Amygdaloid kindled seizures in the rat induce an abrupt elevation of blood
pressure accompanied by a significant decrease in heart rate. The autonomic
pharmacology of this response was examined in unanesthetized kindled rats.
Muscarinic receptor blockade with atropine (1 mg/kg, intravenous (i.v.)) a
bolished the seizure-induced bradycardia. The seizure-induced hypertension
was unaffected by beta-adrenergic blockade with timolol (1 mg/kg, i.v.), bu
t was reduced by phentolamine (5 mg/kg, subcutaneous (s.c.)), an alpha-adre
nergic receptor antagonist. A chemical sympathectomy was induced with 6-hyd
roxydopamine (100 mg/kg, i.v.), an agent that does not cross the blood-brai
n barrier. This eliminated the presser response but did not completely bloc
k the seizure-induced bradycardia. The effectiveness of 6-hydroxydopamine w
as tested with tyramine (0.5 mg/kg, i.v.) an agent that releases endogenous
catecholamines. These results indicate amygdaloid kindled seizures activat
e both branches of the autonomic nervous system. The bradycardia was mediat
ed by the parasympathetic system; the presser response was caused by an inc
rease in peripheral resistance due to alpha-adrenergic receptor activation.
More important, these findings show that kindling is a useful seizure mode
l for future studies on the effect of seizures on cardiovascular function a
nd possible mechanisms of seizure-related sudden unexplained death. (C) 199
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