Abstract
The previous study on the existence and function of alpha-adrenergic receptors in rat myocardium for noradrenaline (NA) has been reported by the auther, in which it was assumed: (1) The rat myocardium contains both alpha- and beta-adrenergic receptors. (2) It is certai n that alpha-receptors play some role in positive ino- and chronotropic effects of NA on atrial and papillary muscle, though it is of course that the stimulation of beta-receptors plays a great role in these effects. (3) The alpha-receptors in rat myocardium consist of two kinds of alpha-receptors: one is the receptor which mediates only the negative inotropic effect of NA and the other is the receptor which mediates only a few parts of positive ino- and chronotropic effect. (4) The former is rich in papillary muscle while lacks in sinus node and atrial muscle, and the latter would be rich in atrial and papillary muscle while poor in sinus node.
In the present study, it was tried to investigate the functions of alpha-adren ergic receptor stimulated by adrenaline (Adr) and the effects of Adr under influences of tolazoline (TLZ), phentolamine (PTL), propranolol (PRP) or carteolol (CTL) on the isolated rat spontaneously beating atria as well as electrically driven left atrium and papillary muscle.
Adr (10-10-10-5g/mL) increased both the rate and contractile ten sion in the spontaneously beating atria: the greatest increase was caused by the drug (10-6-10-5). The rate and contractile tension were not decreased by Adr at these concentrations in the spontaneously beating atria, but the tension of the electrically driven left atrium and papillary muscle was decreased by Adr, though the decrease was transient and followed by the increase of tension: Adr (10-7-10-5) caused the decrease in tension of the left atrium and the drug (10-8-10-4)in tension of the papillary muscle. The increase of tension of the left atrium and papillary muscle were caused by Adr (10-9-10-5) and (10-9-10-4), respectively: the greatest increase of both muscles tension was brought by the drug (10-5): the increase was dose-dependent in concentrations lower than 10-5 of Adr.
In the presence of TLZ (10-7), the positive chronotropic effect of Adr (10-10-10-8) was increased while decreased in presence of concentrations higher than 10-8 of PRP or 10-9 of CTL suggesting the competitive antagonization for Adr. When the TLZ was replaced by PTL (10-7), the effects of Adr (10-9-10-8) were increased as similar as in the presence of the TLZ. However, the increase of the rate was scarcely seen when higher concentrations of TLZ or PTL (10-6) was applied. When higher concentratrations of PRP or CTL (10-6) was applied, the rate was transiently decreased before the increase of rate. In the presence of TLZ or PTL (10-7), the positive inotropic effect of Adr (10-10_10-8) on spontaneously beating atria was remarkably increased while decrease in the presence of concentrations lower than 10-8 of PRP or 10-9 of CTL.
The negative inotropic effect of Adr on both the left atrium and papillary muscle was completely abolished by TLZ or PTL in concentrations higher than 10-7 while increased by PRP or CTL in concentrations lower than 10-6 or 10-8. The positive inotropic effect of Adr on the left atrium was potentiated by TLZ or PTL (10-7) while non-competitively suppressed by PRP or CTL (10-6). However, influences of TLZ or PTL (10-5) were scarce or absence on the effect of Adr. The positive inotropic effect of Adr on the papillary muscle was not influenced by TLZ or PTL (10-5) while competitively suppressed by PRP or CTL (10-8).
