Preglomerular and postglomerular resistance responses to different levels of sympathetic activation by hypoxia.

This study investigated the effects of graded reflex increases in renal sympathetic nerve activity (RSNA) on renal preglomerular and postglomerular vascular resistances. With the use of hypoxia to reflexly elicit increases in RSNA without affecting mean arterial pressure, renal function and stop-flow pressures were measured in three groups of rabbits before and after exposure to room air and moderate (14% O2) or severe (10% O2) hypoxia. Moderate and severe hypoxia increased RSNA, primarily by increasing the amplitude of the sympathetic bursts rather than their frequency. RSNA amplitude increased by 20 +/- 6% (P < 0.05) and 60 +/- 16% (P < 0.05), respectively. Moderate hypoxia decreased estimated renal blood flow (ERBF; 26 +/- 7%; P = 0.07), whereas estimated glomerular capillary pressure (32 +/- 1 versus 34 +/- 1 mmHg; P < 0.05) and filtration fraction (FF; P < 0.01) increased. In response to moderate hypoxia, calculated preglomerular (approximately 20%) and postglomerular (approximately 70%) resistance both increased, but only the increase in postglomerular resistance was significant (P < 0.05). In contrast, severe hypoxia decreased ERBF (56 +/- 8%; P < 0.01), GFR (55 +/- 9%; P < 0.001), and glomerular capillary pressure (32 +/- 1 versus 29 +/- 1 mmHg; P < 0.001), with no change in FF, reflecting similar preglomerular (approximately 240%; P < 0.05) and postglomerular ( approximately 250%; P < 0.05) contributions to the vasoconstriction and a decrease in calculated K(f) (P < 0.05). These results provide evidence that reflexly induced increases in RSNA amplitude may differentially control preglomerular and postglomerular vascular resistances.