Abstract
1. The actions of gamma-aminobutyric acid (GABA) upon rabbit urinary bladder muscle were investigated to determine whether they were mediated through potassium channels. 2. In vitro experiments were undertaken in which bladder muscle strips were caused to contract with carbachol. Addition of GABA or baclofen reduced the size of such evoked contractions in the case of GABA by 20.7 +/- 3.2%, in the case of baclofen by 22.4 +/- 2.2%. 3. Electrical stimulation of autonomic nerves in bladder wall strips also evoked contractions which were significantly smaller in potassium-free Krebs solution. The size of contractions produced by carbachol on the other hand were unaffected by the absence of potassium in the Krebs solution. 4. The inhibitory actions of GABA and baclofen on carbachol-induced contractions of bladder muscle were detected at much lower concentrations in potassium-free compared with potassium containing solutions. 5. The inhibitory effects of baclofen were completely reversed by tetraethyl ammonium chloride between 1 and 5 mM, caesium chloride between 0.5 and 3 mM and barium chloride between 0.5 and 2.5 mM. The actions of baclofen were only partially reversed by 4-amino-pyridine between 1 and 5 mM. 6. It was concluded that the GABAB receptor-mediated inhibitory actions on rabbit urinary bladder smooth muscle cells were produced by activation of potassium channels.
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Selected References
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