Role of renin in the pathogenesis of renal hypertension.

1975 ◽  
Vol 36 (6) ◽  
pp. 187-193 ◽  
Author(s):  
O P Gulati ◽  
O A Carretero ◽  
N B Oza ◽  
L A Fernandez ◽  
A Schork
Keyword(s):  
1960 ◽  
Vol XXXIV (III) ◽  
pp. 411-429 ◽  
Author(s):  
Melvin J. Fregly ◽  
Kenneth M. Cook

ABSTRACT The anti-thyroid drugs, thiouracil, propylthiouracil, and methimazole, prevented both development of elevated blood pressure and cardiac hypertrophy usually accompanying kidney encapsulation with latex envelopes. These drugs also reduced elevated blood pressure of rats with hypertension of 13 to 40 weeks' duration prior to drug administration. Addition of desiccated thyroid powder to diet containing an anti-thyroid drug overcame the anti-hypertensive effect of the latter. Withdrawal of thyroid powder only was followed by return of blood pressure to previous low level within 3 weeks. The results suggest that the anti-hypertensive effect of these drugs is related directly to the hypothyroidism produced rather than to extrathyroidal effects of the drugs. Comparison of potencies of the 3 drugs in terms of anti-hypertensive effect, inhibition of growth rate, increase in testicular size, and increase in thyroid size suggests that propylthiouracil and methimazole are equally potent per unit weight of drug. Thiouracil has approximately half the potency of the other two.


1957 ◽  
Vol 188 (2) ◽  
pp. 371-374 ◽  
Author(s):  
Sol Rothman ◽  
Douglas R. Drury

The blood pressure responses to various drugs were investigated in renal hypertensive, cerebral hypertensive and normotensive rabbits. Hexamethonium bromide and Dibenamine reduced the blood pressures of renal and cerebral hypertensives. Effects in the normal were insignificant. The cerebral hypertensive's blood pressure was slightly affected by benzodioxane. Blood pressure was not reduced at all in the other groups. Blood pressure of the renal hypertensive rabbit was greatly reduced by Veriloid and dihydroergocornine. Blood pressures of cerebral and normal animals were affected to a lesser degree. The results suggest that maintenance of hypertension in the cerebral hypertensive rabbit depends on an overactive sympathetic nervous system, possibly due to the release of medullary pressor centers from inhibitory impulses originating in higher centers; whereas, the maintenance of hypertension in the renal hypertensive rabbit may be attributed to an increased reactivity of the peripheral vasculature to a normal sympathetic tone.


2018 ◽  
Vol 5 ◽  
Author(s):  
Yusuke Sata ◽  
Geoffrey A. Head ◽  
Kate Denton ◽  
Clive N. May ◽  
Markus P. Schlaich

1983 ◽  
Vol 245 (4) ◽  
pp. H683-H689 ◽  
Author(s):  
J. R. Haywood ◽  
G. D. Fink ◽  
J. Buggy ◽  
S. Boutelle ◽  
A. K. Johnson ◽  
...  

This study examined the role of the anteroventral third ventricle (AV3V) in the renin-dependent two-kidney, one-clip model of renal hypertension. AV3V lesion and sham lesion rats were subjected to the placement of a clip on one renal artery or a sham operation. The sham lesion-renal artery clip rats experienced an increase in systolic blood pressure; however, AV3V lesioned animals experienced only a transient rise in arterial pressure during the 1st wk after clip. Body fluid regulation studies during the course of the hypertension revealed that there were no differences in water intake and urine volume between the lesion- and sham lesion-renal artery clip animals. Although significantly greater plasma and blood volumes were demonstrated in the AV3V lesion-sham clip rats compared with sham lesion animals, no differences in vascular volumes were detected in the renal artery clip rats. Finally, the rats were water deprived for 3 days to maximally stimulate vasopressin release. Urine osmolality increased significantly in all groups of rats except the AV3V lesion-renal artery clip animals protected against the hypertension.


1983 ◽  
Vol 64 (3) ◽  
pp. 355-358 ◽  
Author(s):  
Ricardo Exequiel Chatelain

1. To determine the possible role of arterial cyclic AMP in the pathogenesis of hypertensive vascular hypertrophy and hyperplasia, the changes in the level of this nucleotide were studied during the development of renal hypertension in rats with aortic ligation between the renal arteries. 2. A twofold increase in the cyclic AMP level of the thoracic aorta was observed in 9-day hypertensive rats when compared with sham-operated controls. At this time the total amounts of DNA and collagen were unchanged, although a marked increase in arterial fibrous protein was already present. 3. Arterial cyclic AMP remained significantly elevated in the thoracic aorta of 30-day hypertensive animals. At this time the hypertensive vascular alterations had reached completion as shown by the abnormal accumulation of collagen, DNA and non-fibrous protein. 4. Contrary to the events taking place in the thoracic aorta, a marked decrease in cyclic AMP was present in the abdominal portion, which was protected from high blood pressure by the aortic ligature. in this segment decreased cyclic AMP coexisted with an unchanged collagen content and a diminution in the contents of DNA and non-fibrous protein. 5. Thus a marked increase in arterial cyclic AMP precedes the initiation of DNA replication and collagen accumulation in vascular territories subjected to high blood pressure. These studies suggest the participation of this nucleotide in the vascular growth induced by hypertension.


1975 ◽  
Vol 228 (1) ◽  
pp. 11-16 ◽  
Author(s):  
JA Johnson ◽  
JO Davis ◽  
B Braverman

Hypertension was produced in rabbits by constricting the left renal artery; in nine rabbits the opposite kidney was removed and in eight rabbits the opposite kidney was left intact. To investigate the role of angiotensin II (A-II), 1-sarcosine-8-alanine angiotensin II, a competitive antagonist of A-II, was infused at 6 mug/min per kg body wt for 30 min. In a control group of seven unilaterally nephrectomized rabbits mean arterial pressure averaged 81 mmHg and infusion of the A-II antagonist did not alter the arterial pressure. In a group of Na-depleted rabbits, arterial pressure decreased from 81 to 63 mmHg (P less than 0.01) in response to the A-II analogue. Thirty days after renal artery constriction, seven of the nine one-kidney hypertensive rabbits had normal values for plasma renin activity (PRA) and during infusion of the A-II antagonist arterial pressure was unchanged. However, two rabbits had elevated PRA and the arterial pressure decreased during infusion of the angiotension analogue. In the two-kidney hypertensive rabbits, PRA was normal and arterial pressure was unchanged by infusion of the A-II antagonist. These studies provide evidence that hypertension developed with either a high or normal A-II plasma level in the one-kidney animals; the two-kidney rabbits developed chronic hypertension in which no role for A-II could be demonstrated.


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