Abstract

After depletion of intracellular calcium stores sensitive to noradrenaline, a spontaneous increase in the resting tone (IRT) when incubated in Ca²⁺-containing solution was observed in isolated rat aorta, but not in tail artery. This IRT does not depend on agonist activation of α₁-adrenoceptors but it is inhibited by prazosin. A close relationship was found between the inhibitory potencies of prazosin (pIC₅₀ = 9.833), BMY 7378 (pIC₅₀ = 8.924), and 5-methylurapidil (pIC₅₀ = 7.883) against IRT and their affinities for cloned α_1D-adrenoceptors. Chloroethylclonidine (100 μmol · l⁻¹) did not inhibit the IRT. After depletion of internal calcium stores by noradrenaline in absence of the agonist, loading in Ca²⁺-containing solution also brings about an increase in the inositol phosphate (IP) levels in rat aorta (not seen in tail artery) that is inhibited by prazosin (1 μmol · l⁻¹), BMY 7378 (10 μmol · l⁻¹), and 5-methylurapidil (10 μmol · l⁻¹), thus confirming the results obtained in contractile studies. Chloroethylclonidine (100 μmol · l⁻¹) did not inhibit this IP accumulation. The fact that the IRT and the IP accumulation related to it can be selectively inhibited by different α₁-adrenoceptor antagonists suggests the existence of a population of α_1D-adrenoceptors that show constitutive activity in rat aorta, not in tail artery.