Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress.

Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress. Research Abstract Details 

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Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress. Abstract Text:

Ben A Weissman,Chantal M Sottas,Ping Zhou,Costantino Iadecola,Matthew P Hardy,

Immobilization stress (IMO) induces a rapid increase in glucocorticoid secretion [in rodents, corticosterone CORT)] and this is associated with decreased circulating testosterone (T) levels. Nitric oxide (NO), a reactive free radical and neurotransmitter, has been reported to be produced at higher rates in tissues such as brain during stress. The biosynthesis of T is also known to be dramatically suppressed by NO. Specifically, the inducible isoform of nitric oxide synthase (iNOS) was directly implicated in this suppression. To assess the respective roles of CORT and NO in stress-mediated inhibition of T production, adult wild-type (WT) and inducible nitric oxide synthase knockout (iNOS(-/-)) male mice were evaluated. Animals of each genotype were assigned to either basal control or 3-h IMO groups. Basal plasma and testicular T levels were equivalent in both genotypes, whereas testicular weights of mutant mice were significantly higher compared with WT animals. Exposure to 3-h IMO increased plasma CORT and decreased T concentrations in mice of both genotypes. Testicular T levels were also affected by stress in WT and mutant males, being sharply reduced in both genotypes. However, the concentrations of nitrite and nitrate, the stable metabolites of NO measured in testicular extracts, did not differ between control and stressed WT and iNOS(-/-) mice. These results support the hypothesis that CORT, but not NO, is a plausible candidate to mediate rapid stress-induced suppression of Leydig cell steroidogenesis.

Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress. Publishing Authors By Initials

BA Weissman,CM Sottas,P Zhou,C Iadecola,MP Hardy,

For similar polycyclic compounds: steroids: androstanes: androstenes: androstenols: testosterone research abstracts see: polycyclic compounds: steroids: androstanes: androstenes: androstenols: testosterone research

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Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: American journal of physiology. Endocrinology and

VOLUME: 292

Page Numbers: E615-20

Journal Abbreviation: Am. J. Physiol. Endocrinol. Me

ISSN: 0193-1849

DAY: 10

MONTH: 10

YEAR: 2006

Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress. Information

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LANGUAGE: eng

NlmUniqueID: 100901226

Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress. Keywords Mesh Terms:

KEYWORDS: Testosterone

MESH TERMS: blood

Chemical & Substance for Abstract: Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress. Information

Substance Name: Nitric Oxide Synthase Type II

Registry Number: EC 1.14.13.39

Grant and Affiliation Information for Testosterone production in mice lacking inducible nitric oxide synthase expression is sensitive to restraint stress.

AFFILIATION: Department of Pharmacology, Israel Institute for Biological Research, Ness Ziona, Israel. baw@iibr.gov.il

Country: United States

AGENCY: United States NINDS

GRANT: NS-34179

ACRONYM: NS

MEDLINETA: Am J Physiol Endocrinol Metab

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