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Biomedical subjects

J O Davis

Publications and source records attributed to J O Davis.

At least 91 records · Page 5Linked to original sources
PubMed1976

The use of angiotensin II blockade to study adrenal steroid secretion.

In the dog, the renin--angiotensin system appears to be a primary control mechanism for aldosterone secretion since angiotensin II blockade decreased aldosterone production to undetectable levels. Angiotensin II blockade also decreased cortisol secretion strikingly in dogs with thoracic caval constriction, a finding which suggests the presence of an angiotensin II receptor in the two inner zones of adrenal cortex. An important incidental finding after angiotensin II blockade in both sodium-depleted dogs and dogs with thoracic caval constriction was the striking drop in arterial pressure. It is suggested that angiotensin II acts on the peripheral arterioles to provide an important compensatory mechanism and, thereby, maintain arterial pressure in these low cardiac output states. In the rat, both the nonapeptide converting enzyme inhibitor and [Sar1, Ala8]-angiotensin II produced a marked decrease in aldosterone secretion in hypophysectomized, sodium-depleted animals. Both synthetic angiotensin II and its heptapeptide fragment produced striking increases in aldosterone secretion when the obscuring effect of ACTH was excluded in the rat. These findings provide evidence that the renin--angiotensin system is an important control mechanism for aldosterone biosynthesis in the rat.

Adrenal Glands↗
PubMed1975

Role of angiotensin II in experimental renal hypertension in the rabbit.

Hypertension was produced in rabbits by constricting the left renal artery; in nine rabbits the opposite kidney was removed and in eight rabbits the opposite kidney was left intact. To investigate the role of angiotensin II (A-II), 1-sarcosine-8-alanine angiotensin II, a competitive antagonist of A-II, was infused at 6 mug/min per kg body wt for 30 min. In a control group of seven unilaterally nephrectomized rabbits mean arterial pressure averaged 81 mmHg and infusion of the A-II antagonist did not alter the arterial pressure. In a group of Na-depleted rabbits, arterial pressure decreased from 81 to 63 mmHg (P less than 0.01) in response to the A-II analogue. Thirty days after renal artery constriction, seven of the nine one-kidney hypertensive rabbits had normal values for plasma renin activity (PRA) and during infusion of the A-II antagonist arterial pressure was unchanged. However, two rabbits had elevated PRA and the arterial pressure decreased during infusion of the angiotension analogue. In the two-kidney hypertensive rabbits, PRA was normal and arterial pressure was unchanged by infusion of the A-II antagonist. These studies provide evidence that hypertension developed with either a high or normal A-II plasma level in the one-kidney animals; the two-kidney rabbits developed chronic hypertension in which no role for A-II could be demonstrated.

Angiotensin II↗
PubMed1975

High-output heart failure in the dog: systemic and intrarenal role of angiotensin II.

Dogs with experimental high-output heart failure (HOF) exhibit marked retention of salt and water secondary to hypersecretion of both renin and aldosterone. The present study was undertaken to evaluate the systemic and intrarenal arteriolar action of angiotensin II (AII) in dogs with HOF and to provide additional information about the role of AII in low-output states. The intravenous infusion of a specific AII antagonist, [Sar1, Ala8]AII (6 mug/kg min-1), into conscious dogs with HOF decreased the mean arterial pressure (AP) from 101 +/- 7 to 83 +/- 7 mmHg (P less than 0.01) after 45 min of infusion. Intrarenal arterial infusion of the AII antagonist (0.2 and 2.0 mug/kg min-1) into anesthetized dogs with HOF also decreased AP and produced a marked increase in renal blood flow (RBF) with no changes in either creatinine clearance or sodium excretion. Similar results were obtained during the intrarenal infusion of the antagonist into sodium-depleted dogs and dogs with thoracic vena caval constriction, but not in normal dogs. The data demonstrate an important role for AII in the regulation of AP and RBF in high- and low-output states.

Angiotensin II↗
PubMed1975

Des-1-Asp-angiotensin II. Possible intrarenal role in homeostasis in the dog.

The relative effects of des-a-Asp-angiotensin 3I and angiotensin II on renal function, including renin secretion, were investigated in normal and sodium-depleted dogs. Intrarenal arterial infusion of the heptapeptide fragment into normal dogs at a rate which was calculated to increase blood levels by only 7 ng/100 ml decreased renal blood flow from 254 +/- 9 ml/min to 220 +/- 12 and 219 +/- 12 ml/min (P less than 0.01 for both values) after 10 and 30 minutes of infusion, respectively; renin secretion decreased from 502 +/- 214 ng/min to 253 +/- 109 and 180 +/- 53 ng/min (P less than 0.05 for both values). Infusion of angiotensin II at the same rate decreased renal blood flow from 251 +/- 26 ml/min to 224 +/- 22 and 220 +/- 16 ml/min (P less than 0.01 and 0.025, respectively) and decreased renin secretion from 374 +/- 25 ng/min to 166 +/- 76 and 131 +/- 37 ng/min (P less than 0.025 for both values). Neither peptide significantly changed mean arterial blood pressure, creatinine clearance, or excreted sodium in these dogs. Infusion of des-1-Asp-angiotensin II into sodium-depleted dogs decreased renin secretion from 1094 +/- 211 ng/min to 768 +/- 132 and 499 +/- 31 ng/min (P less than 0.025 for both values) after 10 and 30 minutes of infusion. Angiotensin II infusion decreased renin secretion from 1102 +/- 134 to 495 +/- 235 and 502 +/- 129 ng/min in these dogs (P less than 0.05 and 0.025, respectively). Neither peptide significantly altered renal blood flow, arterial blood pressure, creatinine clearance, or excreted sodium in the sodium-depleted dogs. The data demonstrated that these two peptides have similar effects on the renin secretory mechanism and the vascular receptor at the level of the renal arterioles.

