Cardiovascular effects of intracerebral injections of glutamate and kainate in rats

The intracerebral (lateral ventricle, 3rd ventricle, posterior hypothalamus and corpus striatum) administrations of sodium glutamate (G) 0.1-10 mg/rat and kainic acid (K) 0.1-10 Ug/rat induced transitory and dose-dependent increases of arterial BP and bradycardia. These effects were abolished by icv L-glutamic acid diethyl ester hydrochloride l-10 Ug/rat. G-and K-hypertensions were reduced by catecholamine depletion, peripheral adrenergic blocks, central a2-adrenergic stimulation, Ca2+ transmembrane block, ganglionic block, adrenalectomy, and spinal transection. Bilateral vagotomy and carotid sinus denervation augmented the hypertension. The bradycardia seemed to be reflexly mediated via carotid sinus and aortic pressoreceptors.