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Titolo:
[Ca2+](i) signaling in renal arterial smooth muscle cells of pregnant rat is enhanced during inhibition of NOS
Autore:
Murphy, JG; Fleming, JB; Cockrell, KL; Granger, JP; Khalil, RA;
Indirizzi:
Univ Mississippi, Med Ctr, Dept Physiol & Biophys, Jackson, MS 39216 USA Univ Mississippi Jackson MS USA 39216 ol & Biophys, Jackson, MS 39216 USA Univ Mississippi, Med Ctr, Ctr Excellence Cardiovasc Renal Res, Jackson, MS 39216 USA Univ Mississippi Jackson MS USA 39216 sc Renal Res, Jackson, MS 39216 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
fascicolo: 1, volume: 280, anno: 2001,
pagine: R87 - R99
SICI:
0363-6119(200101)280:1<R87:[SIRAS>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHESIS; PROTEIN-KINASE-C; CALCIUM-CHANNEL CURRENTS; PORTAL-VEIN; VASCULAR REACTIVITY; MESENTERIC-ARTERY; BLOOD-PRESSURE; PREECLAMPSIA; HEMODYNAMICS; CONTRACTION;
Keywords:
vascular resistance; hypertension; calcium; contraction;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
66
Recensione:
Indirizzi per estratti:
Indirizzo: Khalil, RA Univ Mississippi, Med Ctr, Dept Physiol & Biophys, 2500 N StateSt, Jackson, MS 39216 USA Univ Mississippi 2500 N State St Jackson MS USA 39216 39216 USA
Citazione:
J.G. Murphy et al., "[Ca2+](i) signaling in renal arterial smooth muscle cells of pregnant rat is enhanced during inhibition of NOS", AM J P-REG, 280(1), 2001, pp. R87-R99

Abstract

Vascular resistance and arterial pressure are reduced during normal pregnancy, but dangerously elevated during pregnancy-induced hypertension (PIH), and changes in nitric oxide (NO) synthesis have been hypothesized as one potential cause. In support of this hypothesis, chronic inhibition of NO synthesis in pregnant rats has been shown to cause significant increases in renal vascular resistance and hypertension; however, the cellular mechanisms involved are unclear. We tested the hypothesis that the pregnancy-associatedchanges in renal vascular resistance reflect changes in contractility and intracellular Ca2+ concentration ([Ca2+](i)) of renal arterial smooth muscle. Smooth muscle cells were isolated from renal interlobular arteries of virgin and pregnant Sprague-Dawley rats untreated or treated with the NO synthase inhibitor nitro-L-arginine methyl ester (L-NAME; 4 mg.kg(-1).day(-1) for 5 days), then loaded with fura 2. In cells of virgin rats incubated in Hanks' solution (1 mM Ca2+), the basal [Ca2+](i) was 86 +/- 6 nM. Phenylephrine (Phe, 10(-5) M) caused a transient increase in [Ca2+](i) to 417 +/- 11 nM and maintained an increase to 183 +/- 8 nM and 32 +/- 3% cell contraction. Membrane depolarization by 51 mM KCl, which stimulates Ca2+ entry from the extracellular space, caused maintained increase in [Ca2+](i) to 292 +/- 12 nM and 31 +/- 2% contraction. The maintained Phe- and KCl-induced [Ca2+](i) and contractions were reduced in pregnant rats but significantly enhanced in pregnant rats treated with L-NAME. Phe- and KCl-induced contraction and [Ca2+](i) were not significantly different between untreated and L-NAME-treated virgin rats or between untreated and L-NAME + L-arginine treated pregnant rats. In Ca2+-free Hanks', application of Phe or caffeine (10 mM), to stimulate Ca2+ release from the intracellular stores, caused a transient increase in [Ca2+](i) and a small cell contraction that were not significantly different among the different groups. Thus renal interlobular smooth muscle of normal pregnant rats exhibits reduction in [Ca2+](i) signaling thatinvolves Ca2+ entry from the extracellular space but not Ca2+ release fromthe intracellular stores. The reduced renal smooth muscle cell contractionand [Ca2+](i) in pregnant rats may explain the decreased renal vascular resistance associated with normal pregnancy, whereas the enhanced cell contraction and [Ca2+](i) during inhibition of NO synthesis in pregnant rats may,in part, explain the increased renal vascular resistance associated with PIH.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 11:06:27