Disease relevance of YC-170

• Using an experimental model of global ischemia of the brain in rats, we have shown that a Ca2+ antagonist nicardipine attenuates, and a Ca2+ agonist YC-170 accelerates, the liberation of free fatty acids in the ischemic whole brain [1].

High impact information on YC-170

• 1. We investigated the voltage-dependence of the agonist actions of YC-170, a dihydropyridine (DHP) derivative, on cardiac L-type Ca2+ channels in rabbit ventricular cells, using the patch clamp technique [2].
• YC-170 (0.1-3 mg/kg i.v.) produced dose-dependent increases in blood pressure, total peripheral resistance and maximum dLVP/dt with slight reductions of heart rate and aortic blood flow [3].
• Like Bay K 8644, however, YC-170 increased the time to peak tension and relaxation time of the isometric tension, and prolonged the action potential duration [4].
• Moreover, we administered calcium channel agonist (0.5 microM YC-170) and calcium channel antagonists to the fibroblasts [5].
• Vascular and insulinotropic effects of YC 170, a calcium agonist, on isolated perfused rat pancreas [6].

Anatomical context of YC-170

• Vascular and insulinotropic effects of YC 170 can be dissociated, suggesting variable abilities to promote calcium transport across membranes of smooth muscle cells and of pancreatic B-cells [6].

Associations of YC-170 with other chemical compounds

• In pithed rats, intravenous injection of YM-16151-4 inhibited a YC-170-induced pressor response and an isoproterenol-induced positive chronotropic response with DR10 values of 4.20 and 0.31 mg/kg, respectively [7].

References