In a rat model, lacidipine demonstrated the highest potency among tested dihydropyridine calcium antagonists in inhibiting depolarization-induced coronary artery contractions.
Does not support clinical preference for lacidipine; extends preclinical dihydropyridine comparisons in rat coronaries but leaves human translation open.
We investigated the effect of 1,4-dihydropyridine calcium antagonists (nifedipine, nisoldipine, and lacidipine) on serotonin (5-HT)- and KCl (120 mM)-induced contractions of rat isolated septal coronary artery. The preparations showed the well-known biphasic response to KCl depolarization. All three calcium antagonists were more potent in inhibiting the second, tonic phase compared to the first, transient phase, with pIC50 values of 7.17 +/- 0.12/8.27 +/- 0.07 (nifedipine), 7.93 +/- 0.21/8.96 +/- 0.06 (nisoldipine), and 8.28 +/- 0.07/9.79 +/- 0.04 (lacidipine) for suppressing the first and the second phase, respectively. Furthermore, the influence of the calcium antagonists on the 5-HT concentration-response curve was investigated. Nifedipine, nisoldipine, and lacidipine concentration dependently depressed the maximum effect of 5-HT on the coronary artery preparations without influencing the pEC50 of the 5-HT concentration-response curve. In conclusion, all three dihydropyridine calcium antagonists are potent and effective inhibitors of depolarization- or 5-HT-induced coronary artery contractions. Lacidipine, a new lipophilic compound, was the most potent one in inhibiting the depolarization-induced contraction, thereby showing a marked selectivity for the tonic phase compared to the initial phasic response.
No takes yet. Share an insight, caveat, or question.
Pfaffendorf et al. (1993) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: