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Title: Effects of the Ca2+ agonists, Bay K 8644 and CGP 28392, on isolated cat cerebral and peripheral arteries. Author: Fernández-Alfonso MS, Alonso MJ, Rico I, Salaices M, Sánchez-Ferrer CF, Marín J. Journal: Brain Res; 1988 Nov 22; 474(1):147-54. PubMed ID: 2463854. Abstract: Ca2+-agonists, Bay K 8644 and CGP 28392, produced concentration-dependent contractions in cat middle cerebral arteries. Only Bay K 8644 induced contractile responses in femoral arteries when they were partly depolarized with 15 mM K+. Nifedipine (0.3 microM) caused a reduction of the contractions elicited by low concentrations of both Ca2+ agonists. In femoral arteries, Bay K 8644 (0.1 microM) increased the contractions elicited by K+ concentrations from 25 to 120 mM, whereas CGP 28392 (0.1 microM) only potentiated the response caused by 25 mM K+. The increase of K+-responses induced by Bay K 8644 was blocked by nifedipine (0.1 microM), whereas that produced by CGP 28392 was not only antagonized but the remaining contractions were less than those obtained in the control situation. In both kinds of arteries preincubated with [3H]noradrenaline, nifedipine (50 microM), CGP 28392 (1 microM and 10 microM) and Bay K 8644 (1 microM) neither modified the spontaneous tritium release nor the stimulated tritium secretion elicited by K+ (25, 50 and 75 mM) or electrical stimulation. These data suggest that CGP 28392 and, mainly, Bay K 8644 facilitate the Ca2+ entry into smooth muscle cells, through voltage-dependent Ca2+ channels (that appear to be preactivated in cerebral arteries), whereas those present in the perivascular adrenergic nerve terminals are unaffected. This fact indicates that the channels existent in both vascular structures seem to have different properties.[Abstract] [Full Text] [Related] [New Search]