Why the study?
Does prolonged intravenous infusion of angiotensin II alter aldosterone excretion and electrolyte metabolism in normal dogs?
Does prolonged intravenous infusion of angiotensin II alter aldosterone excretion and electrolyte metabolism in normal dogs?
Prolonged angiotensin II infusion in dogs stimulates aldosterone excretion and causes mineralocorticoid-like electrolyte changes that depend on intact adrenal glands.
Answers are grounded in this paper and cite their sources.
Confirms adrenal dependence of angiotensin II mineralocorticoid effects in dogs; leaves open translation to human hypertension or HF.
Intravenous infusion of angiotensin II into normal dogs at rates of 20 or 80 µg/kg day for 4–11 days produced elevated urinary excretion of aldosterone without tachyphylaxis. In five of the six animals studied, angiotensin infusion had little or no effect on arterial pressure; in the sixth dog, which received angiotensin at the higher rate, arterial pressure was elevated by 30 mm Hg. Most of the effects of angiotensin II on water and electrolyte metabolism were similar to those of mineralocorticoids: initial transient sodium retention, polyuria, increased fecal potassium excretion, initially negative potassium balance, and diminished plasma potassium concentration. These effects were not observed when angiotensin II was infused into each of three adrenalectomized dogs, which received daily maintenance doses of desoxycorticosterone acetate and cortisone acetate. In addition, however, angiotensin II had a natriuretic action in intact animals, which was more pronounced at the higher rate of infusion. The data suggest that an increase in filtered sodium load was the basis of the natriuresis.
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Urquhart et al. (1963) studied this question.
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