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Effect of isoprenaline on Ca2+ channel current in single smooth muscle cells isolated from taenia of the guinea‐pig caecum.
Author(s) -
Muraki K,
Bolton T B,
Imaizumi Y,
Watanabe M
Publication year - 1993
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1993.sp019916
Subject(s) - forskolin , isoprenaline , chemistry , biophysics , medicine , long term potentiation , endocrinology , membrane potential , biology , biochemistry , in vitro , stimulation , receptor
1. The effects of isoprenaline (Iso) on Ca2+ channel current in enzymatically isolated single cells of the guinea‐pig taenia caeci were examined using the standard whole‐cell voltage‐clamp method. 2. Iso potentiated the voltage‐dependent Ca2+ current; the threshold and maximally effective concentration of Iso to increase Ca2+ current were 3‐10 nM and 1‐3 microM, respectively. The average increase in Ca2+ current produced by 3 microM Iso was 42 +/‐ 6% (mean +/‐ S.E.M.) and the response could be obtained repeatedly in the same cell. The concentration‐response relationship could be fitted by a binding model with a Hill coefficient of 1 and a dissociation constant of 42 nM. 3. The effect of Iso on Ca2+ current was voltage dependent. Although potentiation of Ca2+ current by Iso was obvious between ‐30 and +10 mV, it was small or absent around +20 to +30 mV. Iso had little effect on the relationship between inactivation of the Ca2+ current and voltage obtained using a double‐pulse protocol. 4. External application of forskolin, an adenylyl cyclase activator, or internal perfusion of cAMP or dibutyryl cAMP from the recording pipette, did not increase Ca2+ current and potentiation of Ca2+ current by Iso was observed repeatedly and was unchanged. 5. Internal perfusion of GTP gamma S or GDP beta S increased or did not affect the Ca2+ current and potentiation of Ca2+ current by Iso was unchanged and could be recorded repeatedly for about 20 min after rupture of the cell membrane. In addition, treatment of cells with the potent protein kinase C inhibitor, chelerythrine, had no effect on Ca2+ current or on potentiation of Ca2+ current by Iso. 6. These results suggest that the Ca2+ current in guinea‐pig taenia caeci cells is potentiated by isoprenaline via mechanisms which do not involve either a cAMP pathway, a G‐protein pathway or a protein kinase C pathway. The receptor involved appeared to be an atypical adrenoreceptor not blocked by either alpha‐ or beta‐receptor blocking agents.