|
|
||||||||
Journal of Applied Physiology, Vol 48, Issue 3 473-478, Copyright © 1980 by American Physiological Society
ARTICLES |
N. F. Voelkel, I. F. McMurtry and J. T. Reeves
Chronic beta-receptor blockade has been reported to inhibit right ventricular hypertrophy in rats at high altitude. If so, we wanted to determine whether beta-receptor blockade or some other drug action were involved and whether the heart, the lung vessels, or blood alterations were affected. In rats, chronic treatment with DL-propranolol (2 mg/kg ip once daily) reduced right ventricular hypertrophy and polycythemia of chronic high altitude. D-Propranolol and metoprolol did not reduce hypoxia-induced right ventricular hypertrophy or polycythemia. In isolated lungs from low-altitude rats treated chronically with DL-propranolol or with D-propranolol the pressor response to acute hypoxia was blunted. Chronic DL-propranolol blunted the acute hypoxic pressor response and angiotensin II induced vasoconstriction in lungs from high-altitude rats. Two effects of DL-propranolol treatment were seen: 1) blockade of beta 2-adrenergic receptors, which reduced the right ventricular hypertrophy of high altitude through reduction of hematocrit; and 2) a non-beta-effect, which reduced vascular responsiveness to acute hypoxia in the isolated lung preparation.
This article has been cited by other articles:
![]() |
Y. Hoshikawa, S. Ono, S. Suzuki, T. Tanita, M. Chida, C. Song, M. Noda, T. Tabata, N. F. Voelkel, and S. Fujimura Generation of oxidative stress contributes to the development of pulmonary hypertension induced by hypoxia J Appl Physiol, April 1, 2001; 90(4): 1299 - 1306. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |