The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.
Angiotensin II-induced hypertension increases heme oxygenase-1 expression in rat aorta.
BACKGROUND: We investigated the in vivo effects of angiotensin ( Ang) II- induced hypertension on heme oxygenase (HO) mRNA and protein expression, activity, and localization in rat aortas. METHODS AND RESULTS: Infusion of Ang II (0.7 mg x kg(-1) x d(-1)) increased HO-1 mRNA levels to 169+/-31%, 251+/-47%, 339+/-26%, and 370+/-74% of the control level at 1, 3, 5, and 7 days after operation, respectively. The HO-1 protein level at 7 days was markedly upregulated, as was HO activity. Treatment with either losartan (25 mg x kg(-1) x d(-1)) or hydralazine (15 mg x kg(-1) x d(-1)), both of which prevented the Ang II-induced hypertension, blocked HO-1 mRNA upregulation. Norepinephrine infusion (2.8 mg x kg(-1) x d(-1)) produced a degree of hypertension and degree of HO-1 mRNA upregulation similar to those of Ang II infusion, which was again blocked by treatment with hydralazine (382+/-18% and 150+/-30% of the control level, respectively). Immunohistochemical analysis demonstrated that HO-1 is expressed in medial smooth muscle and adventitial cells in normotensive rat aortas, and this is markedly increased in adventitial and endothelial cells in Ang II-induced hypertensive rat aortas. In contrast, HO-2 protein expression was not changed in hypertensive rat aortas. CONCLUSIONS: These findings indicate that HO-1 is upregulated in hypertensive rat aortas, apparently by mechanisms unique to Ang II and by hemodynamic stress.[1]References
- Angiotensin II-induced hypertension increases heme oxygenase-1 expression in rat aorta. Ishizaka, N., de León, H., Laursen, J.B., Fukui, T., Wilcox, J.N., De Keulenaer, G., Griendling, K.K., Alexander, R.W. Circulation (1997) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Use
