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Titolo:
ACCENTUATED ANTAGONISM BY ANGIOTENSIN-II ON GUINEA-PIG CARDIAC L-TYPECA-CURRENTS ENHANCED BY BETA-ADRENERGIC STIMULATION
Autore:
AI T; HORIE M; OBAYASHI K; SASAYAMA S;
Indirizzi:
KYOTO UNIV,GRAD SCH MED,DEPT CARDIOVASC MED KYOTO 60601 JAPAN KYOTO UNIV,GRAD SCH MED,DEPT CARDIOVASC MED KYOTO 60601 JAPAN
Titolo Testata:
Pflugers Archiv
fascicolo: 2, volume: 436, anno: 1998,
pagine: 168 - 174
SICI:
0031-6768(1998)436:2<168:AABAOG>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONGESTIVE-HEART-FAILURE; VENTRICULAR MYOCYTES; RECEPTOR; IDENTIFICATION; INVOLVEMENT; RENIN; ISOPROTERENOL; MECHANISM; CAPTOPRIL; CYCLASE;
Keywords:
ANGIOTENSIN-II; L-TYPE CA2+ CURRENT; PTX-SENSITIVE G PROTEINS; CAMP; PROTEIN KINASE A;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
44
Recensione:
Indirizzi per estratti:
Citazione:
T. Ai et al., "ACCENTUATED ANTAGONISM BY ANGIOTENSIN-II ON GUINEA-PIG CARDIAC L-TYPECA-CURRENTS ENHANCED BY BETA-ADRENERGIC STIMULATION", Pflugers Archiv, 436(2), 1998, pp. 168-174

Abstract

To examine mechanism(s) underlying the accentuated antagonism by angiotensin II (A-II) on twitch tension, we recorded L-type Ca2+ currents (I-Ca,I-L) using conventional patch-clamp techniques in single, guineapig, ventricular myocytes. I-Ca,I-L was recorded by a step-pulse protocol after eliminating K+ conductances (internal Cs+ plus tetraethylammonium chloride and K+-free extracellular solution). A-II (100 nM) did not affect basal I-Ca,I-L but inhibited I-Ca,I-L that had been enhanced (approximately 200% of control) by (ISO, isoproterenol 100 nM). The inhibitory action of A-II, was concentration dependent (concentration eliciting 50% inhibition 88+/-9 pM, n=41) and the ISO-enhanced component of I-Ca,I-L was completely blocked by A-II at concentrations above 10 nM. CV-11974 (500 nM), an A-II type-1 receptor (AT(1)) antagonist, prevented the inhibitory action of A-II. Pre-incubation with pertussistoxin (PTX) abolished the inhibitory effect of A-II. A-II also inhibited the I-Ca,I-L enhanced by histamine (500 nM) and forskolin (1 mu M), but failed to affect I-Ca,I-L enhanced by intracellular cyclic adenosine monophosphate (1 mM). The inhibitory action of A-II may thereforeinvolve AT(1) receptors/PTX-sensitive, guanine nucleotide-binding (G)proteins (Gi)/adenylate cyclase and partially explains the A-II-dependent accentuated antagonism of inotropy.

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Documento generato il 12/07/20 alle ore 12:05:43