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Titolo:
Pituitary adenylate cyclase-activating polypeptide activates K-ATP currentin rat atrial myocytes
Autore:
Baron, A; Monnier, D; Roatti, A; Baertschi, AJ;
Indirizzi:
Ctr Med Univ Geneva, Dept Physiol, CH-1211 Geneva 4, Switzerland Ctr Med Univ Geneva Geneva Switzerland 4 , CH-1211 Geneva 4, Switzerland
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 3, volume: 280, anno: 2001,
pagine: H1058 - H1065
SICI:
0363-6135(200103)280:3<H1058:PACPAK>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASOACTIVE-INTESTINAL-PEPTIDE; SMOOTH-MUSCLE CELLS; PROTEIN-KINASE; FUNCTIONAL EXPRESSION; NATRIURETIC-PEPTIDE; CORONARY-ARTERIES; CA CHANNELS; PACAP; RECEPTOR; SECRETION;
Keywords:
cAMP; patch-clamping; protein kinase C; RT-PCR; vasoactive intestinal polypeptide;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Baertschi, AJ Ctr Med Univ Geneva, Dept Physiol, 1 Rue Michel Servet, CH-1211 Geneva 4, Switzerland Ctr Med Univ Geneva 1 Rue Michel Servet Geneva Switzerland 4
Citazione:
A. Baron et al., "Pituitary adenylate cyclase-activating polypeptide activates K-ATP currentin rat atrial myocytes", AM J P-HEAR, 280(3), 2001, pp. H1058-H1065

Abstract

Because the electrophysiological effects of pituitary adenylate cyclase-activating polypeptide (PACAP) on the heart are little known, we studied the regulation of the atrial ATP-sensitive K+ (K-ATP) current by PACAP on primary cultured neonatal rat atrial myocytes. PACAP-38 stimulates cAMP production with EC50 = 0.28 nmol/l (r = 0.92, P < 0.02). PACAP-38 and PACAP-27 (10 nmol/l) have similar maximal effects, whereas 100 nmol/l vasoactive intestinal polypeptide (VIP) is 2.7 times less effective (P < 0.05). RT-PCR shows the presence of cloned PACAP receptors PAC(1) (greater than or equal to2 isoforms), VPAC(1), and VPAC(2). PACAP-38 dose dependently activates the whole cell atrial KATP current with EC50 = 1-3 nmol/l (n = 44). Maximal effectsoccur at 10 nmol/l (91 +/- 15 pA/pF, n = 18). Diazoxide further increases the PACAP-activated current by 78% (P < 0.05; n = 6). H-89 (500 nmol/l), a protein kinase A (PKA) inhibitor, reduces the PACAP-activated K-ATP currentto 17.8 +/- 9.6% (n = 5) of the maximal diazoxide-induced current and totally inhibits the cAMP-induced K-ATP current. A protein kinase C (PKC) inhibitor peptide (50 <mu>mol/l) in the pipette reduces the PACAP-38-induced K-ATP current to 33 +/- 17 pA/pF (P < 0.05, n = 6) without significantly affecting the currents induced by cAMP or VIP. The results suggest that: 1) PAC1, VPAC1, and VPAC2 are present in atrial myocytes; and 2) PACAP-38 activates the atrial KATP channels through both PKA and PKC pathways.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 06:54:02