Abstract
Effects of the calcium channel blocker, nifedipine, were examined on the pressor and vasoconstrictor responses to stimulation of alpha-1 and alpha-2-adrenoceptors in chronically instrumented conscious dogs and Rhesus monkeys. Norepinephrine (NE), a mixed alpha-1 and alpha-2 adrenoceptor agonist, phenylephrine (PE) and methoxamine (M), selective alpha-1 adrenoceptor agonists, and B-HT 920, a selective alpha-2 adrenoceptor agonist, were injected i.v. after ganglionic (hexamethonium), beta adrenoceptor (propranolol) and muscarinic receptor (atropine methyl bromide) blockade. In the dog, NE (0.1 microgram/kg i.v.), PE (1 microgram/kg i.v.), M (20 micrograms/kg i.v.) and B-HT 920 (1 microgram/kg i.v.) produced similar increases in mean arterial pressure (NE, 52 +/- 4 mmHg; PE, 42 +/- 4 mm Hg; M, 43 +/- 7 mm Hg; B-HT 920, 45 +/- 6 mm Hg) and total peripheral resistance (NE, 20.8 +/- 5.8 mm Hg/l/min; PE, 23.1 +/- 4.2 mm Hg/l/min; M, 18.2 +/- 2.1 mm Hg/l/min; B-HT 920, 24.8 +/- 7.1 mm Hg/l/min). Nifedipine (0.5 microgram/kg/min i.v.) caused a similar attenuation of the pressor (NE, -54 +/- 8%; PE, -43 +/- 8%; M, -49 +/- 6%; B-HT 920, -56 +/- 8%) and vasoconstrictor (NE, -66 +/- 11%; PE, -52 +/- 9%; M, -60 +/- 13%; B-HT 920, -57 +/- 10%) responses to each of the alpha-adrenoceptor agonists. Nifedipine also attenuated pressor responses to alpha-1 and alpha-2 adrenoceptor agonists similarly in conscious monkeys. Thus, in conscious dogs and monkeys, calcium channel blockade attenuates similarly both alpha-1 and alpha-2 adrenoceptor-mediated vasoconstriction.
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