Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
EFFECT OF RYANODINE ON ATRIAL-NATRIURETIC-PEPTIDE SECRETION BY CONTRACTING AND QUIESCENT RAT ATRIUM
Autore:
LAINE M; WECKSTROM M; VUOLTEENAHO O; ARJAMAA O;
Indirizzi:
UNIV OULU,DEPT PHYSIOL,KAJAANINTIE 52 A SF-90220 OULU FINLAND
Titolo Testata:
Pflugers Archiv
fascicolo: 3-4, volume: 426, anno: 1994,
pagine: 276 - 283
SICI:
0031-6768(1994)426:3-4<276:EOROAS>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARDIAC SARCOPLASMIC-RETICULUM; PERFUSED RABBIT ATRIA; RELEASE CHANNEL; CALCIUM TRANSIENT; SKELETAL-MUSCLE; ANP SECRETION; DISTENSION; STRETCH; PRESSURE; MECHANISM;
Keywords:
RELAXATION; STRETCH; EXOCYTOSIS; VESICLE; SARCOPLASMIC RETICULUM; PRESSURE; CALCIUM CHANNELS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
M. Laine et al., "EFFECT OF RYANODINE ON ATRIAL-NATRIURETIC-PEPTIDE SECRETION BY CONTRACTING AND QUIESCENT RAT ATRIUM", Pflugers Archiv, 426(3-4), 1994, pp. 276-283

Abstract

To elucidate the mechanism involved in the release of atrial natriuretic peptide (ANP), we studied the importance of ryanodine-sensitive Ca2+ release in stretch-secretion coupling. The experiments were made with a left atrial preparation, where the stretch of myocytes was induced by changing the intra-atrial pressure. When external pacing was not applied, the atrial preparation was not spontaneously contracting, andit was therefore possible to investigate the secretory mechanism in the quiescent atrium. The superfusate was collected in 2-min fractions and assayed for ANP immunoreactivity. Filtration analysis revealed that the major fraction in the superfusate in all experimental situationshad a similar molecular weight as the ANP 1-28. Ryanodine (1.0 mu M and 0.1 mu M) inhibited stretch-stimulated ANP secretion dose dependently both in paced and nonpaced atrium, but did not have any effect on basal secretion. The present results support the notion that intracellular Ca2+ transients from the intracellular stores are essential for stretch-stimulated ANP secretion, independently from excitation and contraction. Basal ANP secretion is not inhibited by blocking ryanodine-sensitive Ca2+ channels, either in contracting or in non-contracting atria. In addition our results confirm that the principal stimulus for ANP secretion in response to atrial distension is the stretch of myocytes. Length shortening of myocytes is not essential for ANP release.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/11/20 alle ore 11:44:50