| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Pharmacology and Clinical Pharmacology, St George's Hospital Medical School, London.
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.
This article has been cited by other articles:
|
|
 |
|
  F. Saitow, H. Suzuki, and S. Konishi {beta}-Adrenoceptor-mediated long-term up-regulation of the release machinery at rat cerebellar GABAergic synapses J. Physiol., June 1, 2005; 565(2): 487 - 502. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Aoyama, M. Murakami, T. Iwashita, Y. Ito, K. Yamaki, and S. Nakayama Slow Deactivation and U-Shaped Inactivation Properties in Cloned Cav1.2b Channels in Chinese Hamster Ovary Cells Biophys. J., January 1, 2003; 84(1): 709 - 724. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. D. Keef, J. R. Hume, and J. Zhong Regulation of cardiac and smooth muscle Ca2+ channels (CaV1.2a,b) by protein kinases Am J Physiol Cell Physiol, December 1, 2001; 281(6): C1743 - C1756. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. KURIYAMA, K. KITAMURA, T. ITOH, and R. INOUE Physiological Features of Visceral Smooth Muscle Cells, With Special Reference to Receptors and Ion Channels Physiol Rev, July 1, 1998; 78(3): 811 - 920. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Karaki, H. Ozaki, M. Hori, M. Mitsui-Saito, K.-I. Amano, K.-I. Harada, S. Miyamoto, H. Nakazawa, K.-J. Won, and K. Sato Calcium Movements, Distribution, and Functions in Smooth Muscle Pharmacol. Rev., June 1, 1997; 49(2): 157 - 230. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
