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Titolo:
HYPOXIA STIMULATES RELEASE OF ANP AND BNP FROM PERFUSED RAT VENTRICULAR MYOCARDIUM
Autore:
TOTH M; VUORINEN KH; VUOLTEENAHO O; HASSINEN IE; UUSIMAA PA; LEPPALUOTO J; RUSKOAHO H;
Indirizzi:
UNIV OULU,DEPT PHARMACOL,KAJAANINTIE 52D SF-90220 OULU FINLAND UNIV OULU,DEPT PHARMACOL & TOXICOL SF-90220 OULU FINLAND UNIV OULU,DEPT MED BIOCHEM SF-90220 OULU FINLAND UNIV OULU,DEPT PHYSIOL SF-90220 OULU FINLAND
Titolo Testata:
The American journal of physiology
fascicolo: 4, volume: 266, anno: 1994,
parte:, 2
pagine: 80001572 - 80001580
SICI:
0002-9513(1994)266:4<80001572:HSROAA>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
ATRIAL-NATRIURETIC-PEPTIDE; MAJOR SITE; HEART; ISCHEMIA; ENDOTHELIN-1; BRAIN; MECHANISMS; SECRETION; EXERCISE; BIOLOGY;
Keywords:
ATRIAL NATRIURETIC PEPTIDE; BRAIN NATRIURETIC PEPTIDE; ENDOTHELIN; CELLULAR ENERGY STATE; NUCLEAR MAGNETIC RESONANCE; CARDIAC MYOCYTES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
35
Recensione:
Indirizzi per estratti:
Citazione:
M. Toth et al., "HYPOXIA STIMULATES RELEASE OF ANP AND BNP FROM PERFUSED RAT VENTRICULAR MYOCARDIUM", The American journal of physiology, 266(4), 1994, pp. 80001572-80001580

Abstract

We determined the effect of hypoxia on cellular energy state and ventricular atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and endothelin-1 (ET-1) release in an isolated perfused heart preparation after removal of all atrial tissue in 21- to 24-mo-old Wistar-Kyoto rats. After a control period (14 min), the ventricles (n = 6) were exposed to 30 min of hypoxia by changing the gas mixture to N-2-CO2 (95:5 vol/vol; hypoxic period) and back to O-2-CO2 (95:5 vol/vol) for 30 min (reoxygenation period). Control hearts (n = 6) were perfused throughout the experiment (74 min) with oxygenated Krebs-Henseleit phosphate-free buffer. In parallel experiments, the metabolic state of oxygenated (n = 4) and hypoxic (n = 5) ventricles was assessed using P-31-nuclear magnetic resonance (P-31-NMR). Hypoxia caused a rapid decrease in left ventricular peak systolic pressure associated with a 2.1-fold increase (27.6 +/- 2.2 to 58.0 +/- 13.1 fmol/ml; P < 0.05) in the concentration of immunoreactive (ir) ANP and a 1.6-fold increase (2.5 +/- 0.2 to 3.9 +/- 0.5 fmol/ml; P < 0.05) in the [irBNP] (where brackets signify concentration) in the perfusate. In contrast, perfusate [irET-1] (1.2 +/- 0.2 fmol/ml) did not change significantly during hypoxia. P-31-NMR showed that the [ATP]-to-[ADP].[P-i] ratio was reduced during hypoxia with a simultaneous increase in intracellular monophosphates and perfusate [irANP] and [irBNP]. The decrease in the cytosolic pH during hypoxia was small. High-performance liquid chromatography of the perfusates showed that the ANP-like immunoreactive material releasedcorresponded to the processed, low-molecular weight peptide. The NH2-terminal fragment of proANP, ANP-(1-98), was also found in the perfusate, whereas lactate dehydrogenase activity in the perfusate was at or below the detection limit of the assay. These results show that hypoxia is an independent stimulus for ventricular natriuretic peptide release and that release of ANP and BNP from ventricles contributes to the circulating levels of the peptides during hypoxia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/04/20 alle ore 21:46:36