The effect of acute haemorrhage in the dog and man on plasma‐renin concentration

Brown, Jerry M.; Davies, D. L.; Lever, A. F.; Robertson, J. I. S.; Verniory, A

doi:10.1113/jphysiol.1966.sp007842

Cited by 69 publications

(26 citation statements)

References 49 publications

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“…These circulatory adjustments to severe stress might then be the factor(s) which have previously led to increases in PRA with exercise. This formulation is consistent with results of previous studies in man which showed no increase in PRA with exercise until near-maximal levels of exercise were achieved 12 -' 3 and with a recent study 25 which demonstrated little increase in PRA with exercise but a large increase shortly after exercise. Since the dogs in our study were trained and partially conditioned, it is conceivable that they could exercise to a maximum degree without stressing their circulatory system to the same degree as a less well conditioned man.…”

Section: Discussionsupporting

confidence: 92%

“…This seems unlikely, however, because many of the studies bearing on the control factors for renin release have been performed in the dog, 19 and where these control factors have been studied in man similar results have been obtained. 3 -"• 2 0 In addition,, the hemodynamic changes reported for the dog during exercise in this study and previously 15 are similar to those which occur in man.…”

Section: Discussionsupporting

confidence: 86%

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Plasma renin activity during exercise in the dog.

Lifschitz¹,

Horwitz²

1976

Circulation Research

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SUMMARY Previous workers have suggested that a rise in plasma renin activity (PR A) may mediate some of the hemodynamic changes associated with exercise.To test this hypothesis in nine dogs chronically instrumented for measurement of aortic pressure (catheter) or cardiac output (ascending aorta electromagnetic flow probe) PRA was measured by radioimmunoassay in blood samples drawn before and during running on a level treadmill at 4-8 miles per hour. Exercise caused increases in heart rate from 96 ± 5 (SE) to 186 ± 7 beats/min, cardiac output from 2.8 ± 0.3 to 6.2 ± 0.6 liters/ min, and mean aortic pressure from US ± 5 to 132 ± S mm Hg (P < 0.01). Mean PRA was 6.6 ± 0.7 (SE) ng of angiotensin I/ml per 3 hours before and 7.6 ± 1.2 ng Ang 1 during exercise, values that are not different statistically. Propranolol reduced PRA at rest from 8.6 ± 1.1 to 5.9 ± 1.1 ng Ang 1 (P < 0.05), but there was no significant difference between resting and exercise levels, although the increments in heart rate, cardiac output, and mean aortic pressure were reduced. Standing on hindlimbs for 5 minutes did not cause a change in mean aortic pressure or PRA. However, administration of pentolinium reduced mean aortic pressure, and PRA rose from 6.0 ± 1.1 to 9.8 ± 1.5 ng Ang I. Exercise, with or without /3-adrenergic blockade, does not cause increased PRA in conscious dogs in which the renin-angiotensin system is normally responsive.THERE IS evidence that the renin-angiotensin system plays an important role in the acute regulation of blood pressure in normal animals or man.' For example, hypotension due to postural change 2 or hemorrhage 3 results in prompt increases in renin levels in both peripheral and renal veins. 4 It has been suggested that increased sympathetic nervous system activity may cause the increased renin secretion in these settings.2 -4 If sympathetic tone is an important determinant of the rate of renin release, high renin levels would be expected in other circumstances in which there is increased activity of renal sympathetic nerves, or increased circulating catecholamines. According to this hypothesis, strenuous exercise, during which generalized sympathetic tone is high, should be associated with high plasma renin values. However, results of studies of plasma renin activity (PRA) levels during exercise have been inconsistent, with most showing increases but others concluding that no significant changes occurred.513 Several questions can be raised about these previous studies of renin activity during exercise. Most used a bioassay for renin, which may be less specific than the radioimmunoassay technique.14 Variation in exercise loads may have influenced the data. Also, information has been sparse concerning the influence of pharmacological or surgical blockade of sympathetic stimulation on the response of the renin-angiotensin system to exercise. To clarify the relationship of PRA to sympathetic tone during exercise, we obtained renin levels by radioimmunoassay of blood samples drawn from dogs performing running exerc...

