Inhibition of Renin Release in the Dog by Vasopressin and Vasotocin

Abstract

In anesthetized dogs the intravenous infusion of arginine vasotocin, 25 mU/min, or vasopressin, 10 mU/min, inhibited renin secretion when control secretion rates were normal or when they were elevated by complete ureteral occlusion. Vasotocin, 5 mU/min, or vasopressin, 1 mU/min, was ineffective. Direct intraarterial infusion of vasotocin, 5 mU/min, into the right kidney inhibited renin secretion by the right kidney only. Glomerular filtration rate and renal plasma flow were not changed, and mean arterial pressure was either not changed or was decreased. Vasotocin caused no change in urine flow but did produce a significant natriuresis secondary to decreased tubular reabsorption. The physiological implications of these polypeptide-renal relationships are discussed.ADDITIONAL KEY WORDS posterior pituitary polypeptides sodium balance pineal arginine vasotocin angiotensin renal tubular sodium reabsorption• Bunag, Page, and McCubbin (1) have reported that vasopressin can inhibit renin release. The present studies were performed to test the effects of arginine vasotocin and to extend their observations on vasopressin. Methods Animal Techniques and ProtocolsExperiments were performed on dogs maintained on standard laboratory chow (Friskies) and anesthetized with pentobarbital, 30 mg/kg iv. The right and left ureters were catheterized via a right flank incision. To obtain renal venous blood, a polyethylene catheter (2.4 mm, o.d.) was introduced into the left femoral vein, passed up the inferior vena cava and manipulated into the right renal vein. In three dogs, a catheter was passed from a jugular vein through the vena cavae and right atrium into the left renal vein. In the same dogs, a 24-gauge needle was introduced into the renal artery close to its origin and was left in place throughout the experiment, the needle being constantly perfused via a catheter with isotonic saline, 0.4 ml/min.From the Department of Physiology, University of Michigan, Ann Arbor, Michigan 48104.This investigation was supported in part by U. S. Public Health Service Research Grant AM 05077 from the National Institutes of Health.The author is a John and Mary R. Markle Scholar in Academic Medicine.Accepted for publication September 14, 1968.Arterial blood was obtained from a femoral artery catheter. Arterial blood pressure was monitored continuously using a Statham gauge and Grass polygraph. Renal excretory and hemodynamic data were obtained by the clearance technique; periods were 10 minutes long with arterial and renal venous blood samples taken in the middle of each period. Creatinine clearance was used as a measure of glomerular filtration rate; total renal plasma flow was determined by the Fick principle, using PAH. In experiments employing complete ureteral occlusion, renal blood flow was measured with a Carolina squarewave electromagnetic flowmeter (model 301) and probe. Experimental observations were not begun until at least 45 minutes after completion of all experimental protocols and administration of priming doses of creatini...

Endogenous Angiotensin Stimulation of Vasopressin in the Newborn Lamb

“…Thirst-like behavior was consistently observed between 8 and 20 min after furosemide in the control animals in the present study and this was documented by a measured increase in fluid intake. Finally AVP administration has been shown to suppress renin release (32)(33)(34). This effect also has been well documented in infants and is known to be associated with natriuresis (35).…”

The opposing effects of chronic angiotensin-converting enzyme blockade by captopril on the responses to exogenous angiotensin II and vasopressin vs. norepinephrine in rats.

“…It has been proposed that there is a close interrelation between the renin system and vasopressin (Malvin, 1971: Vander, 1968. However, the emphasis usually has been on the mutual influence of these two pressure systems on their secretion rates.…”

“…Some interactions have been identified among these pressor systems (Gordon et al, 1967;Vander 1968;Malvin 1971;Peach 1974), but their precise role in maintaining normal and elevated blood pressure levels still is poorly understood.…”

The effects of antidiuretic hormone and state of potassium balance on the renin‐angiotensin system in rats with diabetes insipidus.

“…in these rats has not been established. Since DI rats suffer from an absence of antidiuretic hormone (ADH) (Valtin & Schroeder, 1964) and potassium deficiency (Mohring et al 1974), and since both ADH (Bu-nag, Page & McCubbin, 1967; 520 E. FERNANDEZ-REPOLLET AND OTHERS Hesse & Nielsen, 1977;Vander, 1968;Vandongen, 1975) and potassium (Abbrecht & Vander, 1970;Dluhy, Underwood & Williams, 1970;Flamenbaum, Kleinman, McNeil, Hamburger & Kotchen, 1975;Sealey, Clark, Bull & Laragh, 1970;Vander, 1970) are known to exert an inhibitory effect on renin release, one or both of these factors might be involved in the elevation of p.r.a.…”