Abstract
A number of studies indicate that relative to the maximal tone possible, for example, to histamine, noradrenaline produces only weak contractile responses in the rabbit basilar artery. Various factors, including a limited number of α-adrenoceptors, have been proposed to account for the reduced response to noradrenaline. We examined the effect of the Ca2+ -channel activator, Bay K 8644 (0.1 and 1.0 nM) on dose-response curves to noradrenaline, histamine, calcium (Ca2+) and potassium (K+) in ring preparations of rabbit basilar artery and central ear artery. These concentrations of Bay K 8644 (0.1 and 1.0 nM) increased the magnitude of tension developed by noradrenaline (contractility) in the basilar artery, but did not alter its sensitivity (ED50) to the adrenergic vasoconstrictor. Bay K 8644 (0.1 and 1.0 nM) did not alter the contractility or sensitivity to histamine or K+ of the rabbit basilar artery. When dose–response curves to Ca2+ were made in K+-depolarized rabbit basilar artery rings, Bay K 8644 (0.1 and 1.0 nM) dose-dependently augmented tone generated by readmission of Ca2+. Bay K 8644 (0.1 and 1.0 nM) did not alter responses to noradrenaline, histamine, or K+ in rabbit central ear artery preparations. These results are compatible with a voltage-dependent mechanism of action of Bay K 8644 in the rabbit basilar artery, which may be partially depolarized in the resting state. We propose that in addition to other factors, the contractile response of rabbit basilar arteries is limited by a weak or inefficient coupling of α-adrenoceptors to Ca2+ channels. The effect of Bay K 8644 on cerebral vascular tone generated by noradrenaline is to improve coupling thus allowing a greater influx of extracellular Ca2+.