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

The production of renal hypertension by single renal artery constriction in pregnant sheep decreases uteroplacental blood flow. This decrease in uteroplacental perfusion persits for 7-10 days and then returns to normal control levels despite the persistence of hypertension. During hypertension the uteroplacental vascular bed is dependent upon the elevated arterial pressure for perfusion. Therefore, a pharmacologic lowering of this perfusion pressure may reduce uteroplacental blood flow. Antihypertensive agents whose major effect is the lower vascular resistance will tend to reduce uteroplacental blood flow, while those agents which increase cardiac output in addition to lowering the vascular resistance, will tend to maintain or increase uterine blood flow. Of the specific agents tested, hydralazine, which has a positive inotropic and chronotropic effect on the heart, was the only one that consistently increased uteroplacental blood flow. Blockade of these beta-mimetic effects resulted in a fall in uterine blood flow as the perfusion pressure was reduced.
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PMID:Uteroplacental hemodynamic response to antihypertensive drugs in hypertensive pregnant sheep. 100 48

1. The effect of chronic administration of propranolol on the development and maintenance of severe renal hypertension in rats subjected to unilateral renal artery constriction was studied in relation to possible changes in peripheral PRA and the blood and tissue levels of propranolol. Propranolol was administered s.c. twice daily in doses of 1, 10 and 25 mg/kg, starting 2 days before operation. 2. Contrary to expectations, not only did the initial rise in systolic blood pressure become accelerated, but the established level of hypertension attained in the propranolol treated rats was of the same severity as that attained in placebo treated rats. Moreover, the progressive rise in peripheral plasma renin activity following unilateral renal artery constriction was not affected by propranolol administration. 3. The same doses of propranolol were also administered daily for 8 days to rats with established severe hypertension. A slight further rise in blood pressure occurred initially, followed by a moderate decrease of 15-25 mmHg. Propranolol failed to exert this minor hypotensive effect in hypertensive rats treated concomitantly with furosemide. No suppressive effect on the markedly increased levels of plasma renin activity was observed in these severely hypertensive rats in the presence or absence of furosemide administration. 4. These results indicate that in severely renal hypertensive rats propranolol has only a minor hypotensive effect and no blocking action on renin release under the conditions of study.
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PMID:Effects of propranolol on development and maintanance of severe renal hypertension in rats. 100 94

Peripheral plasma renin activity (PRA), vena cava and renal veins PRA were measured in 85 patients; arterial PRA was also measured in several cases. 25 patients had essential hypertension or primary aldosteronism; whereas in 60 patients renal or renovascular abnormalities were present. Peripheral PRA was elevated in 17/30 patients with parenchimal or excretory tract diseases. The following ratios came from the results of vena cava, and renal veins PRA were calculated: Ra/Rc and Rc/P according to Stockigt et al. and V-A/A according to Vaughan et al. The ratios were calculated only when v. cava PRA was greater than 4 ng/ml/3 hrs. A good correlation was found between v. cava can arterial PRA. Among the 60 cases with renal hypertension, 26 underwent either revascularization or nephrectomy surgery. Eleven of the 15 patients operated on for renovascular diseases showed a significant reduction of blood pressure (greater than 30 mmHg); all had high peripheral PRA and 6 had significant Ra/Rc and Rc/P (respectively greater than or equal to 1,5 and less than or equal to 1,3). The same patients also had V-A/A of the affected kidney greater than or equal to 0,48 and 5 also V-A/A of the controlateral kidney less than or equal to 0,23, both values being significant for a unilateral renin secretion and controlateral suppression. Among the 4 patients who were unsuccessfully operated on, only 2 had elevated peripheral PRA and 1 had Ra/Rc and Va-A/A greater than normal, but not significant values of Rc/P and Vc-A/A. 11 patients with small kidney or other forms underwent surgery; among the 6 cases with satisfactory results, 5 had high peripheral PRA, 2 showed significant ratios Ra/Rc and 3 a significant V-A/A for both kidneys. Only 1 of the patients not cured by surgery had supernormal peripheral PRA and none had any significant ratio. Therefore both methods for elaborating data obtained from the measurement of PRA in renal veins seem to offer similar prognostic indications. The finding of significant ratios is an almost sure criterium for predicting a surgical cure of renal hypertension, whereas the cases where we may expect a failure present ratios which are not significant. However, patients of the latter group may sometimes have successful results at surgery too, which demonstrates that other mechanisms may also be involved in the pathogenesis of this form of hypertension.
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PMID:[Plasma renin activity in renal veins in different types of arterial hypertension (author's transl)]. 101 Feb 16

The effect of saralasin in lowering blood pressure and plasma aldosterone concentration in normal subjects, both sodium-replete and sodium-deplete, and in patients with various forms of hypertension, is closely related to the basal plasma angiotensin II concentration. These findings confirm and extend earlier studies of angiotensin II/arterial pressure and angiotensin II/aldosterone dose-response curves. They also emphasize the importance of the renin-angiotensin system in the control of aldosterone in sodium depletion and in renal hypertension.
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PMID:The effects of the angiotensin II antagonist saralasin on blood pressure and plasma aldosterone in man in relation to the prevailing plasma angiotensin II concentration. 101 66

