A. T. Boryczka

Effect of Dietary Sodium Restriction on Adrenal Cortical Response to ACTH.

Summary In dogs fed a low sodium diet for 5 days before being hypophysectomized and nephrectomized, ACTH exerts a greater aldosterone-stimulating effect than it does in dogs fed approximately 40 mEq of sodium/day. Longer periods of sodium restriction produce a further increase in this action of ACTH. Seventeen-hydroxycorticoid output in response to various ACTH doses is unaffected.

Effect of a low sodium diet on aldosterone-stimulating activity of angiotensin II in dogs.

Summary The effect of various doses of angiotensin II on adrenocortical secretion of aldosterone and 17-hydroxycorticoids was determined in dogs fed a low sodium diet for 14 days and in control dogs. The increments in aldosterone secretion produced by angiotensin II in the animals fed the low sodium diet were greater than the corresponding increments in controls. No changes in the increments in 17-hydroxycorticoids or blood pressure were observed. Angiotensin II (1-L-asparaginyl-5-L-valyl angiotensin octapeptide) was provided by Ciba Pharmaceutical Co., Summit, N. J. ACTH was provided by Upjohn Co., and Lonalac for preparation of low sodium diets by Mead Johnson Co. We wish to thank Mr. Roy Shackelford and Miss Margaret Saari for technical assistance.

Effect of Spinal Cord Transection on the Endocrine and Blood Pressure Responses to Intravenous Clonidine

To determine whether the inhibitory effect of clonidine (CLON) on renin secretion is due in part to a direct action on the kidneys or due entirely to an action on the brain, the drug was administered intravenously in a dose of 30 microgram/kg to dogs in which the spinal cord had been transected in the cervical region. Renal perfusion pressure was held constant by adjusting a suprarenal aortic clamp. The decrease in plasma renin activity produced by CLON in dogs with intact spinal cords was abolished, and in 5 of 8 dogs tested, plasma renin activity rose. The decrease in blood pressure seen in control dogs was replaced by a prolonged pressor response. The ACTH response, as measured by plasma corticoids, and the growth hormone (GH) response were not significantly reduced. The data indicate that at least at this dose, the depressor response and the decrease in renin secretion produced by CLON are completely central in origin.

INHIBITION OF STRESS-INDUCED ACTH SECRETION BY NOREPINEPHRINE IN THE DOG: MECHANISM AND SITE OF ACTION

Publisher Summary This chapter discusses the mechanism and site of action for the inhibition of stress-induced adrenocorticotropic hormone (ACTH) secretion by norepinephrine in the dog. In the dog, centrally active sympathomimetic drugs inhibit stress-induced ACTH secretion. The drugs found to have this action include α-ethyltryptamine, α -methyltryptamine, amphetamine, methamphetamine, 2-aminoheptane, and Clopane. L-dopa also inhibits ACTH secretion. In experiments, adrenal venous corticoid output was used as the index of ACTH secretion. Exogenous ACTH was given at the end of each experiment to demonstrate that the adrenal was normally responsive. The stress in all cases was a surgical laparotomy, with adrenal venous blood being collected after the start of the operation. Catecholamines fail to penetrate the brain in appreciable amounts when administered systemically. Norepinephrine and dopamine inhibit ACTH secretion when given directly into the third ventricle, but fail to inhibit ACTH secretion when given systemically.

Lack of Effect of α-Ethyltryptamine on ACTH Secretion When Blood Pressure is Held Constant.

Summary When the rise in blood pressure usually produced by α-ethyltryptamine is prevented by hemorrhage, no inhibition of ACTH Secretion is observed in Surgically stressed dogs. These results suggest that it is the rise in blood pressure produced by α-ethyltryptamine that causes the inhibition of ACTH secretion.