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Department of Physiology, University of Tennessee, Memphis, Tennessee 38163
These studies examined the effects of
1- and
2-adrenoreceptor blockade in the anteroventral portion
of the third cerebral ventricle (AV3V) on modification of
baroreflex-induced changes in heart rate and renal sympathetic nerve
activity (RSNA) induced by hyperosmolality. Local administration of
hypertonic artificial cerebrospinal fluid (aCSF) in the AV3V
significantly increased baroreflex-induced bradycardia during
intravenous phenylephrine but did not alter changes in RSNA during the
pressor response or alter tachycardia and neural responses evoked by
decreased blood pressure. The enhanced cardiac response was not
observed during simultaneous administration of phentolamine
(
1- and
2-antagonist) or yohimbine
(selective
2-antagonist) in the AV3V region. However, treatment with prazosin (
1-antagonist) did not alter the
exaggerated cardiac response evoked by hypertonic aCSF to increased
blood pressure. These data demonstrate that acute, local hypertonic stimulation in the AV3V region selectively enhances baroreflex-induced bradycardia by stimulation of
2-adrenergic receptors
during acute pressor responses.
norepinephrine; anteroventral third ventricle; sympathetic nerve activity; bradycardia; baroreceptor
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