Clonidine has been postulated to produce cardiovascular effects, the most noticeable of which are hypotension and bradycardia, by interaction with the nucleus tractus solitarii (NTS), a cranial nucleus in the dorsal medulla. The experiments reported herein, examined the effects of clonidine (30 μg/kg, i.v.) prior to and following bilateral electrolytic lesioning of the NTS. The studies were performed in conscious, spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY). Clonidine produced marked hypotension and bradycardia in conscious, NTS-intact SHR. Intact WKY exhibited a biphasic response to clonidine with an initial hypertension preceeding a moderate decrease in blood pressure. Heart rate responded similarly to the SHR. Lesioning of the NTS, in both SHR and WKY, induced hypertension. Virtual abolition of the hypotension and bradycardia to clonidine was noted in lesioned SHR upon subsequent administration of clonidine. Nucleus tractus solitarii lesioning in WKY did not significantly alter clonidine-induced hypotension; however, the initial hypertensive phase was abolished following lesioning and bradycardia was blunted. These results indicate that the NTS plays an important role in the mediation of both the hypotension and bradycardia seen with clonidine in SHR. The differing responses of SHR and WKY to clonidine after NTS lesions may also indicate altered functional roles for the NTS in these two strains.
- SHR medullary lesions
- central vasomotor control
- nucleus tractus solitarii
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience