Enhanced pressor response to carotid occlusion in commNTS-lesioned rats: possible efferent mechanisms

Bilateral common carotid occlusion (BCO) over a period of 60 s in conscious rats produces a biphasic presser response, consisting of an early (peak) a nd late (plateau) phase. In this study we investigated 1) the effects of le sions of the commissural nucleus of the solitary tract (commNTS) on the car diovascular responses produced by BCO in conscious rats and 2) the autonomi c and humoral mechanisms activated to produce the presser response to BCO i n sham- and commNTS-lesioned rats. Both the peak and plateau of the presser response produced by BCO increased in commNTS-lesioned rats despite the im pairment of chemoreflex responses induced by intravenous potassium cyanide. In sham rats sympathetic blockade with intravenous prazosin and metoprolol , but not vasopressin receptor blockade with the Manning compound, reduced both components of BCO. In commNTS-lesioned rats the sympathetic blockade o r vasopressin receptor blockade reduced both components of BCO. The results showed 1) the sympathetic nervous system, but not vasopressin, is importan t for the presser response to BCO during 60 s in conscious sham rats; 2) in commNTS-lesioned rats, despite chemoreflex impairment, BCO produces an inc reased presser response dependent on sympathetic activity associated with v asopressin release; and 3) the increment in the presser response to BCO in commNTS-lesioned rats seems to depend only on vasopressin secretion.