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Central sympathoinhibition by protoveratrine may mediate hypotension; leaves open translation to human reflex mechanisms.
Splanchnic outflow was studied along with carotid and aortic presso- and chemoreceptor inflow in cats under a variety of conditions. Splanchnic activity was increased by a decrease in presso- or increase in chemoreceptor activity and vice-versa. Blood pressure rose following splanchnic activation. Protoveratrine and serotonin, reported to activate the "coronary chemoreflex," depressed completely splanchnic outflow, without enhancing pressoreceptor activity. Prolonged hypotension from protoveratrine coincided with partial return of splanchnic activity and tonic discharge of pressoreceptors. ATP increased splanchnic activity simultaneously with the hypotension and it is suggested that it be excluded from the list of drugs eliciting the "coronary chemoreflex."
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A. S. Dontas (1955) studied this question.
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