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Titolo:
Androgen-receptor defect abolishes sex differences in nitric oxide and reactivity to vasopressin in rat aorta
Autore:
Stallone, JN; Salisbury, RL; Fulton, CT;
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, Coll Vet Med, Michael E DeBakey 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 NE Ohio Univ, Coll Med, Dept Physiol, Rootstown, OH 44272 USA NE Ohio Univ Rootstown OH USA 44272 Dept Physiol, Rootstown, OH 44272 USA Univ Akron, Dept Biol, Akron, OH 44325 USA Univ Akron Akron OH USA 44325Univ Akron, Dept Biol, Akron, OH 44325 USA
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 6, volume: 91, anno: 2001,
pagine: 2602 - 2610
SICI:
8750-7587(200112)91:6<2602:ADASDI>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT GENDER DIFFERENCES; TESTICULAR FEMINIZED RAT; L-ARGININE; ENDOTHELIUM; ESTROGEN; MUSCLE; DIMORPHISM; HORMONES; BINDING; BRAIN;
Keywords:
aorta; arginine vasopressin; endothelium-derived relaxing factor; gonadal steroid hormones; testicular-feminized rat; vasoconstriction;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
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:
J.N. Stallone et al., "Androgen-receptor defect abolishes sex differences in nitric oxide and reactivity to vasopressin in rat aorta", J APP PHYSL, 91(6), 2001, pp. 2602-2610

Abstract

Contractions of rat thoracic aorta to vasopressin WP) are threefold higherin females (F) than in males (M), primarily because nitric oxide (NO) attenuation of contraction is greater in M. To determine the role of the androgen receptor (AR) in this mechanism, vascular reactivity to VP was examined in thoracic aorta of the testicular-feminized male (Tfm) rat, which has an X-linked, recessive defect in AR function in affected M. Maximal contraction of normal aortas to VP was fourfold higher in F (4,128 +/- 291 mg/mg ringwt) than in M (971 +/- 133 mg); maximal response of Tfm (3,967 +/- 253 mg)was similar to that of normal F. N-G-nitro-L-arginine methyl ester increased maximal response to VP threefold in M but had no effect in F or Tfm. In contrast, maximal contraction of normal aortas to phenylephrine was 43% higher in M (4,011 +/- 179 mg) than in F (2,809 +/- 78 mg); maximal response of Tfm (2,716 +/- 126 mg) was similar to that of normal F. N-G-nitro-L-arginine methyl ester increased maximal response to phenylephrine by >50% in F and Tfm but had no effect in M. Maximal contractile response to 80 mM KCl did not differ among M, F, or Tfm. Thus androgens and normal vascular AR function are important in the greater NO-mediated attenuation of reactivity to VP in M than in F rat aorta, which may involve specific modulation of endothelial VP signal transduction pathways and NO release by androgens. These data also establish the importance of the Tfm rat as a model to study the effects of androgens on cardiovascular function.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/01/20 alle ore 22:28:47