Effect of S-312, a new calcium channel blocker, on the 1,4-dihydropyridine binding sites in porcine basilar blood vessels and rat aortic smooth muscle cells.

  title={Effect of S-312, a new calcium channel blocker, on the 1,4-dihydropyridine binding sites in porcine basilar blood vessels and rat aortic smooth muscle cells.},
  author={S. Mihara and M. Fujimoto},
  journal={Japanese journal of pharmacology},
  volume={56 3},
We examined the interaction of two isomers of S-312, a new calcium channel blocker with a bicyclic dihydrothienopyridine structure, with 1,4-dihydropyridine binding sites. Specific bindings of [3H]nitrendipine and (+)-[3H] PN200-110 in membranes prepared from porcine basilar blood vessels were saturable, reversible, and stereoselective, and had high affinities. The binding properties were very similar to those in membranes from other tissues such as the aorta, myocardium, and cerebral cortex. 1… Expand
3 Citations
Activity of dihydrothienopyridine S312 enantiomers on L-type Ca2+ channels in isolated rat aorta and cerebral microvessels.
It is concluded that the dihydrothienopyridine S312 could interact with Ca2+ channels in a manner different to that of genuine dihydropyridines. Expand
Pharmacological studies on a new dihydrothienopyridine calcium antagonist, S-312-d. 5th communication: anticonvulsant effects in mice.
Although moderate anticonvulsant effects of S-312-d in higher doses were observed against the clonic convulsions induced by pentylenetetrazole or bemegride, no effects were observed in convulsion induced by N-methyl-D-aspartate, picrotoxin, or electroshock in Slc:ddY mice. Expand
Efficient regioselective one-pot synthesis of partially hydrogenated thiazolo[3,2-a]pyridines
Abstract 7 H -Thiazolo[3,2- a ]pyridin-3(2 H )-ones, 7 H -thiazolo[3,2- a ]pyridin-3(2 H )-imines, and 3-hydroxy-3-methyl(phenyl)-2,3-dihydro-7 H -thiazolo[3,2- a ]pyridines have been obtained inExpand


Specific binding of [3H]nitrendipine to membranes from coronary arteries and heart in relation to pharmacological effects. Paradoxical stimulation by diltiazem.
The results suggest that there may be multiple binding sites for different “subclasses” of calcium channel inhibitors, and that drug binding sites may be different molecular entities from the putative calcium channels. Expand
Binding of a calcium antagonist, [3H]nitrendipine, to high affinity sites in bovine aortic smooth muscle and canine cardiac membranes.
Results suggest that the [(3)H]nitrendipine binding sites are the sites through which dihydropyridines act as calcium channel antagonists. Expand
Comparison of high affinity binding of calcium channel blocking drugs to vascular smooth muscle and cardiac sarcolemmal membranes.
It is concluded that the high affinity binding sites for nitrendipine in bovine aortic smooth muscle membranes are similar to those of canine ventricular sarcolemma. Expand
Characterization of calcium channel antagonist binding sites labeled by [3H]nitrendipine in porcine coronary artery and aorta.
The present study has shown that [3H]NTD selectively labels the pharmacologically relevant dihydropyridine receptors in the porcine coronary artery and that there is no significant difference between the binding characteristics of the receptor sites in the coronary arteries and aorta of pigs. Expand
Effects of S-312, a new calcium antagonist, on the mechanical and electrophysiological responses of isolated cardiovascular preparations.
The present results indicate that S-312 is a potent new calcium antagonist possessing vasculoselectivity, especially for cerebral vessels. Expand
Characterization of binding of the Ca++ channel antagonist, [3H]nitrendipine, to guinea-pig ileal smooth muscle.
The data suggest that [3H]nitrendipine binding in smooth muscle is to a site which mediates the pharmacologic response, which is consistent with previous reports. Expand
Depolarization-dependent binding of the calcium channel antagonist, (+)-[3H]PN200-110, to intact cultured PC12 cells.
Investigation of the effect of K+-depolarization on binding of the dihydropyridine Ca++ channel antagonist, (+)-[3H]PN200-110, to intact PC12 cells in culture provides evidence that this form of Ca++Channel regulation occurs in neural, as well as muscle, cells. Expand
Voltage-dependent binding of dihydropyridine calcium channel blockers to guinea pig ventricular myocytes.
The results demonstrated that the effect of depolarization induced by high extracellular K+ compared to normal K+ was an increase in the observed number of binding sites (Bmax) with no change in the measured affinity of binding (Kd). Expand
Two states of the L-type Ca2+ channel in PC12 cells: Different sensitivity to 1,4-dihydropyridines
The biphasic blockade of the high K(+)-induced [Ca2+]i rise by 1,4-dihydropyridines appears to reflect their different affinities under depolarizing and non-depolarizing conditions. Expand
Pharmacologic and radioligand binding analysis of the actions of 1,4-dihydropyridine activator-antagonist pairs in smooth muscle.
The biphasic response to (-)- (S)-Bay K 8644 and (+)-(S)-202-791 suggests that the properties of Ca++ channel activation and antagonism may reside within a single 1,4-dihydropyridine molecule. Expand