Contribution of intracellular stored calcium to contractile activation in contractures of stomach circular muscle of Bufo vulgaris formosus.

Abstract

Contractile responses of stomach circular muscle of Bufo to high-K, to acetylcholine (ACh) in normal Ringer or in high-K solution, and to calcium in Ca-free high-K solution showed a phasic contraction which relaxed completely in 30-45 sec. K-induced contracture was abolished in Ca-free solution containing 1 mM ethylene glycol bis(j3-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) within 20 sec, while ACh-induced contracture was not abolished and 10-25 % of control tension was kept up to 40 sec. This response increased to 40-50% when all extracellular Na was replaced with tris(hydroxymethyl)-aminomethane (Tris). K-induced contracture was inhibited completely by 1 mM La. ACh-induced contracture in the muscle depolarized by high-K solution was dependent on the depolarization time, 0-10, b0-70, and nearly 100% of control after 1, 3, and 10 min depolarization, respectively. These ACh-induced contractures were not inhibited by 1 mM EGTA or La. All contractures mentioned above were markedly inhibited by 5 mM procaine. These results suggest that activation of both contractures induced by high-K and ACh were, at least partly, dependent on the Ca at the intracellular Ca storage sites. Ca-induced contracture was dependent on depolarization time as was ACh-induced contracture, when the muscle was depolarized by Ca-free high-K solution without pre-treatment with Ca-free Ringer solution. These results suggest that activation of Ca-contracture is also dependent on intracellular stored Ca.

Involvement of calcium channels in the contractile activity of neurotensin but not acetylcholine: studies with calcium channel blockers and Bay K 8644 on the rat fundus

“…The selectivity of Bay K 8644 in the fundus is demonstrated by the fact that the contractile activity of ACh is not significantly altered either by nifedipine or Bay K 8644. Consistent with this finding, some authors have explained that the main source of calcium for the muscarinic contractile responses in visceral smooth muscles is not necessarily of extracellular origin, as in the case of neurotensin, but that part of it may originate from intracellular stores (Ishizawa & Miyazaki, 1977;Bolton, 1979;Shinohara & Kosaka, 1984). In this connection, the physiology ofmuscarinic responses has been hypothesized to occur by degradation of membrane phospholipids via activation of phospholipase C which generates inositol triphosphate and diacylglycerol (Brown & Brown Masters, 1984;Berridge & Irvine, 1984).…”

“…In addition, we have further expanded our arguments by demonstrating that a structural analogue of nifedipine, compound Bay K 8644, a modified dihydropyridine, potentiates the action of neurotensin. This compound has been recently demonstrated to promote calcium influx via a nifedipinesensitive mechanism in a variety of biological systems (Schramm et al, 1983;Janis et al, 1984;Taira et al, 1985 (Ishizawa & Miyazaki, 1977;Bolton, 1979;Shinohara & Kosaka, 1984). In this connection, the physiology ofmuscarinic responses has been hypothesized to occur by degradation of membrane phospholipids via activation of phospholipase C which generates inositol triphosphate and diacylglycerol (Brown & Brown Masters, 1984;Berridge & Irvine, 1984).…”

Depolarization-Stimulated Contractility of Gastrointestinal Smooth Muscle in Calcium-Free Solution: A Review

“…In rat ileal tissue, neither depolarization nor acetylcholine was able to induce a contraction during exposure to calcium-free solution with 1 mM EGTA [2]. Similar effects were found in Bufo gastric smooth muscle strips [3], rat colonic muscle strips [4], and guinea pig ileal longitudinal muscle strips [5]. …”