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

In 16 normal subjects, in 29 patients with essential hypertension and in 25 patients with renal hypertension plasma renin activity was measured together with pulse rate and blood pressure under resting conditions and 15 minutes after the intravenous administration of 5 mg d-1-propranolol subsequently. Basal plasma renin activity (PRA) was correlated significantly to resting pulse rate in normal subjects and in patients with benign essential hypertension but not in patients with renal hypertension from chronic parenchymatous renal disease. In the normal subjects and in the patients with essential hypertension the decrease of not stimulated "basal" PRA 15 minutes after the administration of 5 mg d-1- propranolol was closely ralated to the initial plasma renin activity. In contrast, in the patients with well established renal hypertension the decrease of PRA was generally less pronounced or absent. Whereas in normal subjects as well as in patients with essentail hypertension in the sympathetic nervous system appears to be the major determinant for basal renin release, other factors, possibly the renal baroreceptors, may determine basal renin release in renal hypertension. This difference could possibley provide the basis for a simple biochemical test to differentiate between essential and renal hypertension.
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PMID:[Different reaction of plasma renin activity after propranolol in essential and renal hypertension]. 117 7

Twenty-four conscious male Wistar rats with hypertension induced by left renal artery clipping (two-kidney hypertension) were infused intravenously with 1-Sar-8-Ala-angiotensin II a competitive angiotensin II antagonist. The spectrum of responses was wide, ranging from a mild elevation in blood pressure to a marked fall in blood pressure, despite effective and specific angiotensin blockade in all cases. The change in blood pressure during 1-Sar-8-Ala-AII infusion activity showed a significant correlation with the level of plasma renin prevailing immediately before the infusion (r = - 0.78, P less than 0.01) but not with the prevailing blood urea level (r = 0.27, 0.1 greater than P greater than 0.05), the drgree of hypertension (r = 0.42, 0.1 greater than P greater than 0.05), or the time since clipping (r = 0.02, P greater than 0.05). There was no significant correlation between the degree of hypertension and the plasma renin activity (r = 0.42, 0.1 greater than P greater than 0.05). In rats with blood pressure drops greater than 20 mm Hg in response to 1-Sar-8-Ala-AII, the final blood pressure level was still above the normotensive range. Excision of the clipped kidney reduced blood pressure to normal or to near normal within 24 hours in all of the rats tested. It is concluded that the degree of dependence of renal hypertension on the renin-angiotensin system is directly related to the increase in circulating angiotensin itself and not to an increase in sensitivity to angiotensin. Other factors appear to be involved in renal clip hypertension in addition to circulating renin and angiotensin, especially when the measured activity of plasma renin is normal.
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PMID:Effect of the angiotensin II blocker 1-Sar-8-Ala-angiotensin II on renal artery clip hypertension in the rat. 119 61

In rats with unilateral renal artery stenosis, the malignant phase of hypertension is characterized by: systolic blood pressure above 180-190 mm Hg; sodium and water loss; polyuria and polydipsia; markedly activated renin-angiotensin-aldosterone system; impairment of renal function and malignant nephrosclerosis in the contralateral kidney; some rats exhibit signs of cerebral hemorrhage, heart failure, acute renal failure, and some rats die. After such a phase of malignant hypertension, a period of remission may occur, which is followed by another malignant phase, etc. When malignant hypertensive rats are offered, in addition to water, saline as drinking fluid, they compulsively drink the saline, BP falls transiently, and all signs of malignant hypertension nearly or completely disappear. These observations indicate that, at a critically high BP level, it is salt and water loss which, by activating the renin-angiotensin system, trigger the vicious circle of malignant renal hypertension in rats.
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PMID:Pathogenesis of malignant hypertension: experimental evidence from the renal hypertensive rat. 119 18

Cardiac output, total peripheral vascular resistance, renal, extrarenal, forearm muscle and skin hemodynamics and an indicator of the splanchic vascular resistance were estimated in 20 subjects with chronic renal disease without signs of chronic renal failure and without anemia. The data were compared with a group of subjects with essential hypertension. The high blood pressure of chronic renal disease of mild or moderate severity was maintained in the first place by a high cardiac output, this being due to a rise of the stroke volume, while the heart rate was only slightly increased. The total peripheral vascular resistance was within the normal range in most of the subjects. The vascular resistance in the skin was slightly raised, that in the splanchnic area and muscle unchanged in renal hypertension. The possible pathogenic mechanisms are considered.
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PMID:General and regional hemodynamics in hypertension in chronic renal disease. 119 19

Renal hypertension can usually be recognized only by examining all the features of the hypertensive illness. On the other hand, the investigation of a case of hypertension whose genesis was previously unclear can lead to the diagnosis of a hitherto unrecognized renal disease. The blood pressure values found in patients with renal hypertension are of widely differing degrees of severity. Slight rises in blood pressure (e.g. 140/90 mm Hg), can be a sign of renal disease in adolescent patients. 10-15% of the cases of chronic renal hypertension develop into malignant hypertension. High diastolic values above 120 mm Hg without renal symptomatology and without reduced renal function speak against a primary renal cause of the rise in blood pressure. The finding of hypertension developing during the course of renal disease is, with respect to the hypertensive cardiovascular complications, just as important as in the case of essential hypertension. Complications which can occur during renal hypertension include cardiac insufficiency, hypertensive encephalopathy, retinopathy, hypertensive crises and acceleration of the renal disease.
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PMID:The clinical picture of renal hypertension. 119 21

