Guinea-pig taenia coli suspended in a depolarizing solution without Ca responded to Ca by a contraction. The effects of adrenaline, noradrenaline and isoprenaline on the contractile response were investigated at 20°C and at 37°C. Contractile response to Ca was not significantly affected by adrenaline and noradrenaline, but was reduced by isoprenaline at 37°C. At 20°C, all the three catecholamines inhibited Ca-contraction. The potency in producing the inhibition was isoprenaline, adrenaline, noradrenaline, the same sequence of potency as related to beta-receptor mediated responses. Treatment with a beta-receptor blocking agent markedly reduced or abolished the inhibitory effects, and consequently the Ca-contraction was enhanced by adrenaline and noradrenaline at 37°C. Treatment with an alpha-receptor blocking agent increased the inhibitory effects so that adrenaline and noradrenaline reduced the Ca-contraction at 37°C as well as at 20°C. The order of potency in producing the inhibition after alpha-receptor blockade was again isoprenaline, adrenaline, noradrenaline. It was concluded that the stimulatory effect is mediated by alpha-receptor activation and the inhibitory effect by beta-receptor activation. After beta-receptor blockade and at 37°C, adrenaline and noradrenaline applied after Ca caused further development of tension. The contractile response to adrenaline resembles the slow component of the ACh-induced contraction, regarding time course and susceptibility to removal of Ca from the extracellular medium. Adrenaline enhanced the Ca-contraction to the same extent before and after frequent exposures to ACh to deplete cell-bound Ca. These findings suggest that the enhancement of the Ca-contraction by adrenaline and noradrenaline is dependent on increased permeation of Ca ions across the cell membrane.
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Ohashi et al. (1973) studied this question.
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