PMID- 1330178
OWN - NLM
STAT- MEDLINE
DCOM- 19921218
LR  - 20190509
IS  - 0007-1188 (Print)
IS  - 0007-1188 (Linking)
VI  - 107
IP  - 2
DP  - 1992 Oct
TI  - A pertussis toxin-sensitive mechanism of endothelin action in porcine coronary 
      artery smooth muscle.
PG  - 456-62
AB  - 1. Endothelin-1 (ET-1)-induced contraction of porcine coronary artery strips may 
      be mediated via at least two intracellular signalling mechanisms, the activation 
      of dihydropyridine-sensitive voltage-dependent Ca2+ channels and the stimulation 
      of phosphoinositide breakdown. Here we have investigated the possible involvement 
      of pertussis toxin (PT)-sensitive guanosine-5'-triphosphate (GTP)-binding 
      proteins (G-proteins) in ET-1-induced activation of these two signalling pathways 
      in porcine coronary artery smooth muscle. 2. Increase in extracellular K+ 
      concentration (10, 15 mM) shifted the dose-response relationship for the 
      ET-1-induced contraction to the left. 3. The dihydropyridine Ca2+ channel 
      blocker, nifedipine (10(-8) M), induced a rightward shift in the dose-response 
      curve for ET-1. Pretreatment of the arterial strips with PT (0.1 microgram ml-1) 
      induced a similar rightward shift of the ET-1 dose-response curve but not of the 
      KCl response. Nifedipine (10(-8) M) did not further attenuate the ET-1-induced 
      contraction in the PT-pretreated strips. 4. The pretreatment with PT 
      significantly reduced 45Ca2+ uptake of the arterial strips stimulated by ET-1, 
      but had no effect on ET-1-induced production of inositol phosphates. 5. The 
      contractile response of the arterial strips to phorbol dibutyrate, an active 
      phorbol ester, was not significantly affected by 10(-8) M nifedipine. 6. We 
      confirmed that the pretreatment of the tissue with PT induced ADP-ribosylation of 
      a 41 kDa membrane protein. 7. These findings indicate that activation of 
      dihydropyridine-sensitive voltage-dependent Ca2+ channels by ET-1 in this tissue 
      is mediated via a PT-sensitive G-protein in a manner apparently independent of 
      the ET-1-induced activation of protein kinase C. It is concluded that the action 
      of ET-1 in porcine coronary artery is mediated via two distinct signal 
      transduction pathways, which are coupled to PT-sensitive and PT-insensitive 
      GTP-binding proteins, respectively.
FAU - Kasuya, Y
AU  - Kasuya Y
AD  - Department of Pharmacology, University of Tsukuba, Ibaraki, Japan.
FAU - Takuwa, Y
AU  - Takuwa Y
FAU - Yanagisawa, M
AU  - Yanagisawa M
FAU - Masaki, T
AU  - Masaki T
FAU - Goto, K
AU  - Goto K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Br J Pharmacol
JT  - British journal of pharmacology
JID - 7502536
RN  - 0 (Calcium Channels)
RN  - 0 (Endothelins)
RN  - 0 (Inositol Phosphates)
RN  - 0 (Virulence Factors, Bordetella)
RN  - 20762-30-5 (Adenosine Diphosphate Ribose)
RN  - 37558-16-0 (Phorbol 12,13-Dibutyrate)
RN  - EC 2.4.2.31 (Pertussis Toxin)
RN  - EC 3.6.1.- (GTP-Binding Proteins)
RN  - I9ZF7L6G2L (Nifedipine)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adenosine Diphosphate Ribose/metabolism
MH  - Animals
MH  - Arteries/drug effects
MH  - Calcium/metabolism
MH  - Calcium Channels/drug effects
MH  - Coronary Vessels/*drug effects/physiology
MH  - Dose-Response Relationship, Drug
MH  - Endothelins/*pharmacology
MH  - GTP-Binding Proteins/*physiology
MH  - In Vitro Techniques
MH  - Inositol Phosphates/metabolism
MH  - Muscle Contraction/drug effects
MH  - Muscle, Smooth, Vascular/*drug effects/physiology
MH  - Nifedipine/pharmacology
MH  - *Pertussis Toxin
MH  - Phorbol 12,13-Dibutyrate/pharmacology
MH  - Swine
MH  - Virulence Factors, Bordetella/*pharmacology
PMC - PMC1907892
EDAT- 1992/10/01 00:00
MHDA- 1992/10/01 00:01
PMCR- 1993/10/01
CRDT- 1992/10/01 00:00
PHST- 1992/10/01 00:00 [pubmed]
PHST- 1992/10/01 00:01 [medline]
PHST- 1992/10/01 00:00 [entrez]
PHST- 1993/10/01 00:00 [pmc-release]
AID - 10.1111/j.1476-5381.1992.tb12767.x [doi]
PST - ppublish
SO  - Br J Pharmacol. 1992 Oct;107(2):456-62. doi: 10.1111/j.1476-5381.1992.tb12767.x.