Development of chronic perinephritic hypertension in dogs without volume expansion

1977 ◽  
Vol 233 (4) ◽  
pp. F278-F281 ◽  
Author(s):  
R. H. Freeman ◽  
J. O. Davis ◽  
B. E. Watkins
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Left Kidney ◽  
Renal Hypertension ◽  
Control Level ◽  
Whole Body ◽  
Sodium Balance ◽  
Contralateral Kidney ◽  
Experimental Renal Hypertension

The theory of whole body autoregulation to explain the pathogenesis of experimental renal hypertension states that hypertension is initiated in response to an early increase in salt and water retention and a subsequent elevation of the cardiac output. This hypothesis was evaluated in the present study. Dogs (n,5) were made hypertensive by wrapping the left kidney in cellophane and removing the contralateral kidney 3 wk later. One week prior to right nephrectomy, the dogs were volume depleted by placing them on a low sodium intake (less than 3 meq of sodium/day) and giving them a mercurial diuretic for the first 3 days of the diet. This superimposed sodium depletion (negative sodium balance of 137 +/- 17 meq) increased plasma renin activity 3-5 times but did not change arterial pressure or heart rate. Within 2 days after nephrectomy, the mean arterial pressure increased from the control level of 105 +/- 1 to 135 +/- 6 mmHg (P less than 0.005) and pressure remained elevated throughout an additional 4-wk period in which volume depletion was enforced. The present study suggests, therefore, that initial blood volume expansion with such possible consequences as elevated cardiac output are not essential to the pathogenesis of experimental renal hypertension.

Changes in Cardiac Output during the Development of Renal Hypertension in Sodium-Depleted Dogs

1978 ◽  
Vol 55 (s4) ◽  
pp. 221s-223s
Author(s):  
James O. Davis ◽  
Gregory A. Stephens ◽  
Ronald H. Freeman ◽  
Jack M. Deforrest
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Renovascular Hypertension ◽  
Renal Hypertension ◽  
Whole Body ◽  
High Level

1. Chronic renovascular hypertension developed in uninephrectomized, sodium-depleted dogs in association with a decrease in cardiac output. 2. With sodium and volume repletion of these animals, cardiac output returned to normal but the high level of arterial pressure was unchanged; consequently, the peripheral arterioles dilated. 3. These observations provide evidence against the theory of whole-body autoregulation.

Hemodynamic studies in normotensive and renal hypertensive chronic spinal dogs

1964 ◽  
Vol 206 (3) ◽  
pp. 562-566 ◽  
Author(s):  
Yoshihiro Kaneko ◽  
Irvine H. Page ◽  
James W. McCubbin
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Renal Hypertension ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Marked Rise ◽  
Tetraethylammonium Chloride ◽  
Experimental Renal Hypertension

High spinal cord section caused reduction of stroke volume, cardiac output, aortic pressure, and increase in heart rate. Peripheral resistance was little changed. With time, arterial pressure and heart rate recovered to near control levels; stroke volume, cardiac output, and peripheral resistance tended to increase. Recovery of arterial pressure was due either to increase in peripheral resistance or increase in cardiac output. Elimination of essentially all efferent sympathetic activity caused little or no decrease in peripheral resistance; the small decrease in arterial pressure was accounted for by decrease in stroke volume and cardiac output. Atropine given well after recovery from operation increased heart rate, cardiac output, and aortic pressure while stroke volume decreased. The increase in blood pressure was due to increased cardiac output. Tetraethylammonium chloride given after atropine showed that cardiovascular denervation was essentially complete. Induction of experimental renal hypertension caused marked rise in peripheral resistance without change in stroke volume, heart rate, and cardiac output. Since cardiovascular denervation was complete, the hypertension was of humoral origin.

scholarly journals Relation of Plasma Renin to Sodium Balance and Arterial Pressure in Experimental Renal Hypertension

1966 ◽  
Vol 18 (5) ◽  
pp. 475-483 ◽  
Author(s):  
Torrey C. Brown ◽  
James O. Davis ◽  
Michael J. Olichney ◽  
C. I. Johnston
Keyword(s):  
Arterial Pressure ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Experimental Renal Hypertension

