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ET(B) receptor activates adenylyl cyclase via a c-PLA(2)-dependent mechanism: a novel counterregulatory mechanism of ET-induced contraction in airway smooth muscle.

Abstract：

:Endothelin-1 (ET-1) contracted the rabbit tracheal smooth muscle (RTSM), yielding a bell-shaped tension-concentration curve. Moreover, ET-1 induced concentration- and time-dependent increases in cAMP concentrations in RTSM (EC(50), 58 nM; t(1/2), 2.4 min). Pretreatment with the AC inhibitors, SQ-22536, or 2'-5'-dideoxyadenosine, enhanced contraction to ET-1 and converted its bell-shaped tension curve into a sigmoidal one, but left contraction to carbachol and KCl unaltered. The potent ET(B)-receptor agonists, ET-3 or sarafotoxin-c, mimicked ET-1's effects on cAMP levels (EC(50) values 55 and 50 nM). Further, cAMP formation by ETs was inhibited by BQ-788 (selective ET(B) receptor blocker; IC(50), 8 nM), but not by BQ-610 (selective ET(A) receptor blocker). Removal of the epithelium did not prevent ET-induced increases in cAMP levels. Unlike isoproterenol, ETs failed to activate AC in membrane fractions from RTSM. In intact RTSM, the c-PLA(2) inhibitor, AACOCF3, and the cyclooxygenase inhibitor, indomethacin, blocked ET-induced increases in cAMP levels. These findings reveal a novel, nonepithelial, c-PLA(2)-mediated, regulatory mechanism downstream from ET(B) receptors.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

El-Mowafy AM,Biggs DF

doi

10.1006/bbrc.2001.5389

subject

Has Abstract

pub_date

2001-08-17 00:00:00

pages

388-93

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(01)95389-6

journal_volume

286

pub_type

杂志文章

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