Abstract
To investigate the cellular mechanisms underlying spontaneous excitation of smooth muscle of the guinea-pig urinary bladder, isometric tension was measured in muscle bundles whilst recording the membrane potential from a cell in the bundle with a microeletrode. Changes in the intracellular calcium concentration ([Ca2+]i; Ca transients) were recorded in fura-PE3 loaded strips. Spontaneous action potentials and contractions were abolished by nifedipine (1 μM). Carbachol (0.1 μM) increased the frequency of action potentials and corresponding contractions. Apamin (0.1 μM) potentiated bursting activity and enhanced phasic contraction. Charybdotoxin (CTX, 50 nM) induced prolonged action potentials that generated enlarged contractions. In contrast, levcromakalim (0.1 μM) reduced the frequency of action potentials and contractions. Forskolin (0.1 μM), 8-bromoguanosin 3', 5' cyclic monophosphate (0.1 mM) and Y-26763 (10 μM) suppressed contractions without reducing the amplitude of either action potentials or Ca transients. These results confirm that action potentials and associated Ca transients are fundamental mechanisms in generating spontaneous contractions in smooth muscles of the guinea-pig bladder. However, in parallel with the excitation-contraction coupling, the sensitivity of the contractile proteins for Ca2+ may play an important role in regulating spontaneous excitation and can be modulated by cyclic nucleotides and Rho kinase [Jpn J Physiol 54 Suppl:S124 (2004)]
