Hypertension, Vol 6, 249-254, Copyright © 1984 by American Heart Association
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)
ARTICLES
Alterations in vascular sensitivity to vasoactive agents after discontinuation of propranolol in SHR
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