Central pressor action of neurotensin in conscious rats.

Publisher Website
Google Scholar
Abstract
The effects of neurotensin upon blood pressure in conscious rats were examined after intracerebroventricular (i.v.t.) or intravenous (i.v.) administration of this peptide. Whereas i.v. injected neurotensin (0.1-2.0 microgram/kg) was depressor, i.v.t. injected neurotensin (1 microgram and above) was pressor. Peripheral depressor responses could not be repeated in the same animal due to tachyphylaxis, but central pressor responses were repeatable without reduction in magnitude, showing that the two effects were separate entities. Thyrotropin-releasing hormone (TRH), which is reported to be a potent neurotensin antagonist, completely abolished the neurotensin depressor response, and attenuated the central pressor action. TRH did not alter the central pressor effect of another peptide, angiotensin II (AII). The potent AII receptor antagonist saralasin, while abolishing the central pressor effect of AII, was completely without effect upon the neurotensin-induced pressor response. These results indicate that i.v.t. injected neurotensin and AII stimulate a rise in blood pressure via different receptors. The alpha-adrenergic antagonists phentolamine, prazosin, or yohimbine (injected i.v.t.) involvement of the sympathetic nervous system in this response. These results are discussed in relation to the central pressor actions of other neuropeptides.