scholarly journals RENAL HYPERTENSION IN RATS IMMUNIZED AGAINST ANGIOTENSIN I AND ANGIOTENSIN II

1974 ◽  
Vol 139 (2) ◽  
pp. 239-248 ◽  
Author(s):  
Helen F. Oates ◽  
Gordon S. Stokes ◽  
Brian G. Storey ◽  
Robyn G. Glover ◽  
Beverley F. Snow
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Mechanism Of Action ◽  
Renal Hypertension ◽  
Hypertensive Rats ◽  
Angiotensin I ◽  
Receptor Sites ◽  
Significant Difference ◽  
Blood Pressures ◽  
Renal Artery Constriction

Rats, actively immunized against angiotensin I (AI) and angiotensin II (AII), were subjected to unilateral renal artery constriction to determine whether the resulting hypertension, which may still ensue in the animal immunized against AII, could be prevented by such combined immunity. Sustained immunity to both AI and AII neither changed preoperative blood pressures of the rats from those of control mock-immunized rats nor altered the incidence or severity of renal dip hypertension. Vascular hyperresponsiveness to small quantities of free angiotensin could not be invoked to explain the hypertension, for there was no significant difference between mock-immunized hypertensive animals, and those remaining normotensive, regarding pressor sensitivity to intravenous AI, AII, renin, and norepinephrine. (AI + AII)-immunized hypertensive rats required AI doses averaging 260 times greater than nonimmune hypertensives to elicit equipressor responses, and were refractory to renin, but not to norepinephrine. Thus, while previous studies have not excluded direct participation of endogenous AI in renal clip hypertension in rats, evidence from our experiments makes it extremely difficult to sustain any pressor function therein for circulating AI or AII. Our results also preclude involvement of AII produced from circulating AI by conversion within arteriolar walls, close to receptor sites, since AI immunity would block this mechanism of action.

Paper chromatographic identification of angiotensins

1964 ◽  
Vol 207 (4) ◽  
pp. 759-763 ◽  
Author(s):  
Paul E. Wisenbaugh ◽  
Noah E. Wills ◽  
Robert W. Hill
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Paper Chromatography ◽  
Renal Hypertension ◽  
Nacl Solution ◽  
Angiotensin I ◽  
Experimental Renal Hypertension ◽  
Renal Artery Constriction

The separation of angiotensin I and angiotensin II by paper chromatography using an acid NaCl solution is described. When the pressor material recovered from the blood of dogs infused with renin was analyzed by this method, significant quantities of angiotensin I as well as angiotensin II were found in those infused at rates above 1 Goldblatt U/min. At infusion rates below 1 U/min, only angiotensin II was present. In each of six dogs with malignant experimental renal hypertension, significant increases in circulating pressor material were found 48 hr or more after renal artery constriction. Analysis of the material recovered from the blood of five of these dogs revealed only angiotensin II in four instances, and a mixture of angiotensin I and II in one instance.

Inactivation of Bradykinin and Angiotensin I Conversion in Conscious Rats with Two-Kidney, One-Clip Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 199s-201s ◽  
Author(s):  
Inge E. K. Trindade ◽  
Eduardo M. Krieger
Keyword(s):  
Enzyme Activity ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Renal Artery ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Hypertensive Rats ◽  
Angiotensin I ◽  
Parallel Increase

1. The extents of pulmonary degradation of bradykinin (BK) and angiotensin I (ANG I) to angiotensin II (ANG II) conversion were measured simultaneously to determine whether converting enzyme activity, in vivo, is altered in two-kidney, one-clip hypertensive rats (15, 60 and 180 days after renal artery clipping). 2. Inactivation of BK (estimated by comparing equipressor doses injected intravenously and intra-aortically) was markedly increased in these hypertensive rats: 98.5% (15 days), 98.4% (60 days) and 99.5% (180 days) vs 95.6% in control rats. All groups of hypertensive rats exhibited hyper-reactivity to intra-aortic BK, requiring doses 14–38 times smaller than the control rats to produce the same depressor response. 3. The percentage of ANG I conversion (calculated from equipressor doses of ANG I and ANG II injected intravenously) was elevated after 15 days (46.0% vs 28.1% in control rats), unchanged after 60 days (27.7%) and slightly elevated after 180 days (36.0%). Hyporeactivity to ANG II was observed 15 and 180 days after renal artery clipping (doses six times were needed to produce a standard increase in mean arterial pressure). No alterations were found in the rats at 60 days after artery clipping. 4. The increased degradation of BK cannot be explained solely by elevation of converting enzyme activity since no parallel increase in ANG I conversion was observed, indicating that other bradykininases in the lung may be involved.

