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- Title
Nitric oxide in responses of regional kidney perfusion to renal nerve stimulation and renal ischaemia.
- Authors
Eppel, Gabriela A.; Denton, Kate M.; Malpas, Simon C.; Evans, Roger G.
- Abstract
The mechanisms underlying the relative insensitivity of medullary blood flow (MBF) to sympathetic drive remain unknown. We tested the effects of nitric oxide synthase blockade on regional kidney perfusion responses to electrical renal nerve stimulation (RNS) in pentobarbitone-anaesthetized rabbits. Under control conditions, RNS reduced renal blood flow (RBF), cortical blood flow (CBF) and MBF in a frequency-dependent manner. MBF was always reduced less than CBF or RBF. NG-nitro-l-arginine increased mean arterial pressure (31±3 mmHg), reduced RBF (-8±1 ml/min) and MBF (-33±6 units), enhanced responses to RNS of RBF (from -48±6% to -58±6% at 2 Hz), CBF (from -38±6% to -43±4% at 2 Hz) and, particularly at low frequencies, MBF (from +1±18% to -32±11% at 2 Hz) and potentiated the RBF hyperaemic response following RNS (by 27±6% at 4 Hz). When glyceryl trinitrate was co-infused with NG-nitro-l-arginine to restore basal nitrergic tone, responses to RNS and the subsequent hyperaemia were indistinguishable from control. Since resting renovascular tone or perfusion pressure has little impact on MBF responses to RNS, these present observations suggest that NO contributes to the blunted MBF response to RNS. Paradoxically, NO seems to blunt renal hyperaemia following acute RNS-induced ischaemia.
- Subjects
NITRIC oxide; NITROGEN compounds; ISCHEMIA; HEMODYNAMICS; NEURAL stimulation; BLOOD flow
- Publication
Pflügers Archiv: European Journal of Physiology, 2003, Vol 447, Issue 2, p205
- ISSN
0031-6768
- Publication type
Article
- DOI
10.1007/s00424-003-1149-1