AJP - Heart and Circulatory Physiology, Vol 253, Issue 3 531-H539, Copyright © 1987 by American Physiological Society
Changes in adrenergic pressor responses by calcium channel modulation in conscious dogs
J. C. Wynsen, G. J. Gross, H. L. Brooks and D. C. Warltier
The influence of the slow channel calcium entry blocker, nifedipine, and
the slow channel calcium entry promoter, BAY-K 8644, on receptor-mediated
hemodynamic responses was studied in chronically instrumented, conscious
dogs. Following ganglionic, cholinergic, and beta-adrenergic blockade,
equipressor doses of phenylephrine (0.6 microgram/kg iv), a selective alpha
1-adrenoceptor agonist, and B-HT 933 (20 micrograms/kg iv), a selective
alpha 2-adrenoceptor agonist, as well as a nonadrenergic vasoconstrictor,
vasopressin (0.003 IU/kg) were administered before and after infusions of
nifedipine or BAY-K 8644 (0.25, 0.5, 1.0, and 2.0 micrograms X kg-1 X
min-1). In doses producing minimal or no haemodynamic effects, nifedipine
caused dose-related attenuation from control of phenylephrine- (from 26 +/-
3 to 8 +/- 1 mmHg), B-HT 933- (from 30 +/- 2 to 5 +/- 2 mmHg), and
vasopressin- (24 +/- 1 to 2 +/- 2 mmHg) mediated changes in mean arterial
pressure. In contrast, BAY-K 8644 produced dose-related potentiation from
control of the same pressor responses (phenylephrine, 24 +/- 2 to 41 +/- 3
mmHg; B-HT 933, 28 +/- 3 to 46 +/- 2 mmHg; vasopressin, 25 +/- 3 to 45 +/-
5 mmHg). In addition, BAY-K 8644 produced a marked increase in the duration
of the pressor response produced by all three agonists. Thus, in conscious
dogs, alpha 1-, alpha 2-, and vasopressin-mediated pressor responses are
strongly modulated by transmembrane calcium flux and can be influenced by
dihydropyridine slow channel calcium agonists and antagonists.
