Abstract
The effects of estrogen on arterial function are heterogeneous with respect to vessel and/or species. We have investigated 17β-estradiol-induced relaxation in isolated rat aorta with regard to the role of the vascular endothelium and ionic mechanisms. Estrogen induced a concentration-dependent relaxation of 46.5 ± 7.9% and 70.1 ± 12.2% (10-8 and 10-7 M), which was reduced by endothelial denudation. Furthermore, L-nitroarginine methyl ester completely abrogated this effect; however, estradiol did not relax KCl-contracted rings. Tetraethyl ammonium (1 mmol/l) completely blocked estradiol-induced relaxation. Estradiol increased [cGMP] in isolated aortic rings via NO, but did not significantly affect NOS activity in endothelial cells. Thus, estrogen can relax rat aorta in vitro via both endothelium-dependent and -independent mechanisms involving the NO/cGMP and potassium channel signaling system. Copyright © 2003 S. Karger AG, Basel.
| Original language | American English |
|---|---|
| Journal | Pharmacology |
| Volume | 69 |
| State | Published - Jan 1 2003 |
Keywords
- Animals
- Aorta
- Cattle
- Endothelium
- Estrogen
- Muscle Contraction
- Muscle Relaxation
- NG-Nitroarginine Methyl Ester
- Nitric oxide
- Potassium Channels
- Potassium channel
- Rats
- Sprague-Dawley
- Time Factors
- Vascular
- animal experiment
- animal tissue
- artery endothelium
- article
- concentration response
- cyclic GMP
- drug effect
- drug mechanism
- endothelium cell
- enzyme activity
- estradiol
- in vitro study
- male
- n(g) nitro dextro arginine methyl ester
- nitric oxide synthase
- nonhuman
- potassium chloride
- priority journal
- rat
- signal transduction
- statistical significance
- tetrylammonium
- vasodilatation
Disciplines
- Pharmacology