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Titolo:
17-BETA-ESTRADIOL INHIBITS THE VOLTAGE-DEPENDENT L-TYPE CA2-MUSCLE CELLS( CURRENTS IN AORTIC SMOOTH)
Autore:
NAKAJIMA T; KITAZAWA T; HAMADA E; HAZAMA H; OMATA M; KURACHI Y;
Indirizzi:
UNIV TOKYO,FAC MED,DEPT INTERNAL MED 2,BUNKYO KU,7-3-1 HONGO TOKYO 113 JAPAN GEORGETOWN UNIV,DEPT PHYSIOL & BIOPHYS WASHINGTON DC 00000 OSAKA UNIV,DEPT PHARMACOL 2 SUITA OSAKA 565 JAPAN
Titolo Testata:
European journal of pharmacology
fascicolo: 2-3, volume: 294, anno: 1995,
pagine: 625 - 635
SICI:
0014-2999(1995)294:2-3<625:1ITVLC>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
RABBIT CORONARY-ARTERY; PORTAL-VEIN; EAR ARTERY; RESPONSES; ESTROGEN; CHANNELS; NORADRENALINE; ENDOTHELIN; RECEPTORS; CA-2+;
Keywords:
17-BETA-ESTRADIOL; ESTROGEN; VASCULAR SMOOTH MUSCLE; CA2+ CURRENT, L-TYPE, VOLTAGE-DEPENDENT; ENDOTHELIN-1; VASOPRESSIN; CA2+-PERMEABLE NONSELECTIVE CATION CURRENT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
27
Recensione:
Indirizzi per estratti:
Citazione:
T. Nakajima et al., "17-BETA-ESTRADIOL INHIBITS THE VOLTAGE-DEPENDENT L-TYPE CA2-MUSCLE CELLS( CURRENTS IN AORTIC SMOOTH)", European journal of pharmacology, 294(2-3), 1995, pp. 625-635

Abstract

To elucidate the mechanisms of estrogens-induced relaxation effects on vascular smooth muscle cells, the effects of estrogens and the related hormones were examined in cultured rat thoracic aortic smooth muscle cell lines (A7r5), using the whole-cell voltage clamp technique. Thepatch pipette was filled with 140 mM CsCl- or KCl-containing internalsolution. With CsCl-internal solution, 17 beta-estradiol and synthetic estrogens, ethynylestradiol and diethylstilbestrol (0.1-30 mu M) inhibited the Ba2+ inward current (I-Ba) through the voltage-dependent L-type Ca2+ channel in a concentration-dependent and reversible manner. The potency of the inhibitory effects on I-Ba was 17 beta-estradiol < ethynylestradiol < diethylstilbestrol. 17 beta-Estradiol (10 mu M) appeared to reduce the maximal conductance of I-Ba with only a slight shift of voltage-dependency of inactivation and to affect I-Ba in a use-independent fashion. On the other hand, testosterone and progesterone (30 mu M) failed to affect I-Ba. At a holding potential of -40 mV, bothvasopressin and endothelin-1 (100 nM) activated a long-lasting inwardcurrent. After endothelin-l (100 nM) activated the current, the additional application of vasopressin (100 nM) could not induce it furthermore, suggesting that each agonist activates the same population of thechannels. The reversal potential of the current was about 0 mV and was not significantly altered by replacement of [Cl-], or [Cl-], and theinward current was also observed even when extracellular cations are Ca2+, proposing that it was a Ca2+-permeable non-selective cation channel (I-N.S.). La3+ or Cd2+ (1 mM) completely abolished I-N.S., however, nifedipine (10 mu M) failed to inhibit it at all. Diethylstilbestrol(1-30 mu M) suppressed the I-N.S. evoked by both endothelin-l and vasopressin in a concentration-dependent manner, while 17 beta-estradiol,ethynylestradiol, progesterone and testosterone (30 mu M) failed to inhibit it significantly. In addition, at a holding potential of +0 mV,17 beta-estradiol by itself did not affect the holding currents, and did not inhibit K+ currents evoked by endothelin-l or vasopressin, possibly due to the Ca2+ release from the storage sites. These results suggest that 17 beta-estradiol may play a role in regulating vascular tone, selectively by inhibiting the voltage-dependent L-type Ca2+ current in vascular smooth muscle cells.

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Documento generato il 28/03/20 alle ore 12:17:14