title: Recovery of high blood pressure after chronic lesions of the commissural NTS in SHR.
abstract: Acute electrolytic lesions of the commissural nucleus of the solitary tract (commNTS) reduce blood pressure (BP) in SHR but not in normotensive Wistar-Kyoto and Wistar rats and abolish the pressor response to intravenous injection of potassium cyanide. We investigated the chronic effect of commNTS lesions on mean arterial pressure (MAP), and on baroreceptor and chemoreceptor reflex responses in SHR. The contribution of the sympathetic nervous system and the hormones vasopressin and angiotensin II to maintenance of BP in lesioned SHR was also investigated. MAP fell to normotensive levels the day after lesioning the commNTS but returned to the hypertensive level 9 days later. The reflex tachycardia evoked by sodium nitroprusside remained attenuated for 10 days after commNTS lesions but became enhanced 30 days after commNTS lesions. The pressor component of the chemoreflex elicited by potassium cyanide remained blocked for 30 days after lesions. Vasopressin antagonist or ACE blocker did not change MAP in sham or commNTS-lesioned SHR. Ganglionic blockade with hexamethonium elicited similar reductions in MAP in sham and commNTS-lesioned SHR. Results demonstrated that commNTS lesions in SHR produce a transient fall in BP and a long-lasting inhibition of the pressor response of the chemoreflex. Therefore, the blockade of the pressor response to peripheral chemoreflex activation is not sufficient to chronically reduce MAP in SHR. In the chronic absence of the commNTS, other subnuclei of the NTS or other brain stem nuclei may reorganize to replace the function of commNTS neurons, restoring sympathetic activity and high BP in SHR.
authors.affiliation: Department of Physiology, Universidade Federal de Sao Paulo, Escola Paulista de Medicina, Sao Paulo, SP, Brazil.
authors.forename: Monica Akemi
authors.initials: MA
authors.lastname: Sato
authors.forename: Gerhardus Hermanus Maria
authors.initials: GH
authors.lastname: Schoorlemmer
authors.forename: José Vanderlei
authors.initials: JV
authors.lastname: Menani
authors.forename: Oswaldo Ubríaco
authors.initials: OU
authors.lastname: Lopes
authors.forename: Eduardo
authors.initials: E
authors.lastname: Colombari
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D065092:Antidiuretic Hormone Receptor Antagonists; D001127:Arginine Vasopressin / Q000031:analogs & derivatives* / Q000494:pharmacology; D017704:Baroreflex; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology; D002628:Chemoreceptor Cells / Q000378:metabolism; D004558:Electric Stimulation; D005730:Ganglionic Blockers / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D018738:Hexamethonium / Q000494:pharmacology; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D007700:Kinetics; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR; D017552:Solitary Nucleus / Q000473:pathology / Q000503:physiopathology*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D065092:Antidiuretic Hormone Receptor Antagonists; D005730:Ganglionic Blockers; D001127:Arginine Vasopressin; D018738:Hexamethonium; C025043:vasopressin, 1-(1-mercaptocyclohexaneacetic acid)-2-(O- methyl-L-tyrosine)-8-L-arginine-; D002216:Captopril