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Titolo:
Natriuretic peptides like NO facilitate cardiac vagal neurotransmission and bradycardia via a cGMP pathway
Autore:
Herring, N; Zaman, JAB; Paterson, DJ;
Indirizzi:
Univ Oxford, Physiol Lab, Oxford OX1 3PT, England Univ Oxford Oxford England OX1 3PT Physiol Lab, Oxford OX1 3PT, England
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 6, volume: 281, anno: 2001,
pagine: H2318 - H2327
SICI:
0363-6135(200112)281:6<H2318:NPLNFC>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED INWARD CURRENT; NITRIC-OXIDE DONORS; HEART-RATE RECOVERY; GUINEA-PIG ATRIA; ACETYLCHOLINE-RELEASE; CYCLIC-AMP; INHIBITED PHOSPHODIESTERASE; RECEPTOR SELECTIVITY; GUANYLATE-CYCLASE; PROTEIN-KINASE;
Keywords:
nitric oxide; autonomic nervous system; acetylcholine; heart rate;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Paterson, DJ Univ Oxford, Physiol Lab, Parks Rd, Oxford OX1 3PT, England Univ Oxford Parks Rd Oxford England OX1 3PT OX1 3PT, England
Citazione:
N. Herring et al., "Natriuretic peptides like NO facilitate cardiac vagal neurotransmission and bradycardia via a cGMP pathway", AM J P-HEAR, 281(6), 2001, pp. H2318-H2327

Abstract

We tested the hypothesis that natriuretic peptide receptors (NPRs) that are coupled to cGMP production act in a similar way to nitric oxide (NO) by enhancing acetylcholine release and vagal-induced bradycardia. The effects of enzyme inhibitors and channel blockers on the action of atrial natriuretic peptide (ANP), brain-derived natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) were evaluated in isolated guinea pig atrial-right vagal nerve preparations. RT-PCR confirmed the presence NPR B and A receptor mRNA in guinea pig sinoatrial node tissue. BNP and CNP significantly (P<0.05)enhanced the heart rate (HR) response to vagal nerve stimulation. CNP had no effect on the HR response to carbamylcholine and facilitated the releaseof [H-3] acetylcholine during atrial field stimulation. The particulate guanylyl cyclase-coupled receptor antagonist HS-142-1, the phosphodiesterase 3 inhibitor milrinone, the protein kinase A inhibitor H89, and the N-type calcium channel blocker <omega>-conotoxin all blocked the effect of CNP on vagal-induced bradycardia. Like NO, BNP and CNP facilitate vagal neurotransmission and bradycardia. This may occur via a cGMP-PDE3-dependent pathway increasing cAMP-PKA-dependent phosphorylation of presynaptic N-type calcium channels.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 09:42:30