Abstract
Stimulation of beta-adrenergic receptors (ARs) in response to sympathetic system activation increases heart contractility and rate. The beta1- and 2-ARs are main subtypes expressed in the cardiomyocytes. In the present work, using recording contractions and optical detection of calcium transient and nitric oxide levels, we have studied effects of the beta2-AR stimulation at different temperatures (25 and 35°С) in mice left atria. We found that increase in temperature from 25 to 35°C leads to an attenuation of the positive inotropic effect of beta2-AR stimulation which is accompanied by a decrease in amplitude of Ca2+ transient and an increase in NO synthesis. Under these conditions, pharmacological inhibition of NO production causes recovery of the effects of beta2-AR activation on the contractility and Ca2+ transient. Experiments using hydroxycholesterol interfering with coupling beta2-AR to NO synthesis also confirmed the sensitivity of this link to the temperature. We suggest that temperature plays a role in the coupling between beta2-AR and NO-dependent signaling that could be important for cardiac adaptation.
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