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 86%

Plasma renin activity during exercise in the dog.

Lifschitz¹,

Horwitz²

1976

Circulation Research

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“…In contrast, hemorrhage in the monkey of as much as 10% of blood volume fails to increase ADH unless arterial pressure falls (Amauld et al, 1977). A similar low sensitivity for the volumetric control of ADH and renin during hemorrhage has also been demonstrated in humans (Brown et al, 1966;Hesse et al, 1968;Robertson and Mahr, 1972;Goetz, et al, 1974). In addition, lower body negative pressure (LBNP) at a level which markedly decreases central venous pressure fails to increase plasma ADH (Goldsmith et al, 1982) or renin levels (Mark et al, 1978) in man unless arterial pressure falls.…”

Section: Discussionmentioning

confidence: 79%

Renal responses of the cardiac-denervated nonhuman primate to blood volume expansion.

Peterson¹,

Jones²

1983

Circulation Research

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SUMMARY. Experiments were performed to determine whether total, specific cardiac denervation affects the renal responses of the nonhuman primate to acute inrravascular volume expansion. Adult male Macaca fascicularis monkeys underwent chronic intrapericardial cardiac denervation or sham surgery. After a 14-to 30-day recovery period, each animal was anesthetized with sodium pentobarbital and estimated blood volume was volume-expanded 20% with 6% dextran in isotonic saline. Control renal excretory function did not differ between the two groups, and both groups had similar increases in urine flow, sodium and potassium excretion, osmolar clearance, free water clearance, and renal plasma flow after volume expansion. The times to peak diuresis and natriuresis also were similar in both groups. These results demonstrate that the cardiac-denervated monkey shows unartenuated renal excretory responses to volume expansion. This could indicate that either cardiac receptors do not play a major role in eliciting these responses in the primate or that eliminating a role of cardiac afferents is compensated for by redundant afferents from arterial baroreceptors. (Circ Res 53: 24-32, 1983)

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“…The enhancement ofthe activity ofthe renin-angiotensin system during hemorrhage is a well-accepted phenomena (18)(19)(20) that has stimulated physiologic investigation for a number of years. Studies in the nonfiltering kidney suggest that hemorrhage may provide a multifactorial stimulus for renin release (9 Although Romero et al (11) found that inhibition of prostaglandin synthesis abolished the renin response to hemorrhage in the conscious rabbit, this was not found to be the case in the present study in the anesthetized dog.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Renin Secretion during Hemorrhage in the Dog

1979

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A B S T R A C T The importance of renal perfusion pressure (RPP), the sympathetic beta adrenergic nervous system and renal prostaglandins (PG) on renin release during a uniform 15-17% reduction in blood pressure by hemorrhage (HH) was studied systematically in anesthetized dogs. All groups of animals had similar decrements in systemic and renal hemodynamics with HH. In control dogs (n = 7), both plasma renin activity (PRA, 4.1-9.0 ng angiotensin I/ml per h, P < 0.05) and renin secretory rate (RSR, 26-228 ng/ml per h min, P < 0.005) increased significantly with HH. This increase in renin release during HH was not abolished by any single maneuver alone including beta adre nergic blockade with d,l-propranolol (n = 6), renal PG inhibition with indomethacin (n = 7), or control of RPP (n = 6). However, when beta adrenergic blockade was combined with control of RPP (n = 7) during HH, neither PRA (1.9-2.7 ng/ml per h, NS) nor RSR (16-53 ng/ml per h min, NS) increased significantly. Similarly, a combination ofbeta adrenergic blockade and PG inhibition (n = 6) also abolished the increase in PRA (1.5-1.4 ng/ml per h, NS) and RSR (14-55 ng/ml per h*min, NS) 75216.

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The effect of acute haemorrhage in the dog and man on plasma‐renin concentration

Cited by 69 publications

References 49 publications

Plasma renin activity during exercise in the dog.

Plasma renin activity during exercise in the dog.

Renal responses of the cardiac-denervated nonhuman primate to blood volume expansion.

Mechanisms of Renin Secretion during Hemorrhage in the Dog

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