
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PMID:[A case of primary hyperaldosteronism. Case report]. 55 Jul 63

The relation of plasma dopamine beta-hydroxylase (DBH) activity to age was examined in normotensive and hypertensive subjects. Plasma DBH activity was the highest in the group of 25--34 years and gradually decreased with age. Plasma DBH activity was higher in the hypertensives than in the normotensives in all age groups, and the difference was significant between the groups of 45--54 and 55--64 years. Plasma DBH activity was increased in labile hypertension. Plasma DBH activity was higher in the group of essential hypertension with normal renal function than in that with reduced renal function. It was lower in the severe hypertensives than in the mild cases. Plasma DBH activity was also decreased in the hypertensive patients with cerebrovascular disorders. Plasma DBH activity was lower in the hypertensive patients with renal parenchymal diseases than those of essential hypertension with normal renal function. Plasma DBH activity was also decreased in primary aldosteronism, while it was increased in pheochromocytoma. These observations suggest that measurement of plasma DBH activity may be valuable in the differentiation of essential hypertension from the secondary forms of hypertension, and the evaluation of the hypertensive processes. To evaluate plasma DBH activity, it is important to consider its age-related changes.
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PMID:The evaluation of plasma dopamine beta-hydroxylase activity in essential and secondary hypertension. 57 40


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