These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Captopril therapy decreases both expression and function of alpha-adrenoceptors in pre- hypertensive rat aorta.
    Author: Godínez-Hernández D, Gallardo-Ortíz IA, López-Sánchez P, Villalobos-Molina R.
    Journal: Auton Autacoid Pharmacol; 2006 Jan; 26(1):21-9. PubMed ID: 16371063.
    Abstract:
    1.-- The effects of captopril on alpha(1)-adrenoceptor mRNA and protein and phenylephrine-induced contraction was assessed in aorta of pre-hypertensive spontaneously hypertensive rats. 2.-- Four-week-old SHR and WKY rats were treated with captopril [an angiotensin-converting enzyme (ACE) inhibitor] 3 mg kg(-1) day(-1) for 1 week. 3.-- pA(2) values for BMY 7378, an alpha(1D)-adrenoceptor antagonist, were 8.63-9.20 among the different groups. Schild slopes were close to unity suggesting that contraction was produced primarily by alpha(1D)-adrenoceptor stimulation and was not changed with therapy. 4.-- Alpha(1D)-adrenoceptor mRNA and protein values were higher in pre-hypertensive SHR than in WKY, whereas alpha(1A)-adrenoceptor mRNA was higher in WKY and alpha(1B)-adrenoceptors were similar in both strains, and protein was not significantly different for alpha(1A)- and alpha(1B)-subtypes. 5.-- Captopril decreased maximal contraction in SHR, without having effect in WKY rats, while alpha(1D)-adrenoceptor mRNA was decreased in both rat strains but alpha(1D)-adrenoceptor protein was significantly decreased only in SHR, and increased alpha(1A)-mRNA in SHR, no effect of captopril treatment was observed on alpha(1B)-adrenoceptor mRNA and protein nor on alpha(1A)-adrenoceptor protein. 6.-- These data suggest that ACE inhibition by captopril influences both expression and function of alpha(1D)-adrenoceptors in aorta of pre-hypertensive rats, probably avoiding alpha(1D)-subtype expression by blockade of angiotensin II synthesis.
    [Abstract] [Full Text] [Related] [New Search]