AJP - Heart and Circulatory Physiology, Vol 253, Issue 2 388-H393, Copyright © 1987 by American Physiological Society
Coronary vasoconstriction mediated by alpha 1- and alpha 2-adrenoceptors in conscious dogs
O. L. Woodman and S. F. Vatner
Coronary vasoconstriction was examined in response to the selective
stimulation of alpha 1- and alpha 2-adrenoceptors in chronically
instrumented conscious dogs. Norepinephrine (NE, 0.05 and 0.1 micrograms X
kg-1 X min-1), a mixed alpha 1- to alpha 2-adrenoceptor agonist,
phenylephrine (PE, 0.5 and 1.0 micrograms X kg-1 X min-1), a preferential
alpha 1-adrenoceptor agonist, and B-HT 920 (1.0 micrograms X kg-1 X min-1),
a preferential alpha 2-adrenoceptor agonist, were infused intravenously
after ganglionic (hexamethonium, 30 mg/kg iv), beta-adrenoceptor
(propranolol, 1.0 mg/kg iv), and muscarinic receptor (atropine
methylbromide, 0.1 mg/kg iv) antagonism. Equipressor doses of the
alpha-adrenoceptor agonists caused similar increases in calculated late
diastolic coronary resistance (NE, 0.57 +/- 0.10 mmHg X ml-1 X min; PE,
0.61 +/- 0.13 mmHg X ml-1 X min; B-HT 920, 0.64 +/- 0.09 mmHg X ml-1 X
min). Mechanically increasing aortic root pressure to levels similar to
those observed in response to alpha-adrenoceptor stimulation did not
increase coronary resistance. Preferential antagonism of alpha
1-adrenoceptors with prazosin (1 mg/kg iv) abolished the vasoconstrictor
response to PE but had a lesser effect on the response to B-HT 920.
Antagonism of alpha 2-adrenoceptors with rauwolscine (alpha-yohimbine, 0.1
mg/kg iv) abolished the vasoconstrictor response to B-HT 920 but had a
lesser effect on the response to PE. The response to NE was reduced to a
similar degree by either alpha 1- or alpha 2-adrenoceptor
antagonism.(ABSTRACT TRUNCATED AT 250 WORDS)
