PMID- 8922746
OWN - NLM
STAT- MEDLINE
DCOM- 19970310
LR  - 20220309
IS  - 0007-1188 (Print)
IS  - 0007-1188 (Linking)
VI  - 119
IP  - 5
DP  - 1996 Nov
TI  - Endothelium-derived factors and hyperpolarization of the carotid artery of the 
      guinea-pig.
PG  - 959-64
AB  - 1. Transmembrane potentials were recorded from isolated carotid arteries of the 
      guinea-pig superfused with modified Krebs-Ringer bicarbonate solution. Smooth 
      muscle cells were impaled from the adventitial side with intracellular glass 
      microelectrodes filled with KCl (30-80 M omega). 2. Acetylcholine (1 microM) in 
      the presence of inhibitors of nitric oxide synthase, (N omega-nitro-L-arginine 
      (L-NOARG) 100 microM) and cyclo-oxygenase, (indomethacin 5 microM) induced an 
      endothelium-dependent hyperpolarization (-18.9 +/- 1.6 mV, n = 15). 3. In the 
      presence of these two inhibitors, S-nitroso-L-glutathione (10 microM), sodium 
      nitroprusside (10 microM), 3-morpholinosydnonimine (SIN-1, 10 microM) and 
      iloprost (0.1 microM) induced endothelium-independent hyperpolarizations of the 
      smooth muscle cells (respectively: -16.0 +/- 2.3, -16.3 +/- 3.4, -12.8 +/- 2.0 
      and -14.5 +/- 1.5 mV, n = 4-6). 4. The addition of glibenclamide (1 microM) did 
      not influence the acetylcholine-induced L-NOARG/ indomethacin-resistant 
      hyperpolarization (-18.0 +/- 1.8 mV, n = 10). In contrast, the responses induced 
      by S-nitroso-L-glutathione, sodium nitroprusside, SIN-1 and iloprost were 
      abolished (changes in membrane potential: -0.8 +/- 1.1, 1.3 +/- 3.9, 4.5 +/- 4.6 
      and 0.3 +/- 0.8 mV respectively, n = 4-5). 5. In the presence of NO synthase and 
      cyclo-oxygenase inhibitors, charybdotoxin (0.1 microM) or apamin (0.5 microM) did 
      not influence the hyperpolarization produced by acetylcholine. However, in the 
      presence of the combination of charybdotoxin and apamin, the 
      acetylcholine-induced L-NOARG/indomethacin-resistant hyperpolarization was 
      converted to a depolarization (4.4 +/- 1.2 mV, n = 20) while the 
      endothelium-independent hyperpolarizations induced by S-nitroso-L-glutathione, 
      sodium nitroprusside, SIN-1 and iloprost were not affected significantly 
      (respectively: -20.4 +/- 3.4, -22.5 +/- 4.9, -14.5 +/- 4.7 and -14.5 +/- 0.5 mV, 
      n = 4-5). 6. In the presence of the combination of charybdotoxin and apamin and 
      in the absence of L-NOARG and indomethacin, acetylcholine induced a 
      hyperpolarization (-19.5 +/- 3.7 mV, n = 4). This hyperpolarization induced by 
      acetylcholine was not affected by the addition of indomethacin (-18.3 +/- 4.6 mV, 
      n = 3). In the presence of the combination of charybdotoxin, apamin and L-NOARG 
      (in the absence of indomethacin), acetylcholine, in 5 out of 7 vessels, still 
      produced hyperpolarization which was not significantly smaller (-9.1 +/- 5.6 mV, 
      n = 7) than the one observed in the absence of L-NOARG. 7. These findings suggest 
      that, in the guinea-pig isolated carotid artery, the endothelium-independent 
      hyperpolarizations induced by NO donors and iloprost involve the opening of KATP 
      channels while the acetylcholine-induced endothelium-dependent hyperpolarization 
      (resistant to the inhibition of NO-synthase and cyclo-oxygenase) involves the 
      opening of Ca(2+)-activated potassium channel(s). Furthermore, in this tissue, 
      acetylcholine induces the simultaneous release of various factors from 
      endothelial origin: hyperpolarizing factors (NO, endothelium derived 
      hyperpolarizing factor (EDHF) and prostaglandins) and possibly a depolarizing 
      factor.
FAU - Corriu, C
AU  - Corriu C
AD  - Departement de pneumologie, Institut de Recherches Servier, Suresnes, France.
FAU - Feletou, M
AU  - Feletou M
FAU - Canet, E
AU  - Canet E
FAU - Vanhoutte, P M
AU  - Vanhoutte PM
LA  - eng
PT  - Journal Article
PL  - England
TA  - Br J Pharmacol
JT  - British journal of pharmacology
JID - 7502536
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Potassium Channel Blockers)
RN  - 115422-61-2 (Charybdotoxin)
RN  - 2149-70-4 (Nitroarginine)
RN  - 24345-16-2 (Apamin)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - XXE1CET956 (Indomethacin)
SB  - IM
MH  - Animals
MH  - Apamin/pharmacology
MH  - Carotid Arteries/*drug effects/physiology
MH  - Charybdotoxin/pharmacology
MH  - Enzyme Inhibitors/*pharmacology
MH  - Guinea Pigs
MH  - In Vitro Techniques
MH  - Indomethacin/pharmacology
MH  - Male
MH  - Membrane Potentials/*drug effects
MH  - Nitric Oxide/*physiology
MH  - Nitroarginine/pharmacology
MH  - Potassium Channel Blockers
PMC - PMC1915922
EDAT- 1996/11/01 00:00
MHDA- 1996/11/01 00:01
PMCR- 1997/11/01
CRDT- 1996/11/01 00:00
PHST- 1996/11/01 00:00 [pubmed]
PHST- 1996/11/01 00:01 [medline]
PHST- 1996/11/01 00:00 [entrez]
PHST- 1997/11/01 00:00 [pmc-release]
AID - 10.1111/j.1476-5381.1996.tb15765.x [doi]
PST - ppublish
SO  - Br J Pharmacol. 1996 Nov;119(5):959-64. doi: 10.1111/j.1476-5381.1996.tb15765.x.