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.

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.

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.

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.

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.

Nonuniform Distribution of Vagal Effects on the Atrial Refractory Period

1958 ◽  
Vol 194 (2) ◽  
pp. 406-410 ◽  
Author(s):  
R. Alessi ◽  
M. Nusynowitz ◽  
J. A. Abildskov ◽  
G. K. Moe
Keyword(s):  
Arterial Pressure ◽  
Refractory Period ◽  
Vagal Stimulation ◽  
Nonuniform Distribution ◽  
Right Atrial ◽  
Vagus Nerves ◽  
Anesthetized Dogs ◽  
The Right ◽  
Stimulation Of

The refractory period (RP) was measured at several points on the right atrial surface in anesthetized dogs. Under control conditions with vagi cut the values recorded at various points varied by no more than 40 msec. During stimulation of the vagus nerves, singly or together, the RP varied widely. At some points marked effects were observed, while at others little or no effect was apparent. Reflex excitation of the vagi, induced by increased arterial pressure, yielded similar results. It was concluded that the effects of vagal stimulation are not uniformly distributed.

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