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Titolo:
Testosterone-induced relaxation of rat aorta is androgen structure specific and involves K+ channel activation
Autore:
Ding, AQ; Stallone, JN;
Indirizzi:
Texas A&M Univ, Coll Vet Med, Dept Vet Physiol & Pharmacol, College Stn, TX 77843 USA Texas A&M Univ College Stn TX USA 77843 rmacol, College Stn, TX 77843 USA Texas A&M Univ, Michael E De Bakey Inst Comparat Cardiovasc Sci, College Stn, TX 77843 USA Texas A&M Univ College Stn TX USA 77843 sc Sci, College Stn, TX 77843 USA
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 6, volume: 91, anno: 2001,
pagine: 2742 - 2750
SICI:
8750-7587(200112)91:6<2742:TRORAI>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASOPRESSIN-INDUCED CONTRACTION; CORONARY-ARTERY DISEASE; STEROID-HORMONES; SEXUAL DIMORPHISM; ESTROGEN; 17-BETA-ESTRADIOL; MEN; ENDOTHELIUM; MECHANISMS; RECEPTORS;
Keywords:
endothelium; endothelium-dependent vasodilation; endothelium-independent; vasodilation; vasorelaxation; vasodilation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Stallone, JN Texas A&M Univ, Coll Vet Med, Dept Vet Physiol & Pharmacol, College Stn, TX 77843 USA Texas A&M Univ College Stn TX USA 77843 ge Stn, TX 77843 USA
Citazione:
A.Q. Ding e J.N. Stallone, "Testosterone-induced relaxation of rat aorta is androgen structure specific and involves K+ channel activation", J APP PHYSL, 91(6), 2001, pp. 2742-2750

Abstract

Recent studies have established that testosterone (Tes) produces acute (nongenomic) vasorelaxation. This study examined the structural specificity ofTes-induced vasorelaxation and the role of vascular smooth muscle (VSM) Kchannels in rat thoracic aorta. Aortic rings from male Sprague-Dawley ratswith (Endo+) and without endothelium (Endo-) were prepared for isometric tension recording. In Endo - aortas precontracted with phenylephrine, 5-300 muM Tes produced dose-dependent relaxation from 10 muM (4 +/- 1%) to 300 muM (100 +/- 1%). In paired Endo+ and Endo- aortas, Tes-induced vasorelaxation was slightly but significantly greater in Endo+ aortas (at 5-150 muM Tes); sensitivity (EC50) of the aorta to Tes was reduced by nearly one-half in Endo - vessels. Based on the sensitivity (EC50) of Endo- aortas, Tes, the active metabolite 5 alpha -dihydrotestosterone, the major excretory metabolites androsterone and etiocholanolone, the nonpolar esters Tes-enanthate andTes-hemisuccinate (THS), and THS conjugates to BSA (THS-BSA) exhibited relative potencies for vasorelaxation dramatically different from androgen receptor-mediated effects observed in reproductive tissues, with a rank order of THS-BSA > Tes > androsterone = THS = etiocholanolone > dihydrotestosterone >> Tes-enanthate. Pretreatment of aortas with 5 mM 4-aminopyridine attenuated Tes-induced vasorelaxation by an average of 44 +/- 2% (25-300 muM Tes). In contrast, pretreatment of aortas with other K+ channel inhibitors hadno effect. These data reveal that Tes-induced vasorelaxation is a structurally specific effect of the androgen molecule, which is enhanced in more polar analogs that have a lower permeability to the VSM cell membrane, and that the effect of Tes involves activation of K+ efflux through K+ channels in VSM, perhaps via the voltage-dependent (delayed-rectifier) K+ channel.

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Documento generato il 04/04/20 alle ore 12:30:30