Binding of 125I-[Sar1,Ile8] angiotensin II (AII) to sections of brains from both wild and laboratory rabbits was determined by in vitro autoradiography. In the forebrain, specific high density binding was observed in the olfactory bulb, organum vasculosum of the lamina terminalis (OVLT), subfornical organ, median eminence, lateral septum, median preoptic nucleus and hypothalamic paraventricular, supraoptic and arcuate nuclei. In the midbrain, binding of the radioligand was observed in the interpeduncular and parabrachial nuclei, in the locus coeruleus, and ventrolateral pons. In the hind brain, there was dense binding of 125I-[Sar1,Ile8] AII to the nucleus of the solitary tract (NTS) and to both rostral and caudal parts of the reticular formation of the ventrolateral medulla oblongata. Weaker specific binding of the radioligand to the molecular layer of the cerebellum, to the nucleus of the spinal trigeminal tract, dorsal motor nucleus of the vagus, area postema, and to a band of tissue connecting the NTS to the ventrolateral medulla was also observed. Binding of the ligand to circumventricular organs such as the OVLT, subfornical organ, and median eminence suggests that these are sites in the brain of the rabbit at which blood-borne AII may exert influences on the central regulation of fluid balance and pituitary hormone secretion, although AII of neuronal origin could also act at these sites. Binding of the radioligand in several other brain regions suggests that angiotensin II of cerebral origin may be involved in a number of different aspects of brain function in the rabbit. The finding of dense binding in the NTS and ventrolateral medulla, which are involved in autonomic activity and are also sites of catecholamine-containing neurons, raises the possibility of angiotensin interaction with these neurons and involvement in autonomic function.
The role of sodium concentration of the cerebrospinal fluid (CSF[Na]) in the initiation and/or satiation of Na appetite of Na-deplete or Na-replete sheep was investigated. Slow infusion (1 ml/h) into a lateral brain ventricle of an artificial sheep CSF solution was begun 0-60 min prior to and continued until the end of the Na access period (30-120 min). In Na-deficient sheep, increasing CSF[Na] caused a decrease in Na intake. In both Na-deficient and Na-replete sheep, decreasing CSF[Na] caused an increase in Na intake. The appetite was observed within 25 min of beginning infusion, which represents the most rapid induction of Na appetite yet observed. In Na-replete sheep, the appetite induced by decreasing CSF[Na] was predominantly for Na-containing solutions. A decrease in CSF[Na] of only 4-6 mmol/l was sufficient to induce Na appetite. The results derived by use of different Na, saccharide, or urea containing artificial CSF solutions suggest that there are sensors within the neuropil that respond to change of [Na] and influence salt appetite. They can be accessed by inducing change in [Na] of cerebroventricular CSF.
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