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

The effect of guancydine (1-cyano-3-tert-amylguanidine) on systemic and renal hemodynamics was studied in nine patients with arterial hypertension. Antihypertensive drugs were withheld for 15 days before beginning the investigation. Average sodium intake was 105 meq/24 hours in some patients and 25 meq/24 hours in others. Patients received placebo during a control period that averaged 14 days. Guancydine was given for 7 to 18 days at an average dose of 21 mg/kg of body weight. Although mean arterial blood pressure decreased significantly in all patients, it reached normal levels in only two. There was no change in cardiac output. Glomerular filtration rate and renal plasma flow remained unchanged, whereas urinary sodium excretion diminished, suggesting an activation of the renin-angiotensin-aldosterone system. A substantial gain in body weight was noted. Nausea, vomiting, constipation, somnolence, restlessness, mental confusion, asthenia, and urine retention were observed. The anti-angiotensin effect of guancydine that has been described in animals was not observed.
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PMID:Effect of guancydine on systemic and renal hemodynamics in arterial hypertension. 32 1

The complex hormonal action of angiotensin II in the long-term control of blood pressure or sodium metabolism, or in renal hypertension, is not completely understood. Structure-activity relations with analogues of angiotensin II gave information about the functions responsible for pressor and myotropic response in the molecule that led to the synthesis of competitive antagonists of this hormone. These antagonists, however, show variable agonist/antagonist ratios in different species or different tissues of the same species. This fact necessitates further work to induce tissue specificity. Although des-Asp1-angiotensin II ("angiotensin III") has been recognized as a hormone, its exact role in the biosynthesis of aldosterone is yet to be discovered. The antagonists such as des-Asp1-[Ile8]-angiotensin II or des-Asp1-[Thr8]-angiotensin II have provided important leads in this direction. Many of the biologic effects of angiotensin I have been attributed to its conversion to angiotensin II by the converting enzyme. Recent investigations indicate that angiotensin I itself may play a direct role; however, most of these studies were carried out by inhibiting the converting enzyme activity with peptides obtained from the venom of Bothrops jararaca. Since these peptides also potentiate bradykinin action, the observed biologic activities could be caused by either angiotensin I or bradykinin. Bsides, converting enzyme is no longer thought to be a single enzyme and its nature varies from species to species and from tissue to tissue in the same species. Renin inhibitors related to renin substrate or pepstatin are not freely soluble in plasma and are not effective under physiologic conditions. This points to the importance of renin inhibitors isolated from kidney or other natural sources. Thus, although the renin-angiotensin system appears to be an integral part of the problem of hypertension, characterization of various converting enzymes, roles of extrarenal renin, isorenin, tonin, and brain-renin, and the involvement of other humoral, neurogenic, and immunogenic factors should be pieced together to get a clear picture of the hypertension problem.
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PMID:Pathogenic factors involved in renovascular hypertension. State of the art. 32 61

Hypertension may result from excessive activity of one or more components of the blood pressure-elevating system. These include the adrenergic nervous system, the renin-angiotensin axis, and mineralocorticoids (aldosterone), which potentiate each other, reinforcing their effects on renal hemodynamics and electrolyte transport and thereby affecting extracellular fluid volume, vascular tone, and reactivity. We consider of no less importance in the genesis of hypertension the failure of one or more components of the blood pressure-lowering system: the kallikrein-kinin system, prostaglandin, or one or more lipids associated with the renomedullary interstitial cells. As a corollary of this hypothesis, if one assumes tonic activity of these opposing blood pressure-regulating systems, in the case of a deficiency of the vasodepressor system, hypertension should result. That is, unopposed activity of the pressor system should be sufficient to increase blood pressure without an increase in the "basal level" of its activity. Hypertension, then, may be considered to result from either uncompensated deficiencies or excesses, which may be relative or absolute, of one or more components of the vasodepressor and vasopressor systems.
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PMID:Role of naturally occurring vasoactive principles in hypertension. State of the art. 32 62

Renin-aldosterone profiling was used to classify patients with hypertension: 243 patients with essential hypertension were classified by renin-urinary sodium indexing; 107 were reclassified by response to administration of furosemide and intravenous saline; 45 were further classified by response to a low-sodium diet. Arbitrary "normal ranges" were determined in 89, 32, and 38 volunteers, respectively. Patients with low-renin apparently do not have "high-volume" hypertension. Rather, they show a primary renal abnormality in renin secretion and become relatively deficient in angiotensin II and aldosterone when they are subjected to diuresis. They can maintain aldosterone secretion under normal conditions because their adrenal aldosterone receptor is supersensitive to angiotensin II. No evidence of abnormal sympathetic neural activity was found among the renin subgroups. Renin-aldosterone profiling in current clinical practice seems useful mainly in the detection of patients with curable forms of secondary hypertension. Aldosterone/renin ratios may be particularly helpful in diagnosis when obtained after a patient has undergone expansion or contraction of his extracellular fluid volume.
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PMID:Renin-aldosterone profiling in hypertension. 33 42

