Autoregulatory responses of superficial nephrons and their association with sodium excretion during arterial pressure alterations in the dog.

SUMMARY Micropuncture experiments were conducted to assess autoregulatory behavior of superficial nephrons and to evaluate the possible contribution of alterations in tubular and peritubular capillary pressures to the mechanism responsible for the arterial pressure effects on urine flow and sodium excretion. In response to decreases in renal arterial pressure (RAP), autoregulation of renal blood flow (RBF) and glomerular filtration rate (GFR) was highly efficient to blood pressures as low as 80 mm Hg. Proximal tubule pressure (PTP), peritubular capillary pressure (PCP), distal tubule pressure, and single nephron GFR (SNGFR) remained within 5% of control values with reductions in RAP to 90 mm Hg. Further decreases in RAP to the lower autoregulatory range caused significant decreases in PTP and PCP; the slight decreases in SNGFR were not significant. Within the autoregulatory range, GFR and filtered sodium load were not altered, and urine flow and sodium excretion responses were due to changes in net fractional sodium and water reabsorption. No quantitative relationships could be established between the magnitude of the changes in urine flow or sodium excretion and PTP, PCP, or proximal tubule fractional reabsorp- tion. These experiments demonstrate that superficial nephrons autoregulate in association with the total nephron population except for a proportionately greater reduction when RAP is reduced to the lower autoregulatory range. Furthermore, the urinary responses to reduced arterial pressure occur even in the absence of quantitatively associated alterations in proximal tubule function or PCP. SUMMARY We used 25-/im microspheres to compare blood flow to the V-2 carcinoma in the awake, unanesthe- tized rabbit with blood flow to other organs. Injection of norepinephrine (50 /ig) into the left ventricle caused a 41-fold [95% confidence interval = (25-69)] increase in tumor vascular resistance (P < 0.01). This was more than one order of magnitude greater than the increase in resistance in any other organ. Prostaglandin E 2 (50 /ig) injected into the left ventricle caused a 7-fold (4-13) increase in tumor vascular resistance (P < 0.01) and no significant increase of the vascular resistance of other organs. The change in tumor vascular resistance was not completely due to an increased level of circulating catecholamines because a 2-fold (1.6-3.4) increase in the resistance (P < 0.01) was seen when prostaglandin E, was injected into the left ventricle of animals pretreated with phenoxybenzamine. The prostaglandin E 2 -induced tumor vasoconstriction was not due to an increased level of circulating angiotensin II because in animals in which a and angiotensin receptors were blocked, prostaglandin E 2 increased the tumor vascular resistance by a factor of 3 (2.3-5.5) (P < 0.01). The tumor vasculature appears to be hypersensitive to a-receptor activation and responds to prostaglandin E 2 with vasoconstriction which cannot be accounted for by an increased level of circulating catecholamines or angiotensin II. In these experiments, the vasculature of the tumor responded to pharmacological agents in a manner that was not displayed by the vasculature of other organs. It may be possible to selectively control tumor blood flow without adversely affecting the blood flow to other organs of the host.