Noradrenaline contractions in rabbit mesenteric arteries skinned with saponin.

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Abstract
In rings of small rabbit mesenteric arteries, noradrenaline [norepinephrine] induced oscillatory conctractions. After depolarization with K, which produced in this preparation only a transient contraction, the arteries responded to noradrenaline with tonic contraction. Artery rings, skinned for 6 min with saponin (0.5 mg/ml), were highly sensitive to Ca (half-maximum contraction at 4 .times. 10-7 M Ca2+). In the skinned preparations, a contraction was still elicited by noradrenaline. Treatment with saponin renders virtually all smooth muscle cells of the mesenteric artery preparation hyperpermeable as indicated by both physiological and morphological criteria. While the Ca stores responsible for the noradrenaline-induced contraction of skinned arteries were depleted at a slow rate by 0.1 mM EGTA [ethylene glycol bis(.beta.-aminoethyl ether) N,N,N'',N''-tetraacetic acid], they were completely emptied by a 4-min exposure to 10 mM EGTA. After release of intracellular Ca by noradrenaline, the Ca stores could be partially replenished by incubating the preparation in 10-6 M Ca2+ for 4-min. Noradrenaline failed to contract skinned arteries after part of the intracellular Ca had been released by caffeine but not after Ca release by the ionophore X-537 A. The mitochondrial uncoupler, carbonyl cyanide m-chlorophenylhydrazone, inhibited noradrenaline-induced contractions of skinned arteries. Noradrenaline had no effect on 45Ca translocation in either membrane vesicles or mitochondria isolated from mesenteric arteries. In vascular smooth muscle a certain degree of structural integrity of the cell membrane, but not its selective permeability, is required for the coupling between .alpha.-adrenoceptors and Ca release from intracellular stores. .alpha.-Adrenoceptor stimulation apparently results in release of Ca bound to the plasma membrane rather than indirect release of Ca accumulated in intracellular organelles.