Hypertension, Vol 2, 198-206, Copyright © 1980 by American Heart Association
H Takahashi and RD Bunag
Central alpha-adrenergic mechanisms for cardiovascular regulation were
studied by injecting phenylephrine into a recipient rat whose head was
isolated from its body by cross perfusion with a donor rat. Blood pressure
increases produced in the donor were accompanied by concurrent reduction of
blood pressure and sympathetic nerve activity in the recipient rat's body.
These effects were abolished when alpha- adrenergic receptors in the
perfused head were blocked with phentolamine. By contrast, intracarotid
injections of angiotensin increased blood pressure not only in donor but
also in recipient rats. The magnitude of phenylephrine-induced
vasodepression was significantly greater in spontaneously hypertensive rats
(SHR) than in normotensive or DOCA-salt hypertensive ones. Distribution of
radioactive microspheres indicated that carotid arterial blood went mainly
to the cerebrum, midbrain, and hypothalamus, with almost negligible amounts
going to the lower brainstem. Collectively, our results suggest that
centrally administered phenylephrine reduces sympathetic vasomotor tone and
blood pressure by acting on alpha-adrenergic receptors located in
supramedullary brain areas (possibly in the hypothalamus). In SHR,
augmented, vasodepressor responsiveness may be due to reduced brain levels
of endogenous norepinephrine that could increase the alpha- adrenergic
receptors available.
ARTICLES
Augmentation of centrally induced alpha-adrenergic vasodepression in spontaneously hypertensive rats
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