Salt and water balance and renin activity in renal hypertension of rats

1975 ◽  
Vol 228 (6) ◽  
pp. 1847-1855 ◽  
Author(s):  
J Mohring ◽  
B Mohring ◽  
H-J Naumann ◽  
A Philippi ◽  
E Homsy ◽  
...  
Keyword(s):  
Water Balance ◽  
Renal Artery ◽  
Renal Hypertension ◽  
The Body ◽  
Renin Activity ◽  
Sodium Balance ◽  
Sprague Dawley ◽  
Contralateral Kidney ◽  
Salt And Water Balance ◽  
Renal Artery Constriction

In male Sprague-Dawley rats, renal artery constriction in the presence of an inact contralateral kidney induced sodium retention (for 2-3 wk), moderate potassium loss,elevation of blood volume (BV), and an increase in water turnover. It is suggestedthat renal artery constriction activates the renin-angiotensin-aldosterone system, resulting in disordered regulation of salt and water balance and in blood pressure (BP) elevation. Subsequently, sodium balance was reestablished in one group of hypertensive rats. The previously retained sodium was kept in the body, and BV and reninactivity remained elevated. In a second group of animals, a malignant course of hypertension developed: BP surpassed a critical level of about 180 mmHg; sodium, potassium, and water were lost; BV declined; renin activity was further stimulated; and in the contralateral kidney malignant nephrosclerosis occurred. It is assumed that pressure diuresis and natriuresis induce a vicious circle: the increasing renin activity may maintain or further increase BP level, therby inducing further salt and water loss, etc.; high BP levels and high renin activities induce vascular damage and deterioration of renal function.

Chemical Renal Medullectomy; Effect upon Reversal of Two-Kidney, One-Clip Hypertension in the Rat

1981 ◽  
Vol 61 (s7) ◽  
pp. 335s-338s ◽  
Author(s):  
R. F. Bing ◽  
G. I. Russell ◽  
J. D. Swales ◽  
H. Thurston ◽  
A. Fletcher
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Urine Volume ◽  
Renal Medulla ◽  
Plasma Renin ◽  
Left Renal Artery ◽  
Hypertensive Rats ◽  
Plasma Renin Concentration ◽  
Complete Reversal ◽  
Renal Artery Constriction

1. Chemical renal medullectomy was produced in rats by injection of 2-bromoethylamine hydrobromide. Plasma creatinine and blood pressure were unchanged although urine volume was increased fourfold. 2. Left renal artery constriction resulted in similar degrees of hypertension in both intact and medullectomized rats. This was associated with a significantly smaller rise in plasma renin concentration in the latter. 3. Blood pressure in conscious intact hypertensive rats became normal within 24 h of unclipping whereas blood pressure of medullectomized rats remained significantly elevated. 4. The presence of an intact renal medulla is essential to the complete reversal of two-kidney, one-clip hypertension in the rat. This may reflect the loss of a medullary vasodepressor system.

Snakes and Hypertension

2017 ◽  
Vol 126 (2) ◽  
pp. 321-324
Author(s):  
Edward D. Miller
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Perfusion Pressure ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Renal Perfusion Pressure ◽  
Renal Artery Constriction

Abstract Inhibition of Angiotensin Conversion in Experimental Renovascular Hypertension. By Miller ED Jr, Samuels A, Haber E, and Barger AC. Science 1972; 177:1108–9. Reprinted with permission from AAAS. Constriction of the renal artery and controlled reduction of renal perfusion pressure is followed by a prompt increase in systemic renin activity and a concomitant rise in blood pressure in trained, unanesthetized dogs. The elevated blood pressure induced by the renal artery stenosis can be prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro, which blocks conversion of angiotensin I to angiotensin II. Further, the nonapeptide can restore systemic pressure to normal in the early phase of renovascular hypertension. These results offer strong evidence that the renin– angiotensin system is responsible for the initiation of hypertension in the unilaterally nephrectomized dog with renal artery constriction.

scholarly journals O‐GlcNAc Transferase (OGT) Inhibition Does Not Improve Renal Artery Function in Male Angiotensin II Hypertensive Rats

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Christine Spring Rigsby ◽  
Victor V Lima ◽  
R Clinton Webb ◽  
Rita C Tostes
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Hypertensive Rats ◽  
Glcnac Transferase

Role of angiotensin II in experimental renal hypertension in the rabbit

1975 ◽  
Vol 228 (1) ◽  
pp. 11-16 ◽  
Author(s):  
JA Johnson ◽  
JO Davis ◽  
B Braverman
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renal Artery ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Control Group ◽  
Left Renal Artery ◽  
Chronic Hypertension ◽  
Group Of Seven

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.

