The Role of Plasma and Renal Renin in the Rise in Blood Pressure Following Unilateral Renal Artery Constriction

1982 ◽  
Vol 5 (5) ◽  
pp. 235-244
Author(s):  
Jeffrey Atkinson ◽  
Ernst J. Kirchertz ◽  
Lise Peters-Haefeli ◽  
Pierrette Lüthi
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Renal Artery Constriction

Pathogenesis of Arterial Hypertension after the Constriction of the Renal Artery Leaving the opposite Kidney Intact Both in the Anaesthetized and in the Conscious Dog

1972 ◽  
Vol 42 (6) ◽  
pp. 651-664 ◽  
Author(s):  
G. Bianchi ◽  
E. Baldoli ◽  
R. Lucca ◽  
P. Barbin
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Plasma Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Conscious Dogs ◽  
Plasma Renin Concentration ◽  
Renal Artery Constriction

1. The renal artery was constricted leaving the opposite kidney intact in ten conscious and seven anaesthetized dogs. Intravenous infusion of exogenous renin was done in seven conscious dogs; in four of these the renal artery was constricted 15–17 days later. The following variables were measured in all animals before and after renal artery constriction: plasma renin concentration, blood pressure, cumulative sodium balance, plasma volume, extracellular fluid volume and plasma non-protein nitrogen. Before and after renal artery constriction in the conscious dogs cardiac output, stroke volume, total peripheral resistance and cardiac rate were also measured. In a few dogs angiotensin responsiveness and plasma concentration of renin substrate were also measured. 2. There was no significant difference between the regression of change in blood pressure on change in plasma renin concentration within 2 h from renal artery constriction in the conscious dogs and that observed during intravenous infusion of renin. Comparing the changes of these variables with the ones previously obtained with renal artery constriction to the lone remaining kidney, for a given increase of plasma renin concentration the rise of blood pressure was lower when the contralateral kidney was untouched. The changes of the other variables in the conscious dogs may be divided into three phases: a first phase lasting hours, in which, besides the changes described above, there was an increase of total peripheral resistance while the other variables remain unchanged: a second phase, 24 h after constriction, in which blood pressure, total peripheral resistance and plasma renin clearance decreased while plasma volume, cardiac output and extracellular fluid volume slightly increased; however, only the plasma volume change was statistically significant: and a third phase 6–7 days after constriction, when all the variables returned towards normal values, except that the blood pressure and total peripheral resistance remained significantly higher. Sodium balance remained at equilibrium throughout the study period. It is suggested that these results are compatible with the ‘autoregulation theory’ of renal hypertension. 3. Renal artery constriction in the anaesthetized animals caused a slight but significant sodium retention that very likely influenced the sequence of the events. On the second day after constriction, the plasma renin concentration was significantly increased, whereas the highest values of blood pressure, plasma volume and extracellular fluid volume occurred on the seventh day after constriction.

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.

Experimental hypertension in pregnant sheep

1960 ◽  
Vol 199 (4) ◽  
pp. 633-636 ◽  
Author(s):  
Louis W. Holm ◽  
Yale J. Katz ◽  
Harold R. Parker ◽  
Leon C. Chesley ◽  
Nicholas S. Assali
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Severe Hypertension ◽  
Renal Arteries ◽  
Renal Ischemia ◽  
Experimental Hypertension ◽  
Control Blood Pressure ◽  
Human Hypertension ◽  
Pregnant Sheep ◽  
Renal Artery Constriction

Sheep with spontaneously occurring or experimentally induced toxemia of pregnancy do not develop hypertension despite the presence of a marked renal ischemia. The present study was undertaken in order to investigate whether pregnant sheep, like pregnant dogs and rats, do not exhibit hypertension when subjected to renal artery constriction. Bilateral constriction of the renal arteries was performed on pregnant ewes by a modified Goldblatt-Wakerlin technique, after control blood pressure had been recorded for several days. Blood pressure and BUN were measured throughout pregnancy and following delivery. All the animals which had renal artery constriction developed severe hypertension with retinal changes similar to those of human hypertension. The pregnancy did not affect the course of the hypertension nor did the hypertension alter the course of pregnancy.

scholarly journals Role of endothelin and prostaglandins in radiocontrast-induced renal artery constriction

