@article {Yamada327, author = {S Yamada and R Kimura and Y Harada and K Nakayama}, title = {Calcium channel receptor sites for (+)-[3H]PN 200-110 in coronary artery.}, volume = {252}, number = {1}, pages = {327--332}, year = {1990}, publisher = {American Society for Pharmacology and Experimental Therapeutics}, abstract = {The receptor sites for 1,4-dihydropyridine (DHP) Ca++ channel antagonists in porcine coronary artery were identified and characterized by a binding assay using (+)-[3H]PN 200-110 as a radioligand. Specific (+)-[3H]PN 200-110 binding in porcine coronary artery was saturable, reversible and of high affinity (Kd = 0.24 nM) and it showed a pharmacological specificity as well as stereoselectivity which characterized the receptor sites for DHP Ca++ channel antagonists. DHP antagonists competed for the (+)-[3H]PN 200-110 binding in order: PN 200-110 greater than mepirodipine greater than nisoldipine greater than nicardipine greater than nitrendipine greater than nimodipine greater than nifedipine greater than (-)-PN 200-110. (+)-PN 200-110 was approximately 140 times as potent as the (-)-isomer. The potencies (PKi) of these eight DHP Ca++ channel antagonists in competing for (+)-[3H]PN 200-110 binding sites in porcine coronary artery correlated well with their pharmacological potencies. Specific (+)-[3H]PN 200-110 binding in the coronary artery was enhanced by d-cis-diltiazem and was inhibited incompletely by verapamil and D-600. In EDTA-pretreated coronary artery, the maximal number of binding sites for specific (+)-[3H]PN 200-110 binding was reduced (80\%) markedly, and it was restored to the untreated level by the addition of Ca++ and Mg++.(ABSTRACT TRUNCATED AT 250 WORDS)}, issn = {0022-3565}, URL = {https://jpet.aspetjournals.org/content/252/1/327}, eprint = {https://jpet.aspetjournals.org/content/252/1/327.full.pdf}, journal = {Journal of Pharmacology and Experimental Therapeutics} }