Contribution of vasopressin to hypertension after solitary tract lesioning in the dog.
The relative contributions of vasopressin and sympathetic outflow to the acute hypertension that followed central baroreceptor deafferentation at the level of the rostral solitary tract (TS) were examined. In nine dogs (TS lesion group) baroreflex control of heart rate was abolished, confirmed histologically with bilateral interruption of the solitary tracts. Baroreflex tests were positive and one solitary tract was spared in three dogs (incomplete lesion group). Blood pressure rose rapidly after discontinuation of anaesthesia in the animals of the TS lesion group. Administration of an antagonist of the vascular effects of vasopressin 2 1/2 h after lesioning produced a significant decrease in mean arterial pressure and tachycardia in the TS lesion animals, but did not alter blood pressure in the incomplete lesion group. Subsequent ganglionic blockade with hexamethonium produced comparable falls in mean arterial pressure in both groups of dogs. We conclude that vasopressin contributes significantly to the elevated blood pressure only in animals with complete interruption of the baroreceptor afferents in the rostral TS.
D000208:Acute Disease; D000818:Animals; D001127:Arginine Vasopressin / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D018738:Hexamethonium; D006584:Hexamethonium Compounds / Q000494:pharmacology; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D008526:Medulla Oblongata / Q000502:physiology*; D011311:Pressoreceptors / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000503:physiopathology; D013997:Time Factors
D006584:Hexamethonium Compounds; D001127:Arginine Vasopressin; D018738:Hexamethonium