Alternative mechanism for attenuated pressor responses in AV3V-lesioned dogs

We lesioned the periventricular tissue of the anteroventral portion of the third cerebral ventricle (AV3V) of dogs to evaluate the mechanism that accounts for blunting of the pressor activity of angiotensin II (ANG II). AV3V lesions were done with a microknife using a transbuccal approach; the procedure denervated the organum vasculosum of the laminae terminalis, the nucleus medianus, and the medial preoptic nucleus. Two to four days after surgery, the conscious AV3V-lesioned dogs showed adipsia and their blood contained increased quantities of Na+ (175 +/- 2 meq/l) and an elevated osmolality (352 +/- 5 mosmol/kg). Cardiac rate was faster (131 +/- 8 beats/min) in AV3V-lesioned dogs, but their mean arterial pressure (MAP) was within normal values (99 +/- 4 mmHg). These changes were accompanied by an almost 18-fold increase in the plasma levels of immunoreactive ANG II (irANG II). In contrast, plasma vasopressin (AVP) levels fell to nondetectable values. Pressor responses produced by intravenous infusions of ANG II or injections of norepinephrine (NE) were significantly blunted 3 days after AV3V ablation. Short-term treatment of eight AV3V-lesioned dogs with the synthetic AVP analogue, 1-desamino-8-D-arginine vasopressin, reduced plasma Na+ and irANG II levels. The pressor activity of peripheral infusions of ANG II was restored to prelesion values, whereas pressor responsiveness to NE remained depressed. These data suggest that the blunting of the pressor action of ANG II in AV3V-lesioned dogs is an expression of a disorder in the regulation of renal and behavioral mechanisms maintaining fluid balance and AVP secretion.(ABSTRACT TRUNCATED AT 250 WORDS)