| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Laboratoire de Physiologie Cellulaire et Pharmacologie Moléculaire, INSERM JF, Bordeaux, France.
1. Membrane currents were recorded by a patch-clamp pipette technique in cultured cells from rat portal vein using the whole-cell mode. 2. Noradrenaline (NA, 10(-5) M) and phorbol-12,13-dibutyrate (PDBu, 10(-7) M) produced an increase in voltage-dependent inward current carried by barium (5 mM), but their effects were not additive. Calcium-activated chloride current was evoked by NA but not by PDBu. 3. The NA-induced increase in peak voltage-dependent inward current was inhibited by intracellular application of GDP-beta-S (10(-3) M) while the effect of PDBu was unchanged. GDP-beta-S blocked the NA-induced chloride current but had no effect on the caffeine-induced chloride current. 4. Inclusion of GTP-gamma-S (10(-5)-10(-4) M) in the pipette solution increased the voltage-dependent inward current and inhibited the NA- or PDBu-induced increase in peak current. GTP-gamma-S potentiated the effect of NA on calcium-activated chloride current. At higher concentrations (10(-3) M), GTP-gamma-S activated the chloride current and prevented the effects of NA or caffeine on this current. 5. The combination of 10(-5) M-aluminium chloride and 10(-2) M-sodium fluoride had an effect similar to that of high concentrations of GTP-gamma-S on both inward current and calcium-activated chloride current. In contrast, arachidonic acid (10(-3) M) had no effect on calcium and chloride conductances activated by NA. 6. Cells responded normally to NA after pre-treatment for 4-30 h with 10 micrograms ml-1 pertussis toxin (PTx). 7. It is concluded that the stimulation of calcium and chloride conductances by NA is mediated through activation of a PTx-insensitive GTP-binding protein. This effect may involve activation of phospholipase C enzyme and production of both D-myo-inositol 1,4,5-trisphosphate which depletes calcium stores and diacylglycerol which activates protein kinase C.
This article has been cited by other articles:
|
|
 |
|
  K. Yasuda, T. Nakamoto, M. Yasuhara, H. Okada, T. Nakajima, H. Kanzaki, M. Hori, and H. Ozaki Role of protein kinase C{beta} in rhythmic contractions of human pregnant myometrium Reproduction, April 1, 2007; 133(4): 797 - 806. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Nobe, Y. Sakai, H. Nobe, J. Takashima, R. J. Paul, and K. Momose Enhancement Effect under High-Glucose Conditions on U46619-Induced Spontaneous Phasic Contraction in Mouse Portal Vein J. Pharmacol. Exp. Ther., March 1, 2003; 304(3): 1129 - 1142. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Y. Estevez, T. Bond, and K. Strange Regulation of ICl,swell in neuroblastoma cells by G protein signaling pathways Am J Physiol Cell Physiol, July 1, 2001; 281(1): C89 - C98. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A. Khoyi, L. G. Gregory, A. D. Smith, K. D. Keef, and D. P. Westfall An Unusual Ca2+ Entry Pathway Activated by Protein Kinase C in Dog Splenic Artery J. Pharmacol. Exp. Ther., November 1, 1999; 291(2): 823 - 828. [Abstract] [Full Text]
|
|
|
|
 |
|
 Y. Ohya, T. Tsuchihashi, S. Kagiyama, I. Abe, and M. Fujishima Single L-Type Calcium Channels in Smooth Muscle Cells From Resistance Arteries of Spontaneously Hypertensive Rats Hypertension, May 1, 1998; 31(5): 1125 - 1129. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. N. Orlov, J. Tremblay, and P. Hamet cAMP Signaling Inhibits Dihydropyridine-Sensitive Ca2+ Influx in Vascular Smooth Muscle Cells Hypertension, March 1, 1996; 27(3): 774 - 780. [Abstract] [Full Text]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
