scholarly journals GENETIC INFLUENCE ON THE DEVELOPMENT OF RENAL HYPERTENSION IN PARABIOTIC RATS

1969 ◽  
Vol 129 (3) ◽  
pp. 507-522 ◽  
Author(s):  
J. Iwai ◽  
K. D. Knudsen ◽  
L. K. Dahl ◽  
M. Heine ◽  
G. Leitl
Keyword(s):  
Renal Artery ◽  
Renal Hypertension ◽  
Renin Angiotensin System ◽  
Renal Tissue ◽  
Experimental Hypertension ◽  
Angiotensin System ◽  
Induced Hypertension ◽  
Salt Hypertension ◽  
Genetically Determined ◽  
Renal Artery Constriction

The effects of several renal manipulations including uninephrectomy, unilateral renal artery constriction, and a combination of these two (Goldblatt procedure) were studied in two strains of rats with opposite constitutional predispositions to experimental hypertension. The protective value of intact renal tissue to protect against hypertension was shown to be genetically determined. The Goldblatt procedure carried out on only one member of a parabiotic pair induced hypertension in this operated rat but significant hypertension developed in the intact partner only when the operated animal belonged to the strain predisposed to hypertension. It was speculated that there were qualitative differences in the pressor signals of the two strains of rats. In the strain genetically predisposed to hypertension there are at least two pressor principles: (a) one which is common to both strains, not transmittable via the parabiosis junction and presumably related to the renin-angiotensin system; and (b) a second which is specific for the hypertension-prone strain and can be transmitted through the parabiosis junction. This transmittable agent is probably identical with the factor that produces salt hypertension and is associated with the salt-excreting mechanism.

Inhibition of angiotensin conversion and prevention of renal hypertension

1975 ◽  
Vol 228 (2) ◽  
pp. 448-453 ◽  
Author(s):  
Miller ED ◽  
AI Samuels ◽  
E Haber ◽  
AC Barger
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Renal Hypertension ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin System ◽  
The One ◽  
Renal Artery Constriction

Renal artery constriction in the unilaterally nephrectomized, trained dog, with maintained renal arterial hypotension, produces a prompt increase in systemic renin activity and blood pressure. The hypertension normally induced by renal artery stenosis is prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro (SQ 20, 881), which blocks conversion of angiotensin I to angiotensin II. Constant intravenous infusion of the inhibitor over several days of renal artery constriction prevents the development of chronic renovascular hypertension. Furthermore, a single injection of the nonapeptide restores blood pressure to normal in the early phase of renovascular hypertension, but becomes progressively less effective as salt and water retention occurs in the chronic stage when plasma renin activity returns to control levels. These data provide strong evidence that the renin-angiotensin system is responsible for the initiation of renovascular hypertension in the one-kidney Goldblatt dog, but that other factors become increasingly important in chronic renovascular hypertension.

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.

The Pressor Role of Angiotensin in Salt Deprivation and Renal Hypertension in Rats

1974 ◽  
Vol 48 (s2) ◽  
pp. 45s-48s
Author(s):  
T. G. Coleman ◽  
A. C. Guyton
Keyword(s):  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Enzyme Inhibitor ◽  
Renal Hypertension ◽  
Peripheral Resistance ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renal Artery Constriction ◽  
Normotensive Control

1. Angiotensin may influence arterial pressure either by direct vasoconstriction or by more slowly developing effects on thirst and renal function. The importance of direct vasoconstriction was estimated in rats during salt deprivation and renal hypertension by observing the fall in blood pressure that immediately followed injection of converting-enzyme inhibitor. 2. Chronically salt-deprived rats had normal arterial pressure, cardiac output and total peripheral resistance before inhibition. However, inhibiting the formation of angiotensin II caused marked decreases in arterial pressure (−47 mmHg) and total peripheral resistance (−30%). 3. Animals made hypertensive by renal artery constriction showed large decreases in arterial pressure when angiotensin formation was inhibited only during the first few days after constriction. In the chronic, benign phase of hypertension, animals with both clamp plus contralateral nephrectomy and with unilateral clamp only, showed decreases in pressure after inhibition (−12 to 16 mmHg) that were only slightly greater than decreases observed in normotensive control animals. 4. These results indicate that total peripheral resistance and the activity of the renin-angiotensin system can change separately. In salt deprivation, even though an increased fraction of resistance was due to angiotensin, total peripheral resistance was normal. In chronic renal hypertension, total resistance was undoubtedly elevated, but only partially because of the vasoconstrictor effect of angiotensin.

