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Titolo:
Potentiation of stretch-induced atrial natriuretic peptide secretion by intracellular acidosis
Autore:
Tavi, P; Laine, M; Voutilainen, S; Lehenkari, P; Vuolteenaho, O; Ruskoaho, H; Weckstrom, M;
Indirizzi:
Univ Oulu, Dept Physiol, SF-90220 Oulu, Finland Univ Oulu Oulu Finland SF-90220 lu, Dept Physiol, SF-90220 Oulu, Finland Univ Oulu, Dept Anat, SF-90220 Oulu, Finland Univ Oulu Oulu Finland SF-90220 Oulu, Dept Anat, SF-90220 Oulu, Finland Univ Oulu, Dept Pharmacol & Toxicol, SF-90220 Oulu, Finland Univ Oulu Oulu Finland SF-90220 rmacol & Toxicol, SF-90220 Oulu, Finland Univ Oulu, Dept Phys Sci, Div Biophys, SF-90220 Oulu, Finland Univ Oulu Oulu Finland SF-90220 Sci, Div Biophys, SF-90220 Oulu, Finland Univ Oulu, Bioctr Oulu, SF-90220 Oulu, Finland Univ Oulu Oulu Finland SF-90220 ulu, Bioctr Oulu, SF-90220 Oulu, Finland
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 1, volume: 46, anno: 1999,
pagine: H405 - H412
SICI:
0363-6135(199907)46:1<H405:POSANP>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE MYOCARDIAL-INFARCTION; MAMMALIAN CARDIAC-MUSCLE; RAT VENTRICULAR MYOCYTES; PROTEIN-KINASE-C; CALCIUM TRANSIENTS; ANP SECRETION; PHORBOL ESTER; PLASMA-LEVELS; RELEASE; CA2+;
Keywords:
atrial function; calcium; contractile function; hormones;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Weckstrom, M Univ Oulu, Dept Physiol, Kajaanintie 52A, SF-90220 Oulu, Finland Univ Oulu Kajaanintie 52A Oulu Finland SF-90220 ulu, Finland
Citazione:
P. Tavi et al., "Potentiation of stretch-induced atrial natriuretic peptide secretion by intracellular acidosis", AM J P-HEAR, 46(1), 1999, pp. H405-H412

Abstract

We sought to investigate whether atrial myocyte contraction and secretion of the atrial natriuretic peptide (ANP) are affected in the same manner by intervention in intracellular Ca2+ handling by acidosis. The effects of propionate (20 mM)induced intracellular acidosis on the stretch-induced changes in ANP secretion, contraction force, and intracellular Ca2+ concentration([Ca2+](i)) were studied in the isolated rat atrium. The stretch of the atrium was produced by increasing the intra-atrial pressure of the paced and superfused preparation. Contraction force was estimated from pressure pulses generated by the contraction of the atrium. Intracellular Ca2+ was measured from indo 1-AM-loaded atria, and ANP was measured by radioimmunoassay from the perfusate samples collected during interventions. Intracellular pH of the atrial myocytes was measured by a fluorescent indicator (BCECF)based imaging system. Intracellular acidification caused by 20 mM propionic acid (0.18 pH units) potentiated the stretch-induced (intra-atrial pressure from1 to 4 mmHg) ANP secretion, causing a twofold secretion compared with nonacidotic controls. Simultaneously, the responsiveness of the atrial contraction to stretch was reduced (P < 0.05, n = 7). Stretch augmented the systolic indo 1-AM transients in acidic (P < 0.05, n = 6) and nonacidic atria (P <0.05, n = 6). However, during acidosis this was accompanied by an increaseof the diastolic indo 1-AM ratio (P < 0.05, n = 6). Cooccurrence of stretch and acidosis caused an increase in systolic and diastolic [Ca2+](i) and potentiated the stretch-induced ANP secretion, whereas the contraction forceand its stretch sensitivity were decreased. This mechanism may be involvedin ischemia-induced ANP secretion, suggesting a role for ANP secretion as an indicator of contractile dysfunction.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 00:39:17