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 flow-merry. 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 114 ± 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.
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Issue number||1 49-1|
|Publication status||Published - Jan 2001|
- Anesthetized rabbit
- Cortical blood flow
- Medullary blood flow
- Renal sympathetic nerve activity