Renin Release after Hemorrhage and after Suprarenal Aortic Constriction in Dogs without Sodium Delivery to the Macula Densa

Abstract

To study the possible factors that control renin secretion by the kidney, a model has been developed to prevent glomerular filtration in the dog. Ureteral ligation was combined with a 2-hour period of total renal ischemia to induce tubular degeneration and cessation of glomerular filtration. After the surgical procedures, the dogs were maintained for 4 days by peritoneal dialysis. The absence of lissamine green dye in the renal tubules after an intra-aortic injection provided evidence that filtration had ceased. Plasma renin activity was significantly increased in six conscious dogs at 30, 60, and 90 minutes after hemorrhage of 20 ml/kg body weight. In another group of five conscious animals, suprarenal aortic constriction produced increases in plasma renin activity at 30, 60, and 90 minutes that were 3 to 4 times the control values before aortic constriction. Plasma renin substrate concentration did not change significantly after hemorrhage or after aortic constriction. In a third group of five dogs, only the left kidney was subjected to ureteral ligation and renal ischemia. These dogs were anesthetized and renal blood flow was measured with an electromagnetic flowmeter. After hemorrhage (20 ml/kg), renin secretion increased significantly above control levels at 30, 45, and 60 minutes. It is concluded that sodium delivery to the macula densa is not essential for renin secretion.

Everything we always wanted to know about furosemide but were afraid to ask

“…Recapitulating, furosemide can increase renin release by activation of the sympathetic nervous system (15,32), a decrease in afferent arterial perfusion pressure, and by direct inhibition of NKCC2 in the macula densa (27,151). In addition, macula densa neuronal NO synthase (nNOS)-mediated NO generation can stimulate renin release (18).…”

Mechanism of hyperreninemia in the potassium-depleted rat.

“…In addition, fluid delivery to the macula densa can be maneuvered by altering the colloid concentration of the perfusion medium. By perfusing with hyperoncotic albumin solutions, the kidney can be made nonfiltering, and the renal vascular receptor can be isolated from the macula densa in the absence of ureteral obstruction as occurs in the in situ nonfiltering kidney of Blaine et al (11,12). The purpose of the present study was to determine whether renin secretion was increased in the perfused kidneys of K-deficient rats and to determine the mechanism of the increased renin secretion.…”

“…The nonfiltering kidney developed by Blaine et al (11,12) provided a novel approach to this problem. With this model, the renal vascular receptor is isolated from the macula densa because distal nephron fluid delivery is abolished and from the effects of circulating epinephrine by prior adrenalectomy and from renal nerves by prior renal denervation.…”

An effect of extrarenal beta adrenergic stimulation on the release of renin

“…In some of these circumstances, however, the systemic arterial pressure may either increase (carotid occlusion [2], direct renal nerve [7] and midbrain stimulation [13,14]) or remain unchanged (moderate hemorrhage [2] and hypoglycemia [10,11]). Nevertheless, even in the presence of an increased or unchanged arterial pressure sympathetic neural stimulation could cause renal vasoconstriction and diminish pressure at the level of some intrarenal pressure-sensitive receptors that influence the release of renin from cells of the juxtaglomerular apparatus (3,15,16). Evidence that such could be the case is the finding that, when measured, renal blood flow, glomerular filtration rate, or both may diminish during maneuvers that increase sympathetic discharge (2-5, 8, 9).…”