Renin-angiotensin-aldosterone system in experimental renal hypertension in the rabbit

1976 ◽  
Vol 230 (2) ◽  
pp. 311-318 ◽  
Author(s):  
TE Lohmeier ◽  
JO Davis
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Aldosterone Secretion ◽  
Experimental Renal Hypertension ◽  
Highly Correlated ◽  
The Right

Hypertension was produced in 25 rabbits by constricting the right renal artery and leaving the opposite kidney intact (two-kidney hypertension). After 30 days mean arterial pressure and plasma renin activity (PRA) were significantly elevated (P less than 0.01), and arterial pressure was correlated with PRA (r = 0.551, P less than 0.01); however, not all hypertensive rabbits had elevated PRA, and in animals in which sodium balance was monitored, only rabbits in negative sodium balance had increased levels of PRA. To investigate the role of angiotensin II (A-II) in the hypertension, [1-sarcosine,8-alanine]angiotensin II was infused at 6 mug/kg per min for 30 min in anesthetized hypertensive animals (n = 25). For the group, arterial pressure fell significantly (P less than 0.01), but several animals with minimal hypertension failed to give a depressor response. The declines in arterial pressure were highly correlated with PRA (r = 0.853, P less than 0.01). Aldosterone secretion in hypertensive animals was correlated with PRA (r = 0.851, P less than 0.01). Thus, two-kidney hypertension in the rabbit persists with normal PRA, but during periods of spontaneous sodium depletion, A-II plays a role in the maintenance of the hypertension.

scholarly journals Increased Cardiac Output as a Contributory Factor in Experimental Renal Hypertension in Dogs

1970 ◽  
Vol 27 (5) ◽  
pp. 799-810 ◽  
Author(s):  
CARLOS M. FERRARIO ◽  
IRVINE H. PAGE ◽  
JAMES W. McCUBBIN
Keyword(s):  
Cardiac Output ◽  
Renal Hypertension ◽  
Contributory Factor ◽  
Experimental Renal Hypertension

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.

Euvolemic cirrhotic dogs in sodium balance maintain normal systemic hemodynamics

1988 ◽  
Vol 66 (1) ◽  
pp. 80-83 ◽  
Author(s):  
M. Levy ◽  
Elizabeth Maher ◽  
Marvin J. Wexler
Keyword(s):  
Cardiac Output ◽  
Liver Function ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Systemic Hemodynamics ◽  
Peripheral Vascular Resistance ◽  
Sodium Balance ◽  
Biliary Cirrhosis ◽  
Sodium Retention ◽  
Peripheral Vascular

Dogs with chronic biliary cirrhosis and portal hypertension commonly develop plasma volume expansion, urinary sodium retention, ascites, and perturbed systemic hemodynamics, i. e., a rise in cardiac output and a fall in peripheral vascular resistance. Our laboratory has previously demonstrated that creating a side-side portacaval anastomosis in such animals, and so venting hepatoportal pressure, will prevent sodium retention and ascites formation and will maintain the animals euvolemic. In the present study, in four cirrhotic dogs with such an anastomosis, observations made at 12 weeks postbiliary duct ligation, and in the presence of grossly disturbed liver function and morphology, failed to demonstrate any change from control conditions in arterial blood pressure, cardiac output, or peripheral vascular resistance. We conclude that venting hepatoportal pressure in cirrhotic dogs with markedly disturbed liver function prevents the advent of a hyperdynamic circulation, possibly by preventing volume expansion.