Comparative Pharmacology of New Specific Angiotensin Antagonists

1974 ◽  
Vol 48 (s2) ◽  
pp. 19s-21s
Author(s):  
B. A. Schoelkens
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Pressure Response ◽  
Renal Hypertension ◽  
Antagonistic Activity ◽  
Conscious Rats ◽  
Blood Pressures ◽  
Colon Ascendens

1. The angiotensin II antagonism by newly synthesized 8-C-phenylglycine analogues of [5-isoleucine]angiotensin II in different preparations was investigated in vitro and in vivo. 2. All analogues competitively inhibited the myotropic effect of angiotensin II on the isolated colon ascendens of the guinea-pig and the stomach of the rat. 3. In normotensive dogs, cats, rabbits, guinea-pigs and rats the blood pressure response to infused angiotensin II was inhibited by the antagonists. The angiotensin II-induced fall in renal blood flow in the dog was blocked during infusion of the analogues. Acute renal hypertension in rats was significantly decreased. Of conscious rats variously with normal blood pressures, spontaneous hypertension and chronic renal hypertension, only in the last group could a marked uniform fall in blood pressure be demonstrated. The central pressor effect of angiotensin II was also inhibited in conscious rats. 4. 8-C-Phenylglycine analogues of [5-isoleucine]-angiotensin II exhibit a specific antagonistic activity to endogenous and exogenous angiotensin II.

Faecal Sodium/Potassium Ratio and Aldosteronism in Experimental Hypertension in the Rat

1972 ◽  
Vol 43 (4) ◽  
pp. 577-581 ◽  
Author(s):  
J. D. Swales ◽  
H. Thurston ◽  
F. P. Queiroz ◽  
J. D. Tange
Keyword(s):  
Renal Artery ◽  
Experimental Hypertension ◽  
Sham Operation ◽  
Normal Kidney ◽  
Sodium Depletion ◽  
Hypertensive Rats ◽  
Aldosterone Secretion ◽  
Sodium Potassium ◽  
Renal Artery Constriction

1. Renal artery constriction and sham operation produced a temporary fall in the faecal sodium/potassium (Na/K) ratio of rats. When contralateral nephrectomy had been performed, the ratio rose to normal with the development of hypertension. With an intact opposite kidney the ratio remained low, but was elevated by spironolactone. With or without contralateral nephrectomy, the ratio was normal in chronically hypertensive animals (>28 days). 2. Balance studies showed sodium depletion in hypertensive rats with a normal kidney in situ. It is suggested that this stimulates aldosterone secretion and the faecal electrolyte changes.

Enhanced diurnal variation of blood pressure in the renal hypertensive rat: effect of angiotensin II suppression

1987 ◽  
Vol 73 (3) ◽  
pp. 271-275 ◽  
Author(s):  
E. C. H. Wallace ◽  
A. J. Balmforth ◽  
J. J. Morton
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Diurnal Rhythm ◽  
Blood Pressure Variability ◽  
Renal Hypertension ◽  
Hypertensive Rats ◽  
Computer Data ◽  
Renal Hypertensive Rat ◽  
Collecting System

1. Chronic two-kidney, one-clip hypertensive rats were infused with captopril for 5 days and the daily variability of blood pressure compared with that for both hypertensive rats infused with glucose and normotensive animals. 2. Blood pressure was measured continuously using a computer data collecting system. 3. Normotensive animals showed a stable level of arterial pressure throughout each 24 h period with troughs occurring when they slept during the daytime. 4. Hypertensive animals given glucose had an enhanced diurnal rhythm of blood pressure compared with normotensive rats, with peaks occurring during periods of activity at night as well as troughs when they slept during the day. 5. Hypertensive rats given captopril retained this enhanced pressure variability, in spite of the fact that blood pressure was significantly lower and angiotensin II was suppressed. 6. These results suggest that angiotensin II is not involved in the increased blood pressure variability of renal hypertension and that some other irreversible mechanism is responsible.

Sign in / Sign up

Export Citation Format

Share Document