Enhanced sensitivity to acute angiotensin II is testosterone dependent in adult male growth-restricted offspring
| Autor: | John Henry Dasinger, Norma B. Ojeda, Barbara T. Alexander, Thomas P Royals, Joshua T Black, Jeremy M. Johnson |
|---|---|
| Rok vydání: | 2010 |
| Předmět: |
Male
medicine.medical_specialty Hypertension Renal Physiology Drinking Hemodynamics Blood Pressure Kidney Plasma renin activity Rats Sprague-Dawley Renin-Angiotensin System chemistry.chemical_compound Phenylephrine Sex Factors Pregnancy Physiology (medical) Internal medicine Renin–angiotensin system medicine Animals Birth Weight Vasoconstrictor Agents Testosterone Enalapril Fetal Growth Retardation business.industry Angiotensin II Body Weight Age Factors Organ Size Articles Rats Endocrinology Castration Blood pressure chemistry Prenatal Exposure Delayed Effects Female business Orchiectomy medicine.drug |
| Zdroj: | American journal of physiology. Regulatory, integrative and comparative physiology. 298(5) |
| ISSN: | 1522-1490 |
| Popis: | Placental insufficiency results in intrauterine growth restriction (IUGR) and hypertension in adult male growth-restricted rats. Although renal ANG II and plasma renin activity do not differ between growth-restricted and control rats, blockade of the renin-angiotensin system (RAS) abolishes hypertension in growth-restricted rats, suggesting that the RAS contributes to IUGR-induced hypertension. Moreover, castration abolishes hypertension in growth-restricted rats, indicating an important role for testosterone. Therefore, we hypothesized that enhanced responsiveness to ANG II contributes to hypertension in this model of IUGR and that androgens may play a pivotal role in this enhanced response. Physiological parameters were determined at 16 wk of age in male rats pretreated with enalapril (40 mg·kg−1·day−1) for 1 wk. Baseline blood pressures were similar between growth-restricted (112 ± 3 mmHg) and control (110 ± 2 mmHg) rats; however, an enhanced pressor response to acute ANG II (100 ng·kg−1·min−1 for 30 min) was observed in growth-restricted (160 ± 2 mmHg) vs. control (136 ± 2 mmHg; P < 0.05) rats. Castration abolished the enhanced pressor response to acute ANG II in growth-restricted (130 ± 2 mmHg) rats with no significant effect on blood pressure in controls (130 ± 2 mmHg). Blood pressure was increased to a similar extent above baseline in response to acute phenylephrine (100 μg/min) in control (184 ± 5 mmHg) and growth-restricted (184 ± 8 mmHg) rats, suggesting the enhanced pressor response in growth-restricted rats is ANG II specific. Thus, these results suggest that growth-restricted rats exhibit an enhanced responsiveness to ANG II that is testosterone dependent and indicate that the RAS may serve as an underlying mechanism in mediating hypertension programmed in response to IUGR. |
| Databáze: | OpenAIRE |
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