Effect of acetylcholine on urinary electrolyte excretion

Abstract

Acetylcholine was infused into the aorta of unanesthetized dogs above the origin of the renal arteries. It produced a statistically significant increase in Na, Cl, and K excretion rates and in renal plasma flow with respect to control values in the same experiments and to results obtained in separate control experiments on the same animals. No consistent change was found in glomerular filtration rate, urine flow, and osmolality. In similar experiments Pitressin was also infused. The renal effects of acetylcholine were slightly enhanced by Pitressin. It was concluded that the antidiuretic hormone was not an important mediator in the production of renal effects during acetylcholine infusion. The possible roles of increased medullary blood flow and of increased angiotensin production are discussed.

The effects of combined renal vasodilatation and pressor agents on renal hemodynamics and the tubular reabsorption of sodium.

“…The present results agree with previous studies indicating that renal vasodilatation per se may increase sodium excretion and decrease the net tubular reabsorption of sodium (8,14). In our study unilaterally increased renal plasma flow re-suiting from three different vasodilators was accompanied by decreased tubular reabsorption of sodium.…”

“…We recently suggested that increased renal blood flow, and perhaps increased medullary blood flow specifically, may be one factor that by way of intrarenal mechanisms contributes to diminished reabsorption of sodium during saline loading (5). Furthermore, natriuresis in the absence of salt loading accompanies increased renal blood flow when local vasodilatation is produced by a variety of agents (7)(8)(9)(10)(11)(12)(13), and we have observed that the unilateral natriuresis accompanying increased renal blood flow during the renal arterial infusion of acetylcholine is due in part to diminished net tubular reab-sorption of sodium (14). Leyssac has suggested that angiotensin may depress proximal tubular reabsorption (15), and it has been demonstrated that under certain conditions angiotensin may produce natriuresis (16)(17)(18)(19).…”

Studies on the mechanism of natriuresis accompanying increased renal blood flow and its role in the renal response to extracellular volume expansion.

“…Likewise, increased renal plasma flow and decreased EPAH were not associated with increased sodium excretion when the agent was infused during mannitol diuresis (Table VI). These observations of increased sodium excretion during the infusion of acetylcholine in the first two groups of animals are in agreement with observations previously reported by others (6)(7)(8). Vander reported that the natriuretic effect of acetylcholine was not different in dogs receiving saline infusions than in dogs receiving no saline (6).…”

“…We have suggested that increased renal blood flow during saline loading may be one factor that contributes to the decreased tubular reabsorption of sodium (4,5), since in the saline loaded dog when renal blood flow is decreased experimentally the net tubular reabsorption of sodium may increase (5). Recently, reports have appeared demonstrating that the infusion of several unrelated vasodilators [acetylcholine (6)(7)(8), dopamine (9), pyrogen (10), kallidin (11), and papaverine (12)] may increase the excretion of sodium in association with increased renal hemodynamics. The present studies were undertaken to determine 1) the extent to which local renal vasodilatation may increase the excretion of sodium, 2) whether such increases in sodium excretion may be due to decreased tubular reabsorption, and 3) to what extent an effect of increased blood flow on tubular reabsorption may be operative during different degrees of saline loading.…”

Analysis of Direct Renal Actions of Alpha and Beta Adrenergic Stimulation Upon Sodium Excretion Compared to Acetylcholine

“…Cholinergic drugs injected into the renal artery of the dog have been shown to produce saluresis by a direct renal action (Vander, 1964;Pinter, O'Morchoe & Sikand, 1964;Lavender, Aho & Pullman, 1965;Williams, Pearson & Carter, 1965). This saluresis is effected chiefly by increasing the tubular rejection fraction of the filtered load of sodium (Williams et a)., 1965).…”