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This Article Full Text Full Text (PDF) All Versions of this Article: 92/5/831    most recent expphysiol.2007.037473v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by McBryde, F. D. Articles by Malpas, S. C. Search for Related Content PubMed PubMed Citation Articles by McBryde, F. D. Articles by Malpas, S. C.

¹ Circulatory Control Laboratory, Department of Physiology and Bioengineering Institute, University of Auckland, Auckland, New Zealand ² Department of Physiology, University of Minnesota, Minneapolis, MN, USA

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 (5 mg kg^–1) was used to assess pressor sympathetic drive on days 0, 7 and 21 of a 20 or 50 ng kg^–1 min^–1 continuous I.V. angiotensin II infusion. A 50 ng kg^–1 min^–1 infusion caused an immediate increase in pressure (23 ± 5 mmHg), whereas a 20 ng kg^–1 min^–1 infusion caused a slow increase in pressure, peaking by day 12 (17 ± 4 mmHg). The ganglionic blockade profiles indicated sympathoinhibition in the 50 ng kg^–1 min^–1 group by day 7 and sympathoinhibition in the 20 ng kg^–1 min^–1 group at day 21, corresponding to the development of hypertension. Animals receiving increased dietary salt (0.9% NaCl in drinking water), however, showed a similar slow increase in pressure with 20 ng kg^–1 min^–1 angiotensin II (16 ± 5 mmHg) 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.

(Received 24 February 2007; accepted after revision 24 April 2007; first published online 27 April 2007)
Corresponding author S. C. Malpas: Private Bag 92019, Auckland, New Zealand. Email: s.malpas{at}auckland.ac.nz

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