Angiopeptin is an analog of somatostatin-14, which has been found to inhibit cellular proliferation in several models of systemic vascular injury. As proliferation plays a major role in pulmonary hypertension, we examined the hypothesis that angiopeptin would inhibit the development of chronic hypoxic pulmonary hypertension in the rat. Angiopeptin was infused intravenously (90-100 μg/kg/day) by minipumps in 10 rats during a 3-week exposure to hypobaric hypoxia and in six normoxic rata. Normal saline was infused in six hypoxic control rats and in seven normoxic control rats. Angiopeptin produced no significant difference in mean pulmonary arterial pressure and resistance, right ventricular weight, or medial thickness of small pulmonary vessels. Vasoconstrictor responses of isolated lungs to acute hypoxia were not affected by angiopeptin. We conclude that angiopeptin, at the high intravenous dose used, does not significantly reduce the development of chronic hypoxic pulmonary hypertension in rats.
|Original language||English (US)|
|Number of pages||7|
|Journal||Proceedings of the Society for Experimental Biology and Medicine|
|State||Published - Oct 1996|
Bibliographical noteFunding Information:
To whom requests for reprints should be addressed at VA Medical Center, 1 Veterans Drive, Minneapolis, MN 55417. E. K. W. and S. L. A. are supported by VA Merit Review funding and by the Minnesota Medical Foundation. S. L. A. is also supported by National Institutes of Health Grant HL 45733. V. H. was supported by a Grant-in-Aid from the American Heart Association—Minnesota Affiliate.