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1 The nerve-evoked contractions elicited by transmural electrical stimulation of mouse urinary bladders superfused in modified Krebs Ringer buffer containing 1 IAM atropine plus 3.4 IBM guanethidine were inhibited by adenosine (ADO) and related nucleoside analogues with the following rank order of potency: R-phenylisopropyladenosine (R-PIA) > cyclohexyladenosine (CHA) > 5'N-ethylcarboxamido adenosine (NECA) > ADO > S-phenylisopropyladenosine (S-PIA). Tissue preincubation with 8-phenyltheophylline (8-PT) displaced to the right, in a parallel fashion, the NECA concentration-response curve.2 The contractions elicited by application of exogenous adenosine 5'-triphosphate (ATP) were also inhibited by ADO and related structural analogues. The rank order of potency to reduce the motor response to ATP was: NECA > 2-chloroadenosine (CADO) > R-PIA > ADO > CHA > S-PIA. 3 The ADO-induced ATP antagonism was of a non-competitive nature and was not specific. Tissue incubation with 10 AM NECA not only reduced the motor responses elicited by ATP, but also 5-hydroxytryptamine, acetylcholine and prostaglandin F2CK. The action of NECA was antagonized following tissue preincubation with 8-PT. The inhibitory action of NECA was not mimicked by 10 gM CHA. 4 The maximal bladder ATP contractile response was significantly increased by tissue preincubation with 5-30 gM 8-PT. 5 The 0.15 Hz evoked muscular twitch was significantly increased by 8-PT while dipyridamole consistently reduced the magnitude of the twitch response. These results are consonant with the hypothesis that an endogenous ADO tone modulates the bladder neurotransmission. 6 A working model is proposed suggesting the presence of ADO-Al and A2 receptors in the mouse urinary bladder. The A1 receptor subpopulation is probably of presynaptic origin whereas the smooth muscle membranes contain a population of the A2 receptor subtype.

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A single, intraportal injection of ethanol (0.01 g/kg body weight) in the pentobarbital anesthetized dog elicited an immediate rise in the hepatic resistance to both portal and hepatic blood flows. Similar effects were produced by norepinephrine and these, as well as those of ethanol, were significantly reduced by yohimbine. Increased levels of noradrenaline were found in hepatic venous effluent during the vasoconstriction period induced by ethanol. We postulate that noradrenaline liberated from sympathetic nervous endings of the liver may be involved in vascular response to ethanol.

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