Limited hypertensive effect of infusion of angiotensin

1965 ◽  
Vol 209 (2) ◽  
pp. 264-268 ◽  
Author(s):  
Michael D. Day ◽  
James W. McCubbin ◽  
Irvine H. Page
Keyword(s):  
Arterial Pressure ◽  
Renal Hypertension ◽  
Initial Pressure ◽  
Pressure Level ◽  
Cardiovascular Reflexes ◽  
Vagus Nerves ◽  
Anesthetized Dogs ◽  
Experimental Renal Hypertension ◽  
Maximal Pressure ◽  
Renal Artery Constriction

Though single injections of angiotensin cause extreme rise in arterial pressure, infusion fails to elevate pressure to the degree usually found in experimental renal hypertension. The maximal pressure level obtainable by infusing angiotensin into anesthetized dogs was approximately the same in different dogs and was independent of the initial pressure. The vagus nerves did not importantly influence the "ceiling" response but if arterial pressure was then elevated by carotid occlusion the ceiling was raised. The combination of renal artery constriction and infusion of angiotensin failed to give a higher ceiling than angiotensin alone. In dogs with chronic renal hypertension the ceiling was higher than in normal dogs, presumably because of an upward shift in the range of response of cardiovascular reflexes. The results support the view that compensatory cardiovascular reflexes and tachyphylaxis to large amounts of infused angiotensin suppress the response and that these factors are much less effective in limiting response to quick injection.

Experimental Renal Hypertension: Renin Content of Kidneys in Intact and Adrenalectomized Rats Given Cortexone

1958 ◽  
Vol 195 (3) ◽  
pp. 543-548 ◽  
Author(s):  
F. Gross ◽  
P. Lichtlen
Keyword(s):  
Renal Artery ◽  
Renal Hypertension ◽  
Normal Animal ◽  
Renal Ischemia ◽  
Characteristic Distribution ◽  
Contralateral Kidney ◽  
Moderate Reduction ◽  
Small Doses ◽  
Experimental Renal Hypertension ◽  
Renin Content

The effects were investigated in rats of unilateral renal ischemia, adrenalectomy and varying doses of cortexone on the development of hypertension and on the content of pressor substances in the kidney. Adrenalectomy prevented the hypertension which follows unilateral clamping of the renal artery when a life maintaining dose of 0.1 mg cortexone acetate was injected daily. However, administration of 75 mg cortexone in the form of implants restored but did not enhance the characteristic hypertensive response to renal ischemia. The characteristic distribution of renal pressor material, being normal in the clamped and diminished in the contralateral kidney, was no longer observed after adrenalectomy when only small doses of cortexone were given but was still evident when excess cortexone was given. Overdosage with cortexone without clamping a renal artery led only to a moderate reduction of pressor material in both kidneys while in animals with unilateral renal ischemia the pressor material (renin?) in the contralateral kidney disappeared completely. Clamping the renal artery prevented the diminution of pressor material in the ipsilateral kidney which otherwise occurs under overdosage with cortexone in the normal animal.

Physical and physiological characteristics of pressure-driven hemorrhage

1992 ◽  
Vol 263 (5) ◽  
pp. H1402-H1410 ◽  
Author(s):  
M. Rocha e Silva ◽  
G. A. Braga ◽  
R. Prist ◽  
I. T. Velasco ◽  
E. S. Franca
Keyword(s):  
Cardiac Output ◽  
Blood Loss ◽  
Arterial Pressure ◽  
Plasma Proteins ◽  
Volume Expansion ◽  
Small Volume ◽  
Base Excess ◽  
Complex Function ◽  
Bleeding Rate ◽  
Pressure Driven

Research on hemorrhage has concentrated on its effects rather than the manner of occurrence. A new experimental method in which the rate of bleeding is a function of prevailing arterial pressure is proposed and described. The effects of standard crystalloid volume expansion and of small volume hypertonic treatment on this protocol are demonstrated. In pressure-driven hemorrhage, survival time and the decay of arterial pressure, cardiac output, oxygen consumption, and base excess are functions of the bleeding rate, but plasma proteins and hematocrits are independent. The decay of arterial pressure is also a complex function of blood volume deficit, but this relation is not dependent on the rate of blood removal. Volume expansion induces a recovery of circulatory function despite enhanced blood loss. A comparison between equiosmolar solutions of hypertonic sodium chloride and acetate shows that acetate produces a smaller pressor (hence less blood loss) but larger blood flow (hence higher O2 availability) effect. The possible importance of the isochloremic nature of the response to acetate is highlighted.

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