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Titolo:
THROMBIN RECEPTOR ACTIVATION PEPTIDE INDUCES PULMONARY VASOCONSTRICTION
Autore:
LUM H; ANDERSEN TT; FENTON JW; MALIK AB;
Indirizzi:
RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT PHARMACOL,2242 W HARRISON ST,RM 260 CHICAGO IL 60612 ALBANY MED COLL,ALBANY MED COLL,DEPT BIOCHEM & MOLEC BIOL ALBANY NY 12208 NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES ALBANY NY 12201
Titolo Testata:
The American journal of physiology
fascicolo: 2, volume: 266, anno: 1994,
parte:, 1
pagine: 30000448 - 30000454
SICI:
0002-9513(1994)266:2<30000448:TRAPIP>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN-ENDOTHELIAL-CELLS; VASCULAR SMOOTH-MUSCLE; ALPHA-THROMBIN; INDUCED INCREASE; PROSTACYCLIN PRODUCTION; ALBUMIN PERMEABILITY; CALCIUM; DESENSITIZATION; DEPENDENCE; EXPRESSION;
Keywords:
PULMONARY ARTERIAL PRESSURE; PULMONARY ARTERIAL AND VENOUS RESISTANCE; DESENSITIZATION; SMOOTH MUSCLE CELLS; CALCIUM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
35
Recensione:
Indirizzi per estratti:
Citazione:
H. Lum et al., "THROMBIN RECEPTOR ACTIVATION PEPTIDE INDUCES PULMONARY VASOCONSTRICTION", The American journal of physiology, 266(2), 1994, pp. 30000448-30000454

Abstract

We investigated the involvement of the 11-residue thrombin receptor activating peptide SFLLRNPNDKYEPF (TRAP-14) in mediating the pulmonary vasoconstriction in response to alpha-thrombin. Isolated guinea pig lungs were uniformly perfused with Ringer-albumin solution at a constantflow of 28 ml/min. Addition of TRAP-14 or human alpha-thrombin to theperfusate caused dose-dependent increases of pulmonary arterial pressure within 1 min. TRAP-14 at 1 mu M increased pulmonary arterial pressure to a similar extent as 10 nM alpha-thrombin (i.e., increase of 7.7+/- 0.8 and 7.4 +/- 0.9 cmH(2)O from baseline, respectively). The increases in pulmonary venous resistance induced by TRAP-14 and alpha-thrombin were two- to fivefold greater than the increases in pulmonary arterial resistance, indicating that both agonists mediated pulmonary hypertension secondary to pulmonary venoconstriction. Stimulation of cultured guinea pig pulmonary artery smooth muscle cells with 100 mu M TRAP-14 or 10 nM alpha-thrombin increased cytosolic Ca2+ concentration about five- to sevenfold over baseline. The increase in cytosolic Ca2+ concentration in smooth muscle cells was not observed with a subsequent challenge with either agonist, indicating desensitization. In the perfused lungs, an initial stimulation with alpha-thrombin or TRAP-14 desensitized the lungs to either agonist. The alpha-thrombin-desensitized lungs remained refractile to alpha-thrombin after 1 h of perfusion with fresh Ringer solution, whereas the TRAP-14-desensitized lungs recovered 79% of the vasoconstrictor response by 10 min and 93% of the response by 30 min. Therefore pulmonary vasoconstriction mediated by alpha-thrombin is the result of cleavage of the thrombin receptor, producing a new NH2-terminal ''tethered ligand'' that contains the receptor activating sequence SFLLRNPNDKYEPF. Furthermore, pulmonary vasoconstriction induced by alpha-thrombin involves direct activation of the thrombin receptor on smooth muscle cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 19:50:09