Submitted on June 23, 2006
Accepted on December 21, 2006
The role of renal sympathetic nerve activity in the hypertension induced by chronic nitric oxide inhibition
Rohit Ramchandra1, Carolyn J Barrett2, Sarah-Jane Guild2, Fiona D McBryde2, and Simon C. Malpas3*
1 Howard Florey Institute, Melbourne University, Melbourne, Victoria, Australia
2 Physiology, University of Auckland, Auckland, New Zealand
3 Physiology, University of Auckland, Auckland, New Zealand; Bioengineering Insitute, University of Auckland, Auckland, New Zealand
* To whom correspondence should be addressed. E-mail: s.malpas{at}auckland.ac.nz.
Nitric oxide levels are diminished in hypertensive patients suggesting nitric oxide might have an important role to play in the development of hypertension. Chronic blockade of nitric oxide leads to hypertension which is sustained throughout the period of the blockade in baroreceptor intact animals. It has been suggested that the sympathetic nervous system is involved in the chronic increase in blood pressure, however the evidence is inconclusive. We measured renal sympathetic nerve activity and blood pressure via telemetry in rabbits over 7 days of nitric oxide blockade. Nitric oxide blockade via L-NAME in the drinking water (50mg/kg/day) for 7 days caused a significant increase in arterial pressure (7 ± 1 mmHg above control levels; p < 0.05). While the increase in blood pressure was associated with a decrease in heart rate (from 233 ± 6 bpm before the L-NAME to 202 ± 6 bpm on day 7), there was no change in renal sympathetic nerve activity (94 ± 4 % of baseline levels on day 2 and 96 ± 5 % of baseline levels on day 7 of L-NAME; baseline nerve activity levels were normalised to the maximum 2s of nerve activity evoked by nasopharyngeal stimulation). The lack of change in renal sympathetic nerve activity during the L-NAME induced hypertension indicates that the renal nerves do not mediate the increase in blood pressure in conscious rabbits.
