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Titolo:
HS-142-1, A POTENT ANTAGONIST OF NATRIURETIC PEPTIDES IN-VITRO AND IN-VIVO
Autore:
ZHANG PL; JIMENEZ W; MACKENZIE HS; GUO JZ; TROY JL; ROS J; ANGELI P; ARROYO V; BRENNER BM;
Indirizzi:
BRIGHAM & WOMENS HOSP,DEPT MED,DIV RENAL,75 FRANCIS ST BOSTON MA 02115 HARVARD UNIV,SCH MED,CTR STUDY KIDNEY DIS BOSTON MA 00000 UNIV BARCELONA,HOSP CLIN & PROV,HORMONAL LAB BARCELONA SPAIN UNIV BARCELONA,HOSP CLIN & PROV,LIVER UNIT BARCELONA SPAIN
Titolo Testata:
Journal of the American Society of Nephrology
fascicolo: 4, volume: 5, anno: 1994,
pagine: 1099 - 1105
SICI:
1046-6673(1994)5:4<1099:HAPAON>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
NONPEPTIDE ANTAGONIST; INDUCED RELAXATION; MICROBIAL ORIGIN; RENAL RECEPTORS; DIABETIC RATS; ATRIAL; BRAIN; HYPERFILTRATION; URODILATIN; INHIBITION;
Keywords:
ATRIAL NATRIURETIC PEPTIDE; BRAIN NATRIURETIC PEPTIDE; URODILATIN; C-TYPE NATRIURETIC PEPTIDE; CGMP; RAT FETAL LUNG FIBROBLAST (RFL-6) CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
24
Recensione:
Indirizzi per estratti:
Citazione:
P.L. Zhang et al., "HS-142-1, A POTENT ANTAGONIST OF NATRIURETIC PEPTIDES IN-VITRO AND IN-VIVO", Journal of the American Society of Nephrology, 5(4), 1994, pp. 1099-1105

Abstract

To determine whether HS-142-1 (HS), a potent atrial natriuretic peptide (ANP) receptor antagonist, also inhibits the effects of brain natriuretic peptide (BNP), urodilatin (URO), and C-type natriuretic peptide, in vitro studies were carried out, demonstrating that HS inhibited production of cGMP by rat fetal lung fibroblast cells induced by ANP, BNP, URO, and C-type natriuretic peptide. Acute clearance studies were conducted in euvolemic Munich-Wistar rats under inactin anesthesia to characterize the effects of HS in vivo. In response to ANP, BNP, or URO (4 mu g/kg priming dose plus 0.5 mu g/kg per minute for 20 min), urine flow, absolute sodium excretion rates, and fractional sodium excretion exhibited similar increases (four- to fivefold) in vehicle-treatedrats; these responses were, however, completely abolished by prior HStreatment. The tendency for GFR to rise during the infusion of natriuretic peptides (NP) was also blocked after HS. By contrast, HS did notblock the renal effects of L-arginine, a precursor of nitric oxide, or of furosemide. Furthermore, the inhibition of endogenous NP by HS was associated with small but significant reductions in GFR and absoluteand fractional sodium excretion in normal rats under euvolemic but not hydropenic conditions. These studies provide evidence that the observed effects of HS in vivo and in vitro are mediated exclusively by receptors of NP. Together, these data support the view that HS is a highly specific ligand for NP receptors, capable of antagonizing the renal effects not only of exogenous ANP, but also those of BNP and URO.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 06:52:22