Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 1984;6:249-254

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kubota, T.
Right arrow Articles by Yamada, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kubota, T.
Right arrow Articles by Yamada, T.

Hypertension, Vol 6, 249-254, Copyright © 1984 by American Heart Association


ARTICLES

Alterations in vascular sensitivity to vasoactive agents after discontinuation of propranolol in SHR

T Kubota and T Yamada

Spontaneously hypertensive rats (SHR) were treated with propranolol (P) (70 mg/kg) daily for 2 or 4 weeks and then the effects of vasoactive substances on blood pressure were studied 10 or 36 hours after the last dose of P. At 10 hours after the last dose of P, vascular hyperresponsiveness to norepinephrine (NE) and angiotensin II (AII) had largely disappeared, but the hypotensive action of isoproterenol and prostacyclin was still blocked in P-treated SHR. An increase of cyclic AMP (cAMP) in response to isoproterenol was blocked in the thoracic aorta. Similarly, an increase of circulating cAMP and blood glucose in response to epinephrine (E) was depressed. At 36 hours after the last dose of P, an elevation of blood pressure in response to NE and AII was significantly reduced in P-treated SHR. Although basal blood pressure with or without anesthesia was the same in P-treated SHR and control SHR, a decrease of blood pressure in response to isoproterenol and prostacyclin was augmented significantly in P-treated SHR. This was also true in normal rats similarly treated. In addition, an increase of cAMP in the thoracic aorta in response to isoproterenol and prostacyclin was augmented significantly in P-treated SHR. An increase in blood glucose in response to E was not blocked, but an increase of circulating cAMP in response to E was blocked. These data suggest that cAMP synthesis in the vessels is somehow related to the production of peculiar vascular responses during escape from P action.(ABSTRACT TRUNCATED AT 250 WORDS)