Alpha-1 adrenoceptors and calcium in isolated canine coronary arteries.

Experiments were designed to define the postjunctional alpha adrenoceptor subtype(s) in large canine coronary arteries and to determine the dependency of contractions due to their activation upon the entry of extracellular calcium. Rings of left circumflex coronary artery were mounted at their optimal length for isometric tension recording in organ chambers filled with physiological salt solution. Phenylephrine and cirazoline were full agonists relative to norepinephrine. Methoxamine was a partial agonist relative to norepinephrine whereas clonidine, xylazine, B-HT 920 and B-HT 933 produced minimal contractions. Prazosin competitively inhibited the contractile response to phenylephrine (pA2 = 8.6), whereas rauwolscine caused a noncompetitive inhibition and was more than 100 times less potent than prazosin at inhibiting the response to phenylephrine. Similar results were obtained using norepinephrine (in the presence of propranolol) as the agonist. The calcium-entry blockers nimodipine, verapamil and diltiazem inhibited contractions caused by norepinephrine, phenylephrine and cirazoline. Removal of extracellular calcium abolished the response to cirazoline. These results suggest that in large canine coronary arteries: 1) only alpha-1 adrenoceptors are present postjunctionally and 2) responses due to alpha-1 adrenoceptor activation are dependent upon extracellular calcium.