Source of calcium and cholinergic contraction of the rat portal vein and the sheep coronary artery.

To demonstrate the heterogeneity in behavior of the rat portal vein and the sheep coronary artery, we studied the effect of cholinergic stimulation and its dependence upon extracellular ions. Since acetylcholine produces a contraction antagonized by atropine (pA2 9.5), these effects must be mediated by muscarinic receptors. alpha- and beta-adrenergic blocking agents or a drug which destroys noradrenergic nerve endings (6-hydroxydopamine) do not modify the effects of acetylcholine. In a calcium-free medium (EGTA 10(-4) M), the portal vein, unlike the coronary artery, doses not contract to acetylcholine or caffeine. In the coronary artery only the phasic component of the cholinergic contraction is maintained in a calcium-free medium. Verapamil and cobalt abolish the cholinergic contraction of the portal vein, but inhibit only the tonic component in the coronary artery. In a calcium-free medium, hyperosmotic solutions (290 mM sucrose) produce a moderate contraction which occurs slowly in both vessels. In the coronary artery, a sodium-calcium exchange does not appear to participate in the sustained tonic component of the cholinergic contraction. Electron microscopy demonstrates differences between the two blood vessels regarding the size of the sarcoplasmic reticulum. The coronary artery uses calcium both from extra- and intracellular sources. Portal vein is extremely dependent of the extracellular calcium but we were unable to give direct evidence of the utilization of calcium from intracellular pools during the cholinergic contraction of the rat portal vein.