Prostaglandin F(2alpha) infused into the vertebral artery of the anaesthetized greyhound in doses which had no effect when given intravenously ((8-64 ng/kg)/min) caused an increase in blood pressure and heart rate.2. This response was not significantly altered by beta-adrenoceptor blockade with propranolol (10 mg i.v.) or by cervical cord section at C(4-6).3. The tachycardia was abolished and the pressor response greatly reduced by vagotomy or atropine (250 mug/kg i.v.).4. The pressor response which remained after vagotomy was abolished by subsequent sympathetic blockade with bethanidine (2-3 mg/kg i.v.) or bretylium (10 mg/kg i.v.).5. In contrast to the effects of propranolol or cervical cord section bethanidine (4-5 mg/kg i.v.) or bretylium (10 mg/kg i.v.) significantly reduced blood pressure and heart rate responses to intravertebral prostaglandin F(2alpha). This result suggests that bethanidine and bretylium have some central actions.6. It is concluded that the cardiovascular effects of intravertebral infusions of prostaglandin F(2alpha) are mediated by the autonomic nervous system and that the preferential pathway is withdrawal of vagal tone to the heart.
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LAVERY et al. (1971) studied this question.
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