Nine patients with aortic coarctation were studied. On the fourth day of a low diet, blood samples were obtained for plasma renin activity (PRA) at 8:00 A.M., 11:00 A.M. and 5:00 P.M. On the same day a 24 hour urinary collection was obtained for the determination of aldosterone excretion. The following day 60 mg. of furosemide were given orally at 8:00 A.M. and another blood sample was drawn at noon. This study protocol was done before and after surgical correction of the aortic lesion. Mean systolic and diastolic blood pressure decreased significantly (P less than 0.005), while mean PRA and urinary aldosterone values showed no significant modifications after surgery. With these results, it is concluded that the renin-angiotensin-aldosterone system, does not seem to play a role in the chronic hypertension of the coarctation of the aorta. However, tests with angiotensin II specific blockers have to be performed before a definite conclusion can be drawn on this point.
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PMID:[The renin angiotensin system in the pathology of arterial hypertension of aortic coarctation]. 33 12

Blood pressure (BP), plasma renin concentration (PRC), plasma aldosterone concentration (PAC) and exchangeable sodium (ES) were studied in 19 kidney recipients on different fixed levels of sodium intake after successful kidney transplantation. The following groups of kidney recipients were investigated: group 1: 7 normotensives, group 2:7 hypertensives without transplant renal artery stenosis (TRAS), group 3:5 hypertensives with angiographically verified TRAS. Hypertension in the recipients without TRAS (group 2) was characterized by a positive correlation between BP and ES and a normal response of PRC and PAC to a fixed low (10 mEQ/day) and high (150 mEq/day) sodium intake. In contrast, hypertension in the recipients with TRAS (group 3) was characterized by a normal or varyingly increased PRC on a liberal sodium intake and a reduced response of PRC to sodium restriction, whereas PAC did not differ from the other groups of recipients. In one recipient in group 3 who underwent surgical correction for TRAS, PRC and PAC decreased before operation during sodium restriction, but BP remained high until after operation, when it normalized simultaneously with a decrease in ES. The results indicate that sodium retention is involved in the pathogenesis of posttransplant hypertension and suggest that an increased activity of the renin--angiotensin system is counterbalanced by an accumulation of sodium in TRAS.
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PMID:Plasma renin, plasma aldosterone and exchangeable sodium in normotensive and hypertensive kidney transplant recipients with and without transplant renal artery stenosis. 33 73

Among 9 hypertensive recipients with kidney transplant artery stenosis (KTAS) evidence of increased activity of the renin system was present in 3. Surgical repair of KTAS in 4 recipients resulted in an increase in renal plasma flow and glomerular filtration rate associated with a decrease in exchangeable sodium and blood pressure. Peripheral plasma renin and aldosterone values were normal before and after operation in all. It is suggested that sodium retention may counterbalance increased activity of the renin system in KTAS. Preoperative determinations of plasma renin do not predict the effect of surgical repair of KTAS on hypertension.
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PMID:Kidney transplant artery stenosis. Interrelationship between blood pressure, kidney function, renin-aldosterone system and body sodium content. 34 Nov 39

Functional aspects of the renin-aldosterone axis were investigated in long-term normotensive and hypertensive renal allograft recipients. Unstimulated plasma renin and aldosterone levels were within control range in all patients and rose significantly in response to sodium depletion. However, no difference in the stimulated renin and aldosterone values between normotensive and hypertensive patients was noted. Baseline aldosterone secretory rates were elevated in all patients, but were higher in hypertensive patients than in normotensive patients. In both groups sodium depletion failed to augment this already elevated aldosterone secretion rate. Possibly, changes in the body pool and/or metabolic clearance rate of aldosterone account for elevations in plasma levels despite a relatively fixed secretory rate, though the role played by the lack of normal innervation of the kidneys cannot be ignored. It is unknown whether these observations may be causal or affected by other presently unknown or unmonitored factors. This in part may reflect unfolding problems in the understanding of nonrenal transplant hypertension.
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PMID:Studies of renin-aldosterone axis in stable normotensive and hypertensive renal allograft recipients. 34 66

Spironolactone, an aldosterone antagonist, has been found effective in the treatment of certain forms of hypertension, ascites, and edematous conditions. Since patients may receive daily doses of spironolactone for many years, it is important to determine the chronic effects on tissues. This study reviews the tissue changes in rats, dogs, and monkeys receiving spironolactone daily for up to two years. Dose levels were frequently in excess of 100 times the recommended human dose. The pituitary, adrenals, and kidneys of all animals showed no significant changes. Histologic changes were noted in rat livers, thyroid, and male internal genitalia. There were alterations in monkey testes and male mammary glands. This study found no evidence to suggest that spironolactone is tumorigenic or carcinogenic. Species differences in metabolism may account for the diversity of tissue observations.
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PMID:Effects in animals of chronic administration of spironolactone--a review. 36 67

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


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