PMID- 9007683
OWN - NLM
STAT- MEDLINE
DCOM- 19970508
LR  - 20190724
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 29
IP  - 1
DP  - 1997 Jan
TI  - Endothelin-1 inhibits L-type Ca2+ current enhanced by isoprenaline in rat atrial 
      myocytes.
PG  - 136-43
AB  - Endothelin-1 (ET-1) was shown to exert direct cardiac effects by complex 
      signaling pathways and to interact with neurotransmitter regulation of cardiac 
      activity. The effect of ET-1 was investigated on the beta-adrenergic stimulation 
      of cardiac L-type Ca2+ current (ICaL) on isolated rat atrial myocytes by using 
      the patch-clamp technique. ET-1 (5 x 10(-8) M) reversed the increase in ICaL 
      induced by isoprenaline (10(-6) M) but had no effect on basal ICaL and on (-) Bay 
      K 8644-increased ICaL (10(-6) M); so ET-1 might exert an effect only when the 
      Ca2+ channels are phosphorylated. The antiadrenergic action of ET-1, blocked by 
      BQ-123 (10(-6) M) and unaffected by IRL 1038 (3.5 x 10(-8) M) should be mediated 
      by ET-A receptors. The inhibitory action of ET-1 was still observed when ICaL was 
      previously increased by forskolin (3 x 10(-6) M), 8-bromo-cyclic adenosine 
      monophosphate (8-Br-cAMP; 200 microM), or cAMP (100 microM) in presence of 
      isobutyl methyl xanthine (IBMX; 10(-6) M), suggesting that the antiadrenergic 
      action of ET-1 on ICaL was exerted independent of the cAMP-dependent 
      phosphorylation pathway. ET-1 is known to be an activator of phosphoinositide 
      hydrolysis, resulting in an increased production of IP3 and diacylglycerol (DAG). 
      A Ca(2+)-dependent inhibition of ICaL consequently to an elevation of the 
      intracellular Ca2+ pool via IP3 might be excluded in the action of ET-1, because 
      of the presence of EGTA in the intrapipette medium. ET-1 reversed the 
      isoprenaline-induced increase in ICaL in the presence of protein kinase C 
      inhibitor [PKC(19-31); 100 microM), making unlikely the involvement of a 
      DAG-dependent activation of PKC. Therefore the antiadrenergic action of ET-1 
      might also be independent on the phosphoinositide pathway.
FAU - Delpech, N
AU  - Delpech N
AD  - Laboratory of General Physiology, URA CNRS 1869, Faculty of Sciences, Poitiers, 
      France.
FAU - Soustre, H
AU  - Soustre H
FAU - Potreau, D
AU  - Potreau D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Adrenergic beta-Agonists)
RN  - 0 (Calcium Channel Agonists)
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Calcium Channels)
RN  - 0 (Endothelin-1)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 1F7A44V6OU (Colforsin)
RN  - 71145-03-4 (3-Pyridinecarboxylic acid, 
      1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester)
RN  - E0399OZS9N (Cyclic AMP)
RN  - L628TT009W (Isoproterenol)
SB  - IM
MH  - 3-Pyridinecarboxylic acid, 
      1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl 
      ester/pharmacology
MH  - Adrenergic beta-Agonists/*pharmacology
MH  - Animals
MH  - Calcium Channel Agonists/pharmacology
MH  - Calcium Channel Blockers/*pharmacology
MH  - Calcium Channels/*drug effects
MH  - Cells, Cultured
MH  - Colforsin/pharmacology
MH  - Cyclic AMP/metabolism
MH  - Endothelin-1/*pharmacology
MH  - Heart Atria/*drug effects/metabolism
MH  - Isoproterenol/*pharmacology
MH  - Myocardium/cytology/*metabolism
MH  - Patch-Clamp Techniques
MH  - Protein Kinase Inhibitors
MH  - Rats
EDAT- 1997/01/01 00:00
MHDA- 1997/01/01 00:01
CRDT- 1997/01/01 00:00
PHST- 1997/01/01 00:00 [pubmed]
PHST- 1997/01/01 00:01 [medline]
PHST- 1997/01/01 00:00 [entrez]
AID - 10.1097/00005344-199701000-00021 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 1997 Jan;29(1):136-43. doi: 
      10.1097/00005344-199701000-00021.