Testosterone contributes to marked elevations in mean arterial pressure in adult male intrauterine growth restricted offspring.

Testosterone contributes to marked elevations in mean arterial pressure in adult male intrauterine growth restricted offspring. Research Abstract Details 

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Testosterone contributes to marked elevations in mean arterial pressure in adult male intrauterine growth restricted offspring. Abstract Text:

Norma B Ojeda,Daniela Grigore,Licy L Yanes,Radu Iliescu,Elliot B Robertson,Huimin Zhang,Barbara T Alexander,

Our laboratory uses a model of intrauterine growth restriction (IUGR) induced by placental insufficiency in the rat to examine the developmental origins of adult disease. In this model only male IUGR offspring remain hypertensive in adulthood, revealing sex-specific differences. The purpose of this study was to determine whether testosterone with participation of the renin-angiotensin system (RAS) contributes to hypertension in adult male IUGR offspring. At 16 wk of age a significant increase in testosterone (346 +/- 34 vs. 189 +/- 12 ng/dl, P < 0.05) was associated with a significant increase in mean arterial pressure (MAP) measured by telemetry in IUGR offspring (147 +/- 1 vs. 125 +/- 1 mmHg, P < 0.05, IUGR vs. control, respectively). Gonadectomy (CTX) at 10 wk of age significantly reduced MAP by 16 wk of age in IUGR offspring (124 +/- 2 mmHg, P < 0.05 vs. intact IUGR) but had no effect in control (125 +/- 2 mmHg). A significant decrease in MAP in intact IUGR (111 +/- 3 mmHg, P < 0.05 vs. untreated intact IUGR) and castrated IUGR (110 +/- 4 mmHg, P < 0.05 vs. untreated CTX IUGR) after treatment with enalapril for 2 wk suggests a role for RAS involvement. However, the decrease in blood pressure in response to enalapril was greater in intact IUGR (Delta36 +/- 1 mmHg, P < 0.05) compared with CTX IUGR (Delta15 +/- 2 mmHg), indicating an enhanced response to RAS blockade in the presence of testosterone. Thus these results suggest that testosterone plays a role in modulating hypertension in adult male IUGR offspring with participation of the RAS.

Testosterone contributes to marked elevations in mean arterial pressure in adult male intrauterine growth restricted offspring. Publishing Authors By Initials

NB Ojeda,D Grigore,LL Yanes,R Iliescu,EB Robertson,H Zhang,BT Alexander,

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 contributes to marked elevations in mean arterial pressure in adult male intrauterine growth restricted offspring. Journal Published:

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

Journal: American journal of physiology. Regulatory, integr

VOLUME: 292

Page Numbers: R758-63

Journal Abbreviation: Am. J. Physiol. Regul. Integr.

ISSN: 0363-6119

DAY: 17

MONTH: 08

YEAR: 2006

Testosterone contributes to marked elevations in mean arterial pressure in adult male intrauterine growth restricted offspring. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901230

Testosterone contributes to marked elevations in mean arterial pressure in adult male intrauterine growth restricted offspring. Keywords Mesh Terms:

KEYWORDS: Testosterone

MESH TERMS: physiology

Chemical & Substance for Abstract: Testosterone contributes to marked elevations in mean arterial pressure in adult male intrauterine growth restricted offspring. Information

Substance Name: Renin

Registry Number: EC 3.4.23.15

Grant and Affiliation Information for Testosterone contributes to marked elevations in mean arterial pressure in adult male intrauterine growth restricted offspring.

AFFILIATION: Department of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216-4505, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL-074927

ACRONYM: HL

MEDLINETA: Am J Physiol Regul Integr Comp

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