G. D. Fink

Role of central catecholamines in the control of blood pressure and drinking behavior.

The role of central nervous system (CNS) catecholamines in the development of hypertension and the control of drinking behavior was assessed in rats by depleting these amines with 6-hydroxydopamine (6-OHDA). Intraventricular administration of 6-OHDA completely prevented the development of one-kidney renal hypertension and abolished the associated increase in water consumption. 6-OHDA-treated rats showed deficits in drinking behavior when challenged with subcutaneous injections of angiotensin II (AII) and hypertonic sodium chloride. The acute pressor responses produced by intraventricular injections of AII and carbachol were virtually abolished by central catecholamine depletion. However, drinking produced by central cholinergic stimulation remained intact while AII drinking was significantly reduced. These data demonstrate that the integrity of CNS catecholamines is required for the development of one-kidney renal hypertension and the increased drinking which accompanies it. In addition, destruction of central catecholamine-containing neurons allows for a specific dissociation of the pressor and drinking responses produced by central cholinergic but not AII stimulation.

Interruption of the maintenance phase of established hypertension by ablation of the anteroventral third ventricle (AV3v) in rats

Ablation of tissue surrounding anteroventral third ventricle (AV3V) was studied in three models of hypertensive rats. Lesions were placed in the AV3V at one and six weeks following the initiation of one kidney Grollman renal hypertension. At one week the rise in blood pressure was arrested and water intake was reduced; at six weeks arterial pressure returned to prehypertensive levels in animals surviving the post-lesion hydrational crisis. In two kidney (one clip) Goldblatt animals lesioned two weeks post-clip, arterial pressure was significantly reduced but did not become fully normotensive. Finally, the AV3V was also lesioned in spontaneously hypertensive rats (SHR-Okamoto strain) with established hypertension. The lesion did not reduce arterial pressure in adult SHR although characteristic initial adipsia and weight loss occurred. Ablation of the AV3V thus altered the course of maintenance of renal hypertension; however, the arterial pressure of SHR was not affected.

Prevention of renal hypertension and of the central pressor effect of angiotensin by ventromedial hypothalamic ablation

Various lines of research have implicated the central nervous system in the development of renal hypertension. The ablation of a periventricular region surrounding the anteroventral third ventricle (AV3V) has been shown to block the development of renal hypertension. Because of hemodynamic effects produced by AV3V electrical stimulation can be abolished by a midline lesion of the ventromedial hypothalamic--median eminence region (VMH-ME), the effect of VMH-ME ablation on the development of renal hypertension was studied. Following recovery from surgery that destroyed the VMH-ME region the lesioned rats and controls were subjected to unilateral nephrectomy and figure-of-eight wrapping of the remaining kidney. Control animals developed renal hypertension but those with VMH-ME lesions did not. When the pressor response produced by intracerebroventricular injections of angiotensin II was studied, it was found that rats with VMH-ME lesions, as compared to neurologically intact animals, showed significantly attenuated responses. The data suggest that a neural system related to cardiovascular control descends through the VMH-ME region and that the integrity of this pathway is necessary for the development of renal hypertension.

Alterations in cerebrospinal fluid sodium and osmolality in rats during one-kidney, one-wrap renal hypertension

1. Measurements of plasma and cerebrospinal fluid (CSF) sodium and osmolality were made throughout the course of one‐kidney, one‐wrap Grollman renal hypertension.