The effects of angiotensin II (AII), epinephrine and changes in perfusion pressure on glomerular capillary and afferent arteriolar pressures were assessed using the in vitro blood perfused juxtamedullary nephron (JMN) preparation. At a perfusion pressure of 102 ± 1 mm Hg, glomerular capillary pressure (GCP) averaged 55 ± 1 mm Hg. Afferent arteriolar pressure (AAP), measured at early-to-mid afferent locations, was 88 ± 2 mm Hg and decreased to 71 ± 7 mm Hg at the most terminal segments, 50 to 80 μm from the glomerulus. In some nephrons, readjustments of GCP occurred in response to step changes in perfusion pressure within the range of 90 to 165 mm Hg. In 37 nephrons, bolus injections of AII into the blood caused dose-dependent and reversible decreases in GCP, ranging from -4 ± 1 mm Hg (12 to 25 pg) to -26 ± 4 mm Hg (20 ng). Similar decreases in GCP ranging from -9 ± 3 to -22 ± 3 mm Hg were observed in response to epinephrine (1.25 to 20 ng). Epinephrine also consistently reduced AAP by 37 ± 10% (N = 8). In contrast, AII typically increased pressure in the early and mid segments of the afferent arteriole, but caused variable responses in the late afferent arteriole. The responses to vasoconstrictor agents were not mimicked by increases in perfusion pressure per se. These results indicate that the preglomerular vasculature of in vitro JMN can exhibit autoregulatory behavior and is responsive to humoral vasoconstrictors. The response to epinephrine was generalized occurring along the entire preglomerular vasculature, while the predominant effects of AII were localized to terminal afferent structures, which may include intraglomerular constrictor elements.
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