Acute hypertension after the local injection of kainic acid into the nucleus tractus solitarii of rats.
- 1 February 1981
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 48 (2) , 292-298
- https://doi.org/10.1161/01.res.48.2.292
Abstract
Kainic acid (KA), an analogue of L-glutamate, was microinjected in 0.1 microliter of saline into the nucleus tractus solitarii (NTS) of adult rats. In rats anesthetized with halothane or alpha-chloralose, KA injected unilaterally elicited hypotension, bradycardia, and apnea. The threshold dose was 0.1-0.2 ng (10(-13) mol). Doses greater than 0.2 ng blocked responses to subsequent injections for at least 30 minutes. Doses of KA greater than 15 ng reduced the reflex bradycardia elicited by raising the arterial pressure with phenylephrine and produced arterial hypertension in rats anesthetized with alpha-chloralose or in other rats within 15 minutes of terminating halothane anesthesia. Bilateral injection of KA in doses greater than 15 ng completely blocked baroreflexes and resulted in a dose-dependent elevation of arterial pressure (167 +/- 9.4; P less than 0.001) both in alpha-chloralose-anesthetized rats and in awake rats after the termination of halothane anesthesia. The hypertension rapidly led to pulmonary edema and death. Procaine microinjected also elicited fulminating hypertension; vehicle did not. Doses of KA producing hypertension caused no histological or biochemical evidence of neuronal death. The cardiovascular responses to KA were restricted to sites in the intermediate one-third of NTS and could not be elicited by injection into adjacent sites in brainstem. The results indicate that, in low doses, KA injected into NTS stimulates neurons which mediate the baroreflex, whereas, in higher doses, it produces baroreflex blockade and neurogenic hypertension. The results suggest that fulminating hypertension can be produced by nondestructive perturbations of neurochemical transmission in brain. Since the cardiovascular responses of KA are similar to those produced by microinjection into NTS of the amino acid neurotransmitter glutamic acid, the study adds further support to the hypothesis that L-glutamate is the neurotransmitter released by baroreceptor afferent nerves.This publication has 27 references indexed in Scilit:
- Evidence for L-glutamate as the Neurotransmitter of Baroreceptor Afferent Nerve FibersScience, 1980
- Immunochemical demonstration of increased choline acetyltransferase concentration in rat preoptic area after estradiol administrationBrain Research, 1980
- Regional distribution of [3H] kainic acid after intraventricular injectionLife Sciences, 1980
- Production of sustained hypertension by lesions in the nucleus tractus solitarii of the American foxhound.Hypertension, 1979
- Long-term sequelae of striatal kainate lesionBrain Research, 1978
- Intraventricular kainic acid preferentially destroys hippocampal pyramidal cellsNature, 1978
- Striatal lesions with kainic acid: neurochemical characteristicsBrain Research, 1977
- Hypertension after localized transection of brainstem fibresLife Sciences, 1976
- Actions of several anthelmintics and insecticides on rat cortical neuronesBrain Research, 1970
- A SIMPLIFIED RADIOCHEMICAL ASSAY FOR CHOLINE ACETYLTRANSFERASEJournal of Neurochemistry, 1967