Hypertension, Vol 5, 26-33, Copyright © 1983 by American Heart Association
Y Furukawa, P Scipione and MN Levy
In anesthetized dogs with the left cardiac sympathetic nerves and both
vagal nerves intact, angiotensin II (AII) induced a substantial, dose-
dependent increase in arterial blood pressure and small increments in
cardiac cycle length and ventricular contractile force. In dogs in which
the cardiac sympathetic and vagal nerves had been interrupted, AII produced
similar increases in blood pressure and larger increases in contractile
force, but it decreased the cardiac cycle length. In both groups of dogs,
AII augmented substantially the positive inotropic responses to sympathetic
nerve stimulation, but it enhanced the positive chronotropic responses only
slightly. However, AII did not appreciably prolong the cardiac responses to
sympathetic nerve stimulation, nor did it alter significantly the cardiac
responses to norepinephrine infusions. Hence, at the dosage levels used,
AII probably did not inhibit the neuronal uptake of norepinephrine
appreciably nor did it enhance the responsiveness of the cardiac effector
sites to norepinephrine. Therefore, the potentiation of the cardiac
responses to sympathetic nerve stimulation by AII in these experiments was
probably achieved principally by facilitating norepinephrine release from
the adrenergic nerve terminals in the heart.
ARTICLES
Effects of angiotensin II on the cardiac responses to sympathetic nerve stimulation in dogs
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