Biomedical subjects

I A Reid

Publications and source records attributed to I A Reid.

130 records · Page 8Linked to original sources

PubMedDate not supplied

Role of antidiuretic activity in the inhibition of renin secretion by vasopressin in anesthetized dogs.

The nature of the activity of vasopressin which is responsible for the inhibition of renin secretion was studied by comparing the effects of vasopressin (AVP) and analogs of AVP in anesthetized water-loaded dogs. Infusion of AVP (1.0 ng/kg/min) increased mean arterial pressure (MAP) and decreased heart rate (HR) and free water clearance (CH2O). Plasma renin activity (PRA) decreased from 11.9 +/- 4.7 to 3.8 +/- 1.7 ng/ml/3 hr (p less than 0.05). A selective antidiuretic agonist, 1-deamino-8-D-arginine vasopressin (1.0 ng/kg/min), which had no effect on MAP or HR but was effective as AVP in decreasing CH2O, decreased PRA from 13.5 +/- 4.6 to 7.0 +/- 2.9 ng/ml/3 hr (p less than 0.05). Infusion of a selective vasoconstrictor agonist, 2-phenylalanine-8-ornithine oxytocin (1.0 ng/kg/min), increased MAP and decreased HR but did not decrease CH2O or PRA. A vasoconstrictor antagonist, d(CH2)5Tyr(Me)AVP (10 micrograms/kg), completely blocked the MAP and HR responses to AVP but did not block the decrease in CH2O or PRA (5.9 +/- 1.8 to 2.9 +/- 1.6 ng/ml/3 hr) (p less than 0.001). Infusion of the 0.45% saline vehicle had no significant effect on MAP, HR, CH2O or PRA. These results indicate that the inhibition of renin secretion by vasopressin in anesthetized water-loaded dogs is due to its antidiuretic activity.

Animals↗

PubMedDate not supplied

The cardiovascular effects of intravertebral angiotensin II before and after treatment with clonidine.

1. In anaesthetized mongrel dogs it was shown that intravertebral infusions of angiotensin II (2-4 ng/kg per min) increased mean arterial pressure by causing an increase in cardiac output, while infusions of 10 ng/kg per min increased mean arterial pressure through an effect on peripheral resistance. After intravenous clonidine, intravertebral angiotensin no longer had any stimulatory effect on cardiac output, but arterial pressure still increased to the same extent. 2. It is concluded that intravertebral angiotensin can increase arterial pressure by increasing either cardiac output or peripheral resistance. The effects of intravertebral angiotensin on cardiac output can be reduced by concomitant stimulation of baroreflex pathways but its effects on peripheral resistance are not so readily antagonized.

Angiotensin II↗

PubMedDate not supplied

Correlation of plasma angiotensin II concentration and plasma renin activity during acute hypoxia in dogs.

The effects of isocapnic hypoxia on plasma renin activity (PRA) and angiotensin II (AII) concentration were studied in anaesthetized, artificially ventilated dogs. Regression analysis of plasma AII concentration vs PRA, both measured by radioimmunoassay (RIA), was used as an index of converting enzyme activity in vivo. PaO2 decreased from 82 to 30 mmHg but regression analysis did not reveal any inhibition of AII production within the limits of detection of this method (less than 20% inhibition). We conclude that systemic converting enzyme activity, assessed by in vivo measurement and correlation of PRA and AII, is not inhibited by severe hypoxia.

Acute Disease↗

PubMedDate not supplied

Role of the renin-angiotensin system in the control of vasopressin and ACTH secretion during the development of renal hypertension in dogs.

Experiments were performed to determine if the activation of the renin-angiotensin system that occurs during the development of two-kidney, one clip Goldblatt hypertension in dogs is accompanied by increases in vasopressin and adrenocorticotrophic hormone (ACTH) secretion. Following renal artery constriction, there were marked increases in arterial blood pressure, plasma renin activity (PRA), and plasma angiotensin II (AII) concentration. These changes were accompanied by an increase in plasma vasopressin concentration during the second week following constriction, and there were significant correlations between plasma vasopressin concentration and PRA (r = 0.57, p less than 0.001), and between plasma vasopressin concentration and plasma AII concentration (r = 0.59, p less than 0.001). In contrast, plasma corticosteroid concentration, used as an index of changes in ACTH secretion, did not change significantly. Acute blockade of the renin-angiotensin system with captopril or saralasin produced the expected changes in blood pressure, PRA, and plasma AII concentration but did not decrease plasma vasopressin or corticosteroid concentrations. These results indicate that during the development of renal hypertension in dogs, there may be an interaction between the renin-angiotensin system and vasopressin, but not between the renin-angiotensin system and the pituitary-adrenal axis. They also show that the antihypertensive action of captopril in this experimental model is not mediated via suppression of vasopressin, ACTH, or corticosteroid secretion.

Adrenal Cortex Hormones↗