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Titolo:
Multiple mechanisms are involved in the acute vasodilatory effect of 17 beta-estradiol in the isolated perfused rat heart
Autore:
Hugel, S; Neubauer, S; Lie, SZ; Ernst, R; Horn, M; Schmidt, HHHW; Allolio, B; Reincke, M;
Indirizzi:
Univ Wurzburg, Med Klin, D-97080 Wurzburg, Germany Univ Wurzburg Wurzburg Germany D-97080 d Klin, D-97080 Wurzburg, Germany Univ Wurzburg, Inst Pharmakol & Toxikol, D-97080 Wurzburg, Germany Univ Wurzburg Wurzburg Germany D-97080 oxikol, D-97080 Wurzburg, Germany
Titolo Testata:
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
fascicolo: 6, volume: 33, anno: 1999,
pagine: 852 - 858
SICI:
0160-2446(199906)33:6<852:MMAIIT>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOTHELIUM-INDEPENDENT RELAXATION; NITRIC-OXIDE; SMOOTH-MUSCLE; CORONARY-ARTERIES; K+ CHANNELS; ESTROGEN; PROSTACYCLIN; RELEASE; RABBIT; CELLS;
Keywords:
coronary circulation; estradiol; nitric oxide; K channel; Ca channel; prostaglandins;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Hugel, S Univ Wurzburg, Med Klin, Josef Schneider Str 2, D-97080 Wurzburg,Germany Univ Wurzburg Josef Schneider Str 2 Wurzburg Germany D-97080 any
Citazione:
S. Hugel et al., "Multiple mechanisms are involved in the acute vasodilatory effect of 17 beta-estradiol in the isolated perfused rat heart", J CARDIO PH, 33(6), 1999, pp. 852-858

Abstract

The purpose of this study was to define the dose-dependent effects of 17 beta-estradiol on coronary flow and cardiac function in isolated rat hearts and to identify the mechanisms involved in its vasodilator action. Hearts from female and male Wistar rats were perfused at constant pressure (100 mm Hg). Stereoisomer specificity and the mechanism of vasodilation by 17 beta-estradiol were examined in female rat hearts. Function was measured by a left ventricular (LV) balloon and coronary flow (CF) with an ultrasonic flowmeter. 17 beta-Estradiol at 10(-6), 5 x 10(-6), and 10(-5) M increased CF infemale hearts by 5 +/- 2, 27 +/- 4 (p < 0.05 vs. baseline), and 40 +/- 4% (p < 0.05 vs. baseline), respectively. The effect of 17 beta-estradiol in hearts from male rats was similar but less pronounced compared with females [Delta CF 8 +/- 3, 19 +/- 3 (p < 0.05 vs. baseline)] and 25 +/- 7% (p < 0.05 vs, baseline; p < 0.05 vs, female 17 beta-estradiol). Maximum vasodilation by the stereoisomer 17 alpha-estradiol was significantly smaller [Delta CF 5 +/- 3, 4 +/- 3 (p < 0.05 vs. female 17 beta-estradiol) and 14 +/- 1% (p< 0.05 vs. baseline; p < 0.05 vs. female 17 beta-estradiol)] for 10(-6), 5x 10(-6), and 10(-5) M. Pretreatment with the NO-synthesis inhibitor N-omega-methyl-L-arginine (10(-4) M) had no effect on the maximal vasodilator response to 17 beta-estradiol (10(-5) M) [Delta CF 36 +/- 6% (p < 0.05 vs. baseline)]. When hearts were pretreated with the prostaglandin-synthesis inhibitor diclofenac (10(-6) M), the maximal vasodilator effect of 17 beta-estradiol was partially attenuated [Delta CF 12 +/- 7% (p < 0.05 vs, female 17 beta-estradiol)]. Similarly, pretreatment with the K-ATP(+)-blocker glibenclamide (10(-6) M) partially inhibited the maximal vasodilator effect of 17 beta-estradiol [Delta CF 22 +/- 6% (p < 0.05 vs. baseline; p < 0.05 vs. female 17 beta-estradiol)]. Pretreatment with the Ca2+ channel antagonist nifedipine (7.2 x 10(-8) M) completely blocked the vasodilator effect. In isolated perfused rat hearts, 17 beta-estradiol induced marked acute coronary vasodilation; this effect is in pare gender specific, and in female hearts, largely stereoisomer specific. The dilator effect is mediated predominantly by calcium channel blockade, but prostaglandin release and K-ATP(+) channelactivation also are involved. In the isolated pet-fused rat heart, NO production does not contribute to the acute vasodilator effect of 17 beta-estradiol.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/10/20 alle ore 23:17:35