Received February 24, 2007
Revised March 16, 2007
Accepted after revision April 24, 2007
Cardiovascular Control [210]
|
Angiotensin II-based Hypertension and the Sympathetic Nervous System. The Role of Dose and Increased Dietary Salt
Fiona D McBryde 1,
Sarah-Jane Guild 1,
Carolyn J Barrett 1,
John W Osborn 2,
Simon C Malpas 1*
1 University of Auckland
2 University of Minnesota
* To whom correspondence should be addressed. E-mail: s.malpas{at}auckland.ac.nz.
 |
Abstract |
|---|
There is accumulating evidence that angiotensin II may exert its hypertensive effect through increasing sympathetic drive. However this action may be dependent on the dose of angiotensin II as well as salt intake. We determined the effect of different doses of angiotensin II, and different levels of salt intake on neurogenic pressor activity. We also examined the effect of renal denervation. New Zealand white rabbits were instrumented to continuously measure arterial pressure. The depressor response to the ganglionic blocker pentolinium tartrate (5mg/kg) was used to assess pressor sympathetic drive on days 0, 7 and 21 of a 20ng/kg/min or 50ng/kg/min continuous i.v. angiotensin II infusion. A 50ng/kg/min infusion caused an immediate increase in pressure (23±5mmHg) whereas a 20ng/kg/min infusion caused a slow increase in pressure peaking by Day 12 (17±4mmHg). The ganglionic blockade profiles indicated sympathoinhibition in the 50ng/kg/min group by Day 7, and sympathoinhibition in the 20ng/kg/min group at Day 21, corresponding to the development of hypertension. Animals on increased dietary salt (0.9% NaCl in drinking water) however showed a similar increase in pressure with 20ng/kg/min angiotensin II (16±5mmHg) but no sympathoinhibition at Day 21. Bilateral renal denervation delayed the onset but not the extent of hypertension in this group. We conclude that different doses of angiotensin II produce distinct profiles of hypertension and associated changes in pressor sympathetic drive and that increased dietary salt intake disrupts the normal sympathoinhibitory response to angiotensin II-based hypertension.
Key Words:
Angiotensin, Blood pressure, Sympathetic nervous system