Angiotensin II↗
PubMed1975

Control of aldosterone secretion in the spontaneously hypertensive rat.

Adrenal secretion rates of aldosterone, corticosterone, and deoxycorticosterone were studied sequentially in the spontaneously hypertensive rat and the normotensive Kyoto Wistar rat. Steroid secretion was studied at three different ages: 7-8, 11-13, and 22-25 weeks. Also, peripheral plasma levels of aldosterone and plasma renin activity were determined in both the spontaneously hypertensive and the normotensive rats at 7-8 weeks of age. Aldosterone secretion was elevated markedly in dexamethasone-morphine-treated spontaneously hypertensive rats at both 7-8 and 11-13 weeks of age but was not significantly different from control in 22-25-week-old spontaneously hypertensive rats. No statistically significant differences in corticosterone or deoxycorticosterone secretion rates were observed between the spontaneously hypertensive rats and the normotensive Kyoto Wistar controls; however, the data suggested that dexamethasone did not suppress adrenocorticotropic hormone in the 7-8- and 11-13-week-old spontaneously hypertensive rats to the same extent that it did in the normotensive Kyoto Wistar rats. Therefore, aldosterone secretion was reexamined in acutely hypophysectomized 7-8-week-old rats to eliminate completely the influence of the anterior pituitary; no differences in aldosterone, corticosterone, or deoxycorticosterone secretion rates were observed between hypophysectomized spontaneously hypertensive rats and normotensive Kyoto Wistar rats. Moreover, aldosterone secretion in the hypophysectomized 7-8-week-old spontaneously hypertensive rats was reduced markedly compared with that in the intact 7-8-week old spontaneously hypertensive rats, thus confirming the importance of the pituitary in these animals. Determinations of peripheral plasma aldosterone concentration and plasma renin activity in unstressed 7-8-week-old spontaneously hypertensive and normotensive rats revealed that both parameters were depressed significantly in the spontaneously hypertensive rats. Thus, the present data indicate that the renin-angiotensin-aldosterone system is suppressed in the spontaneously hypertensive rat but do not suggest that the system is critically involved in the hypertensive process in these animals

Adrenal Glands↗
PubMed1975

DES-ASP1--angiotensin II: possible role in mediating responses of the renin-angiotensin system.

In dexamethasone-treated dogs, both antiogensin II and its heptapeptide fragment (des-asp1-angiotensin II) stimulated the secretion of the adrenal steroids aldosterone, corticosterone, and cortisol. Further, there was no statistically significant difference in the steroidogenic potency of the two peptides. An interesting incidental finding was the decrease in PRA with both peptides, again with no demonstrable difference in the magnitude of the responses. The present data are consistent with the hypothesis that the heptapeptide mediates responses produced by the renin-angiotensin system in both the adrenals and the kidneys.

Adrenal Cortex Hormones↗
PubMed1975

Metablism of aldosterone in dogs with renovascular hypertension (38476).

The rate of metabolism of aldosterone was measured in seven normal dogs, 4 dogs with chronic renal hypertension and five dogs with malignant renal hypertension. Tritiated aldosterone was injected intravenously and the rate of disappearance of authentic aldosterone was determined. The disappearance curves were resolved into two exponential components and the plasma half-life was measured from the slow component which reflects the rate of metabolism of aldosterone. The half-life of aldosterone was essentially the same for the three groups of dogs. It is concluded, therefore, that the rate of aldosterone metabolism is normal in dogs with experimental renal hypertension.

Aldosterone↗
PubMed1973

Angiotensin. II. Important role in the maintenance of arterial blood pressure.

An angiotensin II antagonist, [1-sarcosine, 8-alanine]-angiotensin II, was given intravenously to anesthetized dogs with thoracic caval constriction and ascites to investigate the role of angiotensin II in the control of arterial pressure. The antagonist produced a striking fall in arterial pressure and in aldosterone secretion and an accompanying increase in plasma renin activity. In a control experiment, normal anesthetized dogs were given the angiotensin analog, but it failed to reduce arterial pressure or to influence plasma renin activity. In conscious dogs with caval constriction, the antagonist produced essentially the same drop in arterial pressure as observed in anesthetized animals. These results suggest an important role for angiotensin II in the maintenance of arterial pressure by its action on specific receptor sites in arteriolar smooth muscle and in the adrenal cortex.

Adrenal Glands↗