Inhibition by suloctidil of [3H] nitrendipine binding to cerebral cortex membranes.
[3H] Nitrendipine binds specifically with high affinity and high capacity (KA congruent to 0.20 +/- 0.01 nM, Bmax = 4.4 +/- 0.3 pM/g tissue, means +/- S.E.M.; N = 4) to guinea-pig cerebral cortex membranes. Suloctidil fully inhibits [3H] nitrendipine binding with a Ki value of 0.45 microM. The interaction between suloctidil and the putative Ca2+ channels is allosteric as shown by competition experiments performed in the presence of D 600 or diltiazem. Comparison of the activity of some close analogs of suloctidil provides evidence for the importance of the amino group and of the hydrophobic amino substituent in the interaction of suloctidil and the putative Ca2+ channel. It is suggested that part of the previously reported blockade of Ca2+ entry induced by suloctidil is due to a blockade of the Ca2+ channels.
D000818:Animals; D001665:Binding Sites; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002462:Cell Membrane / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism*; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008297:Male; D009543:Nifedipine / Q000031:analogs & derivatives* / Q000378:metabolism; D009568:Nitrendipine; D011412:Propanolamines / Q000494:pharmacology*; D013329:Structure-Activity Relationship; D013468:Suloctidil / Q000494:pharmacology*; D014316:Tritium
D002121:Calcium Channel Blockers; D011412:Propanolamines; D014316:Tritium; D009568:Nitrendipine; D009543:Nifedipine; D013468:Suloctidil