Conference Publication Details
Mandatory Fields
Ahmeda, Ahmad F; Johns, Edward J;
Bristol, UK, Physiological Society Meeting
Role of nitric oxide in neural control of intra-renal homodynamic in anaesthetised normotensive and hypertensive rats
2005
January
Validated
1
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Optional Fields
J Physiol 567P: C104
Bristol

Nitric oxide (NO) produced in the renal cortex and medulla by nitric oxide synthase (NOS) regulates basal levels of renal haemodynamics and may be involved in neurally mediated vasoconstriction. This study investigated whether NO modulated renal sympathetic nerve (RSN) mediated reductions in renal cortical and medullary blood flow normally and in hypertension. Four groups (n= 6-10) of male Wistar and stroke-prone spontaneously hypertensive rats (SHRSP), 250-300g, were anaesthetised with 1 ml chloralose/urethane, 16.5/250 mg/ml, i.p. The right femoral vein and artery were cannulated for saline infusion (154mM NaCl, at 3ml/h) and measurement of blood pressure (BP), respectively. The left kidney was exposed via the flank and a cannula inserted 4.5mm for intramedullary (i.m.) saline or drug infusion at 0.6-1.0 ml/h. Laser-Doppler microprobes were inserted 1.5 and 4.0 mm into the kidney to measure cortical and medullary blood perfusion (CP and MP), respectively (100 perfusion units (PU) = 1 V). Bipolar stainless steel electrodes were applied to the the renal nerves. After 90 min, baseline CP and MP were taken, and the RSN stimulated, 15V, 2 ms for 1 min, at 0.5, 1, 2 and 4 Hz, then either vehicle or L-NAME, 10 μg/kg/min, was infused i.m. for 90 min and the stimulation protocol was repeated. Data±SEM were subjected to Student’s t test and significance taken at P<0.05. The animals were killed with an anaesthetic overdose. In the Wistar rats, baseline levels of BP, MP and CP were 109±5 mmHg, 125±17 PU and 61±13 PU. respectively and for the SHRSP rats, BP was 123±3 mmHg, CP was 108±18 PU and MP was 60±9 PU. L-NAME infusion i.m. increased BP in both Wistar and SHRSP rats by 15±4% and 7±2% mmHg, respectively (both P<0.05), and reduced MP in the Wistar rats by 15±5% (P<0.05), with no significant change in the SHRSP; L-NAME had no effect on CP in either Wistar or SHRSP. In the Wistar rats, RSN stimulation reduced the MP and CP by 18 and 32%, respectively (both P<0.05), at 4 Hz while in the presence of L-NAME, the reductions in MP and CP were similar reaching 16 and 32% at 4 Hz, respectively (P<0.05). In the SHRSP, the RSN-mediated reductions in MP and CP were 7 and 8% at 4 Hz, respectively (both P<0.05). Following L-NAME infusion i.m., both MP and CP were reduced by 14 and 29% at 4 Hz, respectively (both P<0.05). These results indicate that over the low frequency range of stimulation NO plays little role in buffering the renal medulla from the RSN induced vasoconstrictions. However, NO does appear to have modulatory action in the hypertensive state.

http://www.physoc.org/proceedings/abstract/J%20Physiol%20567PC104
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