Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 1980;2:90-96

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jackson, E. K.
Right arrow Articles by Campbell, W. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jackson, E. K.
Right arrow Articles by Campbell, W. B.

Hypertension, Vol 2, 90-96, Copyright © 1980 by American Heart Association


ARTICLES

Inhibition of angiotensin II potentiation of sympathetic nerve activity by beta-adrenergic antagonists

EK Jackson and WB Campbell

Since beta-adrenergic blockers are effective in the therapy of hypertension by a mechanism related to the degree of activation of the renin-angiotensin system, the effect of eight beta blockers was examined on angiotensin II potentiation of nerve stimulation (NS) in isolated perfused rat mesenteric vessels. The vasoconstrictor response to periarterial NS was obtained by monitoring changes in perfusion pressure while a beta blocker or a beta blocker and angiotensin II (3 ng/ml) were added to the perfusate. Although each beta blocker tended to decrease responses to NS, in the concentrations used, only metoprolol significantly inhibited responses to NS. Angiotensin II, when infused alone, potentiated the responses to NS by 63% (p less than 0.01). These enhanced responses following angiotensin II were inhibited in a dose-related manner (10--300 ng/ml) by beta 1, beta 2, and mixed beta blockers. At the 100 ng/ml concentration, DL-propranolol, timolol, metoprolol, practolol, butoxamine, and H35/25 inhibited the angiotensin II potentiation of NS by 83%, 76%, 77%, 59%, 72%, and 41% respectively. The order of potency for this action was as follows: timolol = metoprolol = butoxamine greater than propranolol greater than practolol greater than H35/25. Administration of D- and L-propranolol also reduced the responses by 75%. The vasoconstrictor responses to injected norepinephrine (NE), in the presence and absence of angiotensin II, were not altered by DL-propranolol or timolol. In conclusion, beta- adrenergic blockers were found to interfere with the effect of angiotensin II on the sympathetic neuron, a property that could contribute to the antihypertensive action of these drugs.


This article has been cited by other articles:


Home page
J. Pharmacol. Exp. Ther.Home page
E. K. Jackson, Z. Mi, D. G. Gillespie, and R. K. Dubey
Metabolism of cAMP to Adenosine in the Renal Vasculature
J. Pharmacol. Exp. Ther., October 1, 1997; 283(1): 177 - 182.
[Abstract] [Full Text]