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Am J Physiol Lung Cell Mol Physiol 280: L555-L564, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 3, L555-L564, March 2001

17beta -Estradiol increases nitric oxide-dependent dilation in rat pulmonary arteries and thoracic aorta

Rayna J. Gonzales, Benjimen R. Walker, and Nancy L. Kanagy

Vascular Physiology Group, Department of Cell Biology and Physiology, Health Sciences Center, University of New Mexico, Albuquerque, New Mexico 87131-5218

Past studies have demonstrated that 17beta -estradiol (E2beta ) increases endothelial nitric oxide (NO) synthase (eNOS) activity in uterine, heart, and skeletal muscle and in cultured human endothelial cells. However, little is known about E2beta regulation of NO synthesis in the pulmonary vasculature. The present study evaluated E2beta regulation of eNOS function in pulmonary arteries and thoracic aortas. We hypothesized that E2beta upregulates vascular NO release by increasing eNOS expression. To test this, NO-dependent vasodilation was assessed in isolated perfused lungs and aortic rings from ovariectomized Sprague-Dawley rats treated for 1 wk with 20 µg/24 h of E2beta or vehicle. Expression of eNOS was evaluated by Western blot and immunohistochemistry. Also, a RNase protection assay determined eNOS mRNA levels in lung and aortic homogenates from control and treated rats. Vasodilation to ionomycin in lungs from the E2beta -treated group was enhanced compared with that in control animals. Endothelium-intact aortic rings from E2beta -treated animals also demonstrated augmented endothelium-dependent dilation. Both responses were blocked with NOS inhibition. Immunostaining for eNOS was greater in pulmonary arteries and aortas from E2beta -treated compared with control rats. However, mRNA levels did not differ between groups. Thus we conclude that in vivo E2beta treatment augments endothelium-dependent dilation in aorta and lung, increasing expression of eNOS independently of sustained augmented gene transcription.

endothelium-dependent vasodilation; isolated rat lungs; endothelial nitric oxide synthase


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