The small molecular weight peptide, atrial natriuretic peptide (ANP), produces marked sodium and water excretion. The peptide, extracted from several species of vertebrate heart, also has been shown to increase glomerular filtration and reduce plasma volume. Several mechanisms have been proposed to account for the action of the peptide but remain undefined. In the present report, the ANP-induced alterations in transcapillary water movement were directly assessed. The modified Landis technique was used to measure single capillary hydraulic conductivity (Lp) of vessels from the frog mesenteric circulation. In 6 individual microvessels, Lp was measured under control conditions and again during perfusion with 10 X 10(-6) M ANP. The Lp increased in each vessel by a mean of 3.79-fold (+/- 2.09 SD). In 4 of these vessels, an additional measurement of Lp was repeated under control conditions; the capillary filtration coefficient returned to control levels. It was concluded that ANP directly and reversibly elevates capillary hydraulic conductivity; this response is independent of changes in capillary hydrostatic pressure or surface area.
The influence of renal perfusion pressure on renin release was examined in rats administered the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). Compared with the control plasma renin of 6.0 +/- 0.7 ng angiotensin I (ANG I).ml-1.h-1, plasma renin activity was suppressed (1.8 +/- 0.2 ng ANG I.ml-1.h-1, P < 0.05) in L-NAME-treated animals in which the renal perfusion pressure was permitted to increase and reached 141 +/- 8 mmHg. Plasma renin activity also was suppressed (2.5 +/- 0.4 ng ANG I.ml-1.h-1, P < 0.05) in a second L-NAME-treated group in which the renal perfusion pressure was controlled to a level of 105 +/- 5 mmHg via tightening of a suprarenal aortic snare. Plasma renin activity was increased (12.0 +/- 1.4 ng ANG I.ml-1.h-1, P < 0.05) in a third L-NAME-treated group in which renal perfusion pressure was reduced to 59 +/- 1 mmHg. Overall, these findings suggest that the intrarenal pressure-sensing mechanism for renin release does not stringently require nitric oxide synthesis. In a second experimental series, bilaterally renal-denervated rats were administered L-NAME, and again plasma renin activity was suppressed significantly whether renal perfusion pressure was permitted to increase or was controlled. Thus L-NAME also suppressed plasma renin activity independently of reflex reductions in renal neuroadrenergic activity even when renal perfusion pressure was controlled. Infusions of sodium nitroprusside completely inhibited L-NAME-induced suppression of plasma renin activity in these renal-denervated rats. Nitric oxide may function as a paracrine stimulatory mechanism for the local regulation of renin release.
Constriction of the thoracic inferior vena cava to decrease venous return and atrial filling markedly elevates plasma renin activity (PRA) and plasma aldosterone concentration (PAC) and produces chronic sodium retention and ascites in the dog. Infusion of a synthetic atrial natriuretic factor into conscious dogs with caval constriction and ascites at doses of 175 and 350 ng X kg-1 X min-1 for 30 min each produced striking increases (P less than 0.05) in creatinine clearance, diuresis, and kaliuresis but failed to increase urinary sodium excretion. Infusions of atrial natriuretic factor at these doses into conscious normal dogs, however, produced a striking increase in sodium excretion from 41 +/- 14 and 55 +/- 19 mu eq/min to 150 +/- 58 and 181 +/- 49 mu eq/min (P less than 0.05 for both values). Creatinine clearance and urine flow also increased in these normal dogs, but potassium excretion remained unchanged during the infusion periods. Atrial natriuretic factor produced parallel suppression (P less than 0.05) of the elevated levels of PRA and PAC in the caval dogs but failed to significantly decrease either PRA or PAC in the normal animals. Arterial pressure, heart rate, and PAH clearance were unchanged in both groups of dogs during infusion of atrial natriuretic factor. These results suggest that the pattern of renal electrolyte excretion elicited in response to the acute infusion of atrial natriuretic factor is dependent, at least partially, on the preexisting status of the renal tubules to facilitate sodium reabsorption and potassium excretion. The results also are consistent with the concept that atrial natriuretic factor might function to tonically inhibit the renin-angiotensin-aldosterone system.
Unilateral renal artery plication in dogs reduced renal blood flow by 80% and produced a sustained elevation in arterial pressure whereas plasma renin activity increased for only 4 days. Sodium was retained for 3 days after plication, but this response is similar to that after a sham operation. Of seven dogs studied chronically, elevated arterial pressure was sustained for 27 days or longer in six animals. In three dogs hypertension continued for 2 mo before collateral vessels developed and arterial pressure fell; ligation of these collaterals restored hypertension. Arterial pressure was unaffected by an infusion of [1-sarcosine, 8-alanine] angiotensin II in chronic hypertensive dogs on a normal sodium intake. This angiotensin antagonist lowered arterial pressure after sodium depletion, but became ineffective following rapid sodium repletion. Chronic hypertensive dogs showed normal responses to deoxycorticosterone acetate. These findings suggest that the renin-angiotensin system is not critically involved in maintenace of chronic two-kidney renovascular hypertension in the dog. The data also show that the homeostatic role played by the renin-angiotensin system in the maintenance of arterial pressure remained intact in chronic hypertension.
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