The involvement of prostaglandins in the contractile function of the aorta by aldosterone.
| Autor: | Eatman D; Department of Pharmacology/Toxicology, Morehouse School of Medicine, Atlanta, Georgia, USA. deatman@msm.edu., Peagler K, Watson J, Rollins-Hairston A, Bayorh MA |
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| Jazyk: | angličtina |
| Zdroj: | BMC research notes [BMC Res Notes] 2011 Apr 14; Vol. 4, pp. 125. Date of Electronic Publication: 2011 Apr 14. |
| DOI: | 10.1186/1756-0500-4-125 |
| Abstrakt: | Background: Aldosterone, one of the major culprits associated with the renin-angiotensin-aldosterone system (RAAS), is significantly elevated following high salt administration in Dahl rats. Since we have previously demonstrated that aldosterone (ALDO) upregulates cyclooxygenase (COX) expression in the kidney, the present study was design to assess whether prostaglandin release is involved in the effects of chronic aldosterone treatment on vascular function of the aorta from nonhypertensive Dahl salt-sensitive rats. Findings: The effects of aldosterone on arachidonic acid metabolism and on the expression of cyclooxygenase (COX)-2 were evaluated in the Dahl salt sensitive (DS) rat aorta, renal, femoral and carotid arteries. DS rats on a low salt (0.3% NaCl) diet were treated with or without ALDO for four weeks. Indirect blood pressure (BP), the release of prostacyclin (PGI2) and prostaglandin E2, and the expression of COX-2 were measured to assess the vascular remodelling by aldosterone. Vascular function was also assessed by contractile responsiveness in the aorta to phenylephrine. ALDO increased BP (17 ± 1%) and inhibited the basal release of PGE2. ALDO enhanced vascular reactivity to phenylephrine and up regulated the expression of COX-2 in both aorta and renal vessels but reduced COX-2 expression in the femoral artery. Conclusions: These data reveal that the effect of ALDO in the vasculature is tissue specific and may involve the inhibition of PGE2 release. Thus, suggesting a role for prostaglandins in the vasculopathic aspects of aldosterone. |
| Databáze: | MEDLINE |
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