The bioelectrical activity of the aortic nerve was studied in normal rabbits and in those with experimentally induced hypertension. Electroneurograms of the aortic nerve of rabbits with renal and coarctational (stenosis of the abdominal aorta) hypertension demonstrated the same burst-like activity synchronous with the systolic contractions of the heart that was noted in normotensive animals. The threshold of the transit of the burst-like activity of the aortic nerve into the uniform one in cases of acutely elevated arterial pressure (induced by injections of noradrenalin and angiotensin) and the threshold of the disappearance of the mentioned activity after an acute reduction of the arterial pressure (induced by injections of acetylcholine, tetra-ethylammonium or by acute bleeding) in rabbits with renal and coarctational hypertension are shifted upwards, as compared to those in normotensive rabbits. It is the more true of the former threshold. The depressor reaction to the administration of the ganglionic blocker -- tetra-ethyl-ammonium -- in renal hypertension during the initial 2 months of the disease remains unchanged, with the exception of the 4th and 8th weeks, when it is elevated. It is concluded that the baroreceptors of the aortic arch percept the chronically elevated arterial pressure as a normal one reacting adequately to its acute changes in either direction. Thanks to this the barorecptors of the aortic arch strive to maintain a high level of the arterial pressure and provide for a stabilization of hypertension.
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PMID:[Functional state of baroreceptors of the aortic arch in experimental hypertension]. 119 46

The main haemodynamic indices were studied in rabbits of two age groups (young -- 10--12 month, and old -- 3--4 years) under normal conditions and those with experimentally induced renal hypertension. Significant changes were observed in the proportion of the main parameters of haemodynamics -- cardiac output per 1 min and total peripheral resistance -- in the presence of persistent arterial hypertension, which permitted to single out three haemodynamic forms of experimentally induced renal hypertension. The first and second haemodynamic forms are characterized by a sharp enhancement of the total peripheral resistance and diverse changes in the values of cardiac output per 1 min.: the third haemodynamic form is predmoninatly characterized by an elevation of the cardiac output. The compensatory hyper-function of the myocardium in the first and second forms of renal hypertension develops usually isometrically, in the third form -- according to the mixed variant.
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PMID:[Peculiarities of cardiac activity in renal form of experimental hypertension with different hemodynamic characteristics]. 119 49

The effect of renal hypertension on dry defatted tissue mass and lipid accumulation in different segments of the aortic intima was studied in both normally-fed and cholesterol-fed rabbits. In normally-fed rabbits hypertension caused an increase in intimal dry weight in the aorta. The increase was greatest in the lower thoracic intimal segment but was not significant in the aortic arch. The increase in tissue mass was not influenced by the addition of cholesterol to the diet and no regression of the increased tissue mass occurred when a 4-week period of hypertension was followed by a 4-week period of normotension. Hypertension did not increase the intimal cholesterol or phospholipid concentrations in normally-fed rabbits, suggesting that an observed increase in lipid content represented the cellular component of the intimal hypertrophy. Hypertension in cholesterol-fed animals caused preferential lipid accumulation in the lower thoracic segment, an effect that was independent of the total intimal cholesterol level. Intimal cholesterol, cholesterol ester and phospholipid were all increased. When a 4-week period of normotension and cholesterol feeding was preceded by a 4-week period of hypertension with normal feeding the amount of cholesterol deposited did not exceed that of the normotensive control, suggesting either that hypertension increased intimal permeability to lipid only in the presence of hypercholesterolaemia, or that healing of damaged intima had occurred before hypercholesterolaemia was fully established.
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PMID:The effect of renal hypertension on the regional deposition of cholesterol and phospholipid in the aorta of normally- and cholesterol-fed rabbits. 120 Nov 50

Experimental studies on 22 hypertonic rats which had previously one kidney removed show that the deviation of the renal vein blood into the portal vein through a cavorportal or splenoportal anastomosis does not result in a lowering of the experimentally induced renovascular hypertension. These anastomoses did not alter the blood pressure in 3 normotonic rats. The prophylactic use of these anastomoses could not prevent the development of experimental renal hypertension in 2 of 3 test animals.
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PMID:[Blood-pressure behavior in rats following the diversion of renal-vein blood into the portal vein]. 120 77

Continuing interest in the mechanism of hypertension have produced considerable new information on the underlying pathophysiologic processes involved. Elucidation of the role of renal malperfusion, the renin-angiotensin-aldosterone mechanism, and renal medullary antihypertensive substances continues to clarify our understanding of renal hypertension. Current evidence suggests that angiotensin can produce hypertension by a direct effect on peripheral blood vessels in malignant hypertension and in renin-secreting renal tumors and by an intrarenal mechanism influencing intrarenal distribution of blood flow, and, thereby, sodium resorption in chronic renovascular hypertension. The current diagnostic techniques used to determine the presence of renal atery stenosis and its functional significance are reviewed. Arteriographic evidence of renal artery collaterals and a positive differential venous renin ratio are the two parameters whose usefulness and practicality have been best documented in recent years. The results of surgical procedures reported in the world literature show a 50 per cent rate with a further 30 per cent improvement rate in terms of control of hypertension. When functional significance of stenosis is demonstrated before surgical procedures, cure rates of the order of 80 per cent can be achieved. Recent developments of technique of operating room upon less extensive lesions of the renal artery branch extend the possibilities of surgical benefit which should also be considered in the presence of renal failure of renovascular origin.
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PMID:Renal hypertension. 120 80


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