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• W2186118727 abstract "To investigate the effects and mechanisms of calcitonin gene-related peptide (CGRP) on ventricular contractility, ventricular myocytes isolated from adult rat and mouse hearts were exposed to CGRP. Myocyte contractility was assessed by a video edge motion detector, and the intracellular [Ca 2+ ] transients were measured by a spectroflurophotometer in fura 2-loaded myocytes. CGRP exerted a potent concentration-dependent (10 pM–10 nM, EC 50 = 44.1 pM) positive inotropism on rat ventricular myocytes. CGRP (1 nM) increased cell shortening during contraction by 140 ± 40% above baselines and increased maximum velocity of contraction and relaxation by 98 and 106%, respectively. CGRP failed to produce any response in the presence of the CGRP 1 receptor antagonist. CGRP induced similar inotropic response in mouse ventricular myocytes. CGRP increased the amplitude of [Ca 2+ ] transients of ventricular myocytes by 120 ± 25% above baseline and shortened the time of half-maximum myoplasmic Ca 2+ clearance by 30 ± 5%. Increase in intracellular Ca 2+ mobilization by CGRP was dependent on Ca 2+ influx through the activation of the L-type Ca 2+ channel, because nifedipine blocked the CGRP-induced increase in [Ca 2+ ] transients. Furthermore, CGRP failed to increase [Ca 2+ ] transients after the inhibition of protein kinase A in ventricular myocytes. These data indicate that stimulation of mammalian ventricular myocardial CGRP 1 receptors enhances [Ca 2+ ] transients through the activation of protein kinase A, which in turn activates voltage-dependent L-type Ca 2+ channels. These events lead to Ca 2+ -induced intracellular Ca 2+ release and enhanced myocyte contraction and facilitated relaxation." @default.
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• W2186118727 date "1999-01-01" @default.
• W2186118727 modified "2023-10-15" @default.
• W2186118727 title "Ca²⁺-induced Ca²⁺release involved in positive inotropic effect mediated by CGRP in ventricular myocytes" @default.
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• W2186118727 doi "https://doi.org/10.1152/ajpregu.1999.276.1.r259" @default.
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