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Am J Physiol Regul Integr Comp Physiol 280: R62-R68, 2001;
0363-6119/01 $5.00
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Vol. 280, Issue 1, R62-R68, January 2001

Differential control of intrarenal blood flow during reflex increases in sympathetic nerve activity

Bridget L. Leonard1, Simon C. Malpas1, Kate M. Denton2, Anna C. Madden2, and Roger G. Evans2

1 Circulatory Control Laboratory, Department of Physiology, University of Auckland, Auckland, New Zealand; and 2 Department of Physiology, Monash University, Melbourne, Victoria 3168, Australia

The role of renal sympathetic nerve activity (RSNA) in the physiological regulation of medullary blood flow (MBF) remains ill defined, yet regulation of MBF may be crucial to long-term arterial pressure regulation. To investigate the effects of reflex increases in RSNA on intrarenal blood flow distribution, we exposed pentobarbital sodium-anesthetized, artificially ventilated rabbits (n = 7) to progressive hypoxia while recording RSNA, cortical blood flow (CBF), and MBF using laser-Doppler flowmetry. Another group of animals with denervated kidneys (n = 6) underwent the same protocol. Progressive hypoxia (from room air to 16, 14, 12, and 10% inspired O2) significantly reduced arterial oxygen partial pressure (from 99 ± 3 to 65 ± 2, 51 ± 2, 41 ± 1, and 39 ± 2 mmHg, respectively) and significantly increased RSNA (by 8 ± 3, 44 ± 25, 62 ± 21, and 76 ± 37%, respectively, compared with room air) without affecting mean arterial pressure. There were significant reductions in CBF (by 2 ± 1, 5 ± 2, 11 ± 3, and 14 ± 2%, respectively) in intact but not denervated rabbits. MBF was unaffected by hypoxia in either group. Thus moderate reflex increases in RSNA cause renal cortical vasoconstriction, but not at vascular sites regulating MBF.

cortical blood flow; hypoxia; medullary blood flow; renal sympathetic nerve activity; anesthetized rabbit


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