1993 ◽  
Vol 44 (6) ◽  
pp. 1217-1223 ◽  
Author(s):  
Lloyd G. Cantley ◽  
Katherine Spokes ◽  
Barbara Clark ◽  
Ellen G. McMahon ◽  
Jeffrey Carter ◽  
...  
Keyword(s):  
Renal Artery ◽  
Renal Artery Constriction

Blood pressure response to chronic episodic hypoxia: role of the sympathetic nervous system

1997 ◽  
Vol 83 (1) ◽  
pp. 95-101 ◽  
Author(s):  
Gang Bao ◽  
Naira Metreveli ◽  
Rena Li ◽  
Addison Taylor ◽  
Eugene C. Fletcher
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Renal Artery ◽  
Adrenal Medulla ◽  
Blood Pressure Response ◽  
Episodic Hypoxia ◽  
Sympathetic Nervous ◽  
Renal Artery Denervation

Bao, Gang, Naira Metreveli, Rena Li, Addison Taylor, and Eugene C. Fletcher. Blood pressure response to chronic episodic hypoxia: role of the sympathetic nervous system. J. Appl. Physiol. 83(1): 95–101, 1997.—Previous studies in several strains of rats have demonstrated that 35 consecutive days of recurrent episodic hypoxia (7 h/day) cause an 8- to 13-mmHg persistent increase in diurnal systemic blood pressure (BP). Carotid chemoreceptors and the sympathetic nervous system have been shown to be necessary for development of this BP increase. The present study was undertaken to further define the role of renal artery sympathetic nerves and the adrenal medulla in this BP increase. Male Sprague-Dawley rats had either adrenal medullectomy, bilateral renal artery denervation, or sham surgery. Rats from each of these groups were subjected to episodic hypoxia for 35 days. Control groups received either compressed air or were left unhandled. Adrenal demedullation or renal artery denervation eliminated the chronic diurnal mean BP response (measured intra-arterially) to episodic hypoxia, whereas sham-operated controls continued to showed persistent elevation of systemic BP. Plasma and renal tissue catecholamine levels at the end of the experiment confirmed successful adrenal demedullation or renal denervation in the respective animals. The chronic episodic hypoxia-mediated increase in diurnal BP requires both intact renal artery nerves as well as an intact adrenal medulla.

Changes of Plasma and Cerebrospinal Fluid Noradrenaline during Frusemide Administration and Acute Renal Artery Constriction in Dogs

1982 ◽  
Vol 63 (s8) ◽  
pp. 343s-345s ◽  
Author(s):  
Yoshiaki Masuyama ◽  
Yuji Ueno ◽  
Mikio Arita ◽  
Hidetoshi Suruda ◽  
Osamu Mohara
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Renal Artery ◽  
Arterial Blood Pressure ◽  
Plasma Noradrenaline ◽  
Direct Role ◽  
Arterial Blood ◽  
Renal Artery Constriction

1. The effects of circulating angiotensin II on cerebrospinal fluid and plasma noradrenaline during frusemide administration and acute renal artery constriction were studied in dogs. 2. The administration of frusemide produced significant increases in cerebrospinal fluid and plasma noradrenaline. Intravertebral artery infusion of [Sar1, Ala8]angiotensin II (saralasin) significantly suppressed the frusemide-induced increases in cerebrospinal and plasma noradrenaline and resulted in a fall in arterial blood pressure. 3. Acute renal artery constriction produced the marked elevation of plasma noradrenaline and arterial blood pressure, although no significant increase was found in cerebrospinal fluid noradrenaline. Though intravertebral artery infusion of saralasin did not affect cerebrospinal fluid and plasma noradrenaline, intravenous infusion of saralasin reduced the increases in arterial blood pressure and plasma noradrenaline induced by acute renal artery constriction. 4. Plasma volume was significantly reduced by frusemide administration, but unchanged by acute renal artery constriction. 5. Therefore it is suggested that circulating angiotensin II may contribute to the regulation of blood pressure at least partially by acting on the central nervous system in the sodium- and volume-depleted states. However, the renin-angiotensin system appears to play a rather direct role in the mechanism of hypertension induced by renal artery constriction, not through the action of angiotensin II on the central sympathetic nervous system.

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.

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