Why the study?
Does captopril treatment prevent pregnancy-induced changes in α1-adrenergic receptor vascular expression in female Wistar rats?
Does captopril treatment prevent pregnancy-induced changes in α1-adrenergic receptor vascular expression in female Wistar rats?
In a rat model, angiotensin II levels during pregnancy appear to mediate a decrease in aortic α1-adrenergic receptor expression, which is prevented by captopril.
Answers are grounded in this paper and cite their sources.
Captopril may preserve α1-AR expression in pregnant rats; leaves open human vascular relevance and clinical translation.
Vessels from pregnant animals show a blunted response to adrenergic agonists. In this work, we explored if pregnancy reduces α₁-adrenergic receptor (α₁-AR)-mediated vascular smooth muscle protein expression as well as agonist-induced contraction in rat aorta, and if angiotensin II (Ang II) levels during pregnancy are related to these changes. Female Wistar rats were divided randomly into nonpregnant (NP) and pregnant groups (first week: P1, second week: P2, third week: P3). Subsets of animals were treated with captopril (5 mg kg–¹ day–¹ for 7 days; n = 6). Phenylephrine (PHE) concentration-response curves were constructed (1 × 10–⁹ to 3.1 × 10–⁵ mol/l) and α1A-, α1B- and α1D-AR were measured in the aorta by immunoblot. Captopril decreased α-AR expression in the NP group. In contrast, pregnancy decreased α1A-, α1B- and α1D-AR levels and captopril prevented this reduction. PHE sensitivity was decreased in the thoracic and abdominal aorta in the P2 group, with no changes in Emax, and Emax was decreased in the abdominal aorta in all experimental groups. Our results suggest that Ang II levels during pregnancy are related to a decrease in aortic α₁-AR expression. The physiological meaning of this finding remains to be established.
No takes yet. Share an insight, caveat, or question.
López‐Sánchez et al. (2009) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: