Abstract
1. In the longitudinal muscle of guinea-pig gastric fundus, adrenaline and phenylephrine (1-30 microM) both produced a slow contraction preceded by a relaxation. The slow contraction was strongly inhibited by prazosin (0.1 microM), but only weakly by yohimbine (1 microM), suggesting main contribution of alpha 1-adrenoceptors. 2. Most of the slow contraction was blocked by meclofenamate or indomethacin (0.1-0.3 microM). Both these drugs also inhibited spontaneously generated muscle tone. In some preparations, obtained from the apical fundus, a small contraction remained in the presence of meclofenamate. 3. During contraction induced by prostaglandin E2, adrenaline produced sustained relaxation and phenylephrine often transient relaxation, in the presence of meclofenamate. The transient relaxation, but not the sustained relaxation, was suppressed by prazosin. 4. In the presence of prostaglandin E2 (5 nM), after treating with phenoxybenzamine (30 microM) for 30 min, isoprenaline and adrenaline produced concentration-dependent relaxation, with IC50 s of 3.9 nM and 64 nM, respectively. Propranolol shifted these concentration-response curves to the right, with apparent pA2 s of 8.15 and 7.34, respectively. 5. It is suggested that in the fundic longitudinal muscle, adrenaline-induced contraction is mediated mainly by an increase in endogenous prostaglandin production through activation of alpha 1-adrenoceptors and that adrenaline produces transient relaxation through alpha 1-adrenoceptors and sustained relaxation through beta-adrenoceptors. The beta-adrenoceptors in the longitudinal muscle are more sensitive to adrenaline and isoprenaline than those in the circular muscle.
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