Hypertension, Vol 2, 90-96, Copyright © 1980 by American Heart Association
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.
ARTICLES
Inhibition of angiotensin II potentiation of sympathetic nerve activity by beta-adrenergic antagonists
This article has been cited by other articles:
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