The dependence of renal hypertension on increased levels of angiotensin II was investigated in conscious dogs at various stages of hypertension of four different types. Two of the most potent angiotensin inhibitors, Sar1-Ile8- and Sar1-Thr8-angiotensin II, were infused separately in various doses and at different times throughout the evolution of renal hypertension. The results of these experiments are consistent with the view that the renin-angiotensin system may participate in the acute and malignant phases of renal hypertension; they do not provide evidence for its participation when hypertension enters the chronic phase.
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PMID:Effects of angiotensin antagonists in various forms of experimental arterial hypertension. 101 72

Tests conducted on anesthetized rats with experimental renal hypertension demonstrated that octadine, reserpine and methyl-DOPA with their one-time administration produce at the onset of the maximal hypotensine effect of fall of the arterial pressure at the expense of the lowered total peripheral resistance. Most characteristic of the action exercised by these drugs is an increased fraction of the cardiac ejection going to the gestro-intestinal tract. In hypertension all the substances under study reduce the coronary and splenic fractions of the cardiac ejection. Reserpine and methyl-DOPA do not change, while octadine reduces the fraction of the cardiac ejection that goes to the kidney.
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PMID:[Effect of reserpine, octadine and methyldopa on the distribution of cardiac output in hypertension]. 102 83

1. In 20 of 20 patients (100%) with borderline hypertension Visken normalized the labile blood pressure. The high renin values after stimulation due to orthostasis and saluresis decreased significantly (p less than 0,01). 2. In 3 of 12 patients (25%) with hyporeninemic essential hypertension Visken alone normalized the blood pressure. The low renin values increased to the normal range. 3. In 4 of 18 patients (22%) with normoreninemic essential hypertension Visken normalized the blood pressure. The normal renin values showed a decreasing tendency within the normal range. 4. In 4 of 10 patients (40%) with hyperreninemic essential hypertension Visken normalized the high blood pressure. In 3 of these patients renin decreased distinctly. 5. In 4 of 20 patients (20%) with renal hypertension a therapy with Visken alone normalized the blood pressure. In 3 patients the high renin values decreased to the normal range. 6. In the most other patients of the groups II to V the additional therapy with diuretics and reserpine normalized the blood pressure. In these cases the renin values showed different reactions corresponding to the different effects of betablocking agents, saluretics or reserpine on the plasma renin activity [7]. 7. It is interesting, that Visken not only suppresses high renin values (borderline hypertension [6], hyperreninemic essential hypertension), but also increases low renin values to the normal range in patients with hyporeninemic essential hypertension. Because in essential hypertension the high blood pressure per se may be responsible for the renin suppression [3,4], this increase of renin activity is possibly the consequence of blood pressure reduction, while the decrease of renin activity after Visken may be the cause of blood pressure reduction.
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PMID:[Effect of pindolol (Visken) on blood pressure and plasma renin activity in various forms of hypertension]. 103 71

The peripheral arterial blood vessels in the cerebrum of 36 experimental animals and 9 controls were studied by electron microscopy. In 5 rats of these renal hypertension was produced (the animals were sacrificed 3 to 15 days following the second operation). 24 animals were treated with depot angiotensin (0.02 to 2.5 mg/daily) for 3 hr up to 40 days, and 7 rats were neurotized for 1 to 41/2 months. The alterations of the cerebral vessels were distinctly different within these 3 models already in the early reactions. Thus, even in the first 14 days of the experiment with renal and angiotensinogenic hypertension alterations were observed that did never occur in the neurotized rats. There were always observed disturbances in permeability of the cerebral vessels, but they were never followed by such heavy wall insudations as usually noticed in the splanchnic vessels. The less frequent occurrence of hemorrhages and malacic processes in the rat brain is ascribed aside from the physiological properties of the brain supply, to genetic factors and the absence of arteriosclerotic burden to the vascular wall in the non-dietetically pretreated experimental animals.
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PMID:Ultrastructural investigation of peripheral arterial vessels in the cortex of rats with experimental hypertension. 103 81

In hypertensive patients with unilateral renal artery stenosis, intravenous diazoide increased renal vein renin activity more on the involved side than on the contralateral side, whereas, in a group with predominantly unilateral renal parenchymal disease, the increase in renal vein was similar for both kidneys. In patients with bilateral renal artery stenosis, the use of diazoxide was helpful in lateralizing the dominant ischaemic lesion. Diazoide administration appears to be a safe, rapid and convenient method of increasing the sensitivity of the renal vein renin test used in predicting the outcome of surgical treatment of renovascular hypertension. Bilateral renal vein renin determination of established value in the diagnosis of functional renal ischaemia. 1-4 However, in the use of this procedure to predict the efficacy of corrective surgery, false positive and false negative results still occur. Thus, various manoeuvres which stimulate renin release have been employed to improve the sensitivity of the test. 5-7 We report a new application the practical approach to of this procedure in the diagnosis of renal hypertension, which both basal and stimulated levels of renal venous renin activitity can be measured during a brief period of bilateral renal vein catherization.
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PMID:Diazoxide-induced renin release in diagnosis of remediable renovascular hypertension. 106 96

1. Sodium-deficient diet failed to alter development and maintenance of severe renal hypertension produced in the rat by ligation of the aorta between the renal arteries. 2. High sodium diet did not alter the early phase of this hypertension, but significantly decreased blood pressure elevation in the late phases. 3. The decrease in blood pressure produced by high sodium intake does not appear to be mediated by renin suppression. 4. Frusemide effectively reduced blood pressure and renin at all phases.
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PMID:Salt, frusemide and renin in severe experimental renal hypertension. 107 87


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