Generation of Angiotensin II at Peripheral Vascular Level: Studies Using Angiotensin II Antisera

1973 ◽  
Vol 45 (5) ◽  
pp. 691-700 ◽  
Author(s):  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Angiotensin Ii ◽  
Renal Hypertension ◽  
Renin Angiotensin System ◽  
Sodium Balance ◽  
High Salt Diet ◽  
Angiotensin System ◽  
Salt Diet ◽  
High Doses ◽  
Renal Artery Constriction ◽  
Local Generation

1. When the renin-angiotensin system of rats had been suppressed by a high salt diet or by bilateral nephrectomy, large doses of angiotensin II antiserum were required to block the pressor action of exogenous angiotensin II. Infusion of renin profoundly lowered the blocking requirement of such animals. 2. It is postulated that renin bound to blood vessels generates angiotensin locally which is taken up by vascular receptors. Where such receptors are left unoccupied and free to bind exogenous angiotensin, high doses of blocking antisera are required. 3. Animals with hypertension produced by renal artery constriction with contralateral nephrectomy were shown to be in positive sodium balance. Nevertheless their blocking requirement was low. 4. It is suggested that the local generation of angiotensin may play a role in the production of renal hypertension and that this accounts for the development of hypertension even in animals immunized against angiotensin.

Insulin-Induced Hypertension in Rats Depends on an Intact Renin-Angiotensin System

Hypertension ◽  
1997 ◽  
Vol 29 (4) ◽  
pp. 1014-1019 ◽  
Author(s):  
Michael W. Brands ◽  
David L. Harrison ◽  
Henry L. Keen ◽  
Angela Gardner ◽  
Eugene W. Shek ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Induced Hypertension

Renal–adrenal interrelationships in experimental hypertension

1968 ◽  
Vol 46 (2) ◽  
pp. 179-188 ◽  
Author(s):  
D. Ostrovsky ◽  
F. R. Papsin ◽  
A. G. Gornall
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Renal Artery ◽  
High Blood Pressure ◽  
Salt Intake ◽  
Renal Tissue ◽  
Experimental Hypertension ◽  
Normal Blood Pressure ◽  
Renal Hypertrophy ◽  
High Salt Intake

For several weeks after partial constriction of one renal artery, the fate of this "clipped" kidney seems to exert a determining influence on blood pressure. Rats that remained hypertensive throughout the experiment almost invariably had clipped kidneys averaging 0.16 to 0.22% of body weight. Below 0.1%, this kidney was usually quite atrophic, and its presence was consistent with falling or normal blood pressure. The untouched kidney in such rats was, on the average, heavier in the hypertensive than in the normotensive animals. Since the latter also had less renal tissue on the clipped side, it appears that factors leading to high blood pressure stimulated hypertrophy beyond the level provoked by renoprival factors. In rats on a high salt intake, 5 μg/day of D-aldosterone for 3 months stimulated significant true renal hypertrophy in the absence of a rise in blood pressure. Such hypertrophy was more pronounced in similar rats that had been getting 250 μg DOCA/day for 3 months but were also normotensive. Rats that developed hypertension on this latter regimen had still heavier kidneys. Renal hypertrophy appears to be a prehypertensive phenomenon which persists and can become even more pronounced in hypertension. The highest levels of renal hypertrophy were usually associated with significant adrenal hypertrophy. Endocrine functions may be involved in renal hypertrophy. This concept is discussed in relation to a phospholipid "renin inhibitor" recently isolated from dog and hog kidneys.

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.

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