Intravenous injection of exogenous ATP (10(-4) M) to rats aging 21, 56, and 100 days increased the heart rate by the 15th sec postinjection. Stable ATP analogue alpha,beta-methylene-ATP in an equimolar concentration increased the heart rate in rats aging 56 and 100 days (by the 15th second after treatment), but had no effect on 21-day-old animals. alpha,beta-Methylene-ATP in a concentration of 10(-7) M increased the heart rate in 21-day-old rat pups, which attests to high sensitivity of P2 purinoceptors. Administration of ATP and alpha,beta-methylene-ATP after treatment with nonselective purinoceptor antagonist suramin did not increase the heart rate in rats of different age groups. Infusion of ATP and its stable analogue after administration of selective P2Y receptor antagonist reactive blue 2 increased the heart rate in rats of different age groups. These changes reflect activation of P2X receptors in the heart.
Stable agonist of P2 receptors 2-methylthio-ATP and selective antagonists of P2X and P2Y receptors PPADS and reactive blue-2 were used for evaluation of the role of P2 receptors in positive contractile reaction of atrial and ventricular myocardium in rats. PPADS significantly moderated the effects of 2-methylthio-ATP in 14-, 21-, and 56-day-old rat pups, but potentiated them in 100-day-old rats. Under conditions of reactive blue-2 treatment, the positive effect of the agonist was preserved in the atria and ventricles in all age groups and was age-dependent.
In all examined age groups of rats, the threshold amplitude of stellate ganglion stimulation is higher for the positive chronotropic effect than for the inotropic effect. The stimulation produced a more pronounced effect on stroke volume than on heart rate.
In vivo effects of exogenous ATP on cardiac activity were studied on adult rats. Intravenous administration of ATP produced a positive chronotropic effect, but did not affect the stroke volume. This was due to activation of type II purine receptors, rather than due to the influence of ATP hydrolysis products, since P1 receptor agonist adenosine was ineffective. The blockade of beta-adrenoceptors and muscarinic receptors did not modify the positive chronotropic effect of ATP, which indicated that this action was not realized via sympathetic or parasympathetic nerves. ATP applied against the background of atropine blockade produced a 4-fold increase in the variability of heart rate typical of activation of the parasympathetic myocardial regulation.
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