Attenuated vascular reactivity in dogs with anteroventral third ventricle lesions.

Lesion of the anteroventral portion of the third cerebral ventricle causes hypernatremia, adipsia, and attenuation of the pressor response to intravenous administration of angiotensin II and norepinephrine. In addition, these lesions prevent the development of several experimental models of hypertension. In this study, a lesion of the third cerebral ventricle region was made in 14 dogs. In seven dogs in which hypernatremia developed the lesions included the organum vasculosum of the lamina terminalis; seven animals in which the circumventricular organ was spared by the lesion remained normonatremic. Vascular responsiveness of isolated right carotid artery rings to angiotensin II and phenylephrine was assessed 3 days after lesioning the anteroventral portion of the third cerebral ventricle. In endothelium-denuded ring vessels, vasoconstrictor responses to phenylephrine were significantly decreased in animals both with and without inclusion of the organum vasculosum of the lamina terminalis. A similar effect was observed in intact vessels of dogs in which the circumventricular organ was spared but not in those with lesions that included this area. In contrast, angiotensin II-induced vasoconstriction was significantly decreased in the arteries with intact endothelium of both groups of lesioned animals. These data show that lesion of the anteroventral third ventricle area alters alpha 1-adrenergic and angiotensin II vascular responsiveness in isolated carotid artery rings with the possible participation of the endothelium.

Neurovascular mechanisms and sodium balance in the pathogenesis of hypertension.

Physiological studies have clarified the role that the brain has in the interplay between salt balance and hypertension. Neural mechanisms and endocrine secretions play a pivotal role in the adaptation of mammals to changes in the intake and excretion of sodium. Maneuvers that alter the concentration of sodium in the plasma modify the sensitivity of baroreceptor reflexes and alter vascular reactivity. These changes may be mediated in part by the release of vasopressin. The research also suggests that the brain indirectly modulates the ability of the vascular endothelium to release vasoactive factors. Collectively, these studies illustrate the multiple effects of the sodium ion on the peripheral neural and central endocrine mechanisms that participate in the regulation of arterial pressure.

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)