Polyuria and imparied ADH release following medial preoptic lesioning in the rat

Abstract

Studies were carried out in the rat to detemine if hypothalamic lesions which caused polydipsia and polyuria had their effect mediated through an alteration of the ability of the neurohypophyseal system to release ADH. Rats with medial preoptic lesions hadincreased water intake while on ad libitum access to water and slightly impaired ability to conserve water following dehydration, but with no impairment of urine-concentrating ability. These were associated with an increase in plasma osmolality both during ad libitum fluid intake and after dehydration. Urinary ADH excretion was at leastas great as in shamoperated controls during ad libitum water intake, but failed to increase during dehydration in spite of a marked increase in plasma osmolality. Pituitary ADH content did not differ from control animals either during ad libitum water intake of after dehydration. Animals with lesions in the lateral preoptic and septal areas did not differ from control animals during ad libitum fluid intake and after dehydration even though lateral preoptic lesions produced polydipsia. In all animals, lesions were remote from the supraoptic nuclei, which showed no histological evidence of damage. It is concluded thatareas of the central nervous system away from the supraoptic nuclei are involved in the regulation of both water intake and ADH release.

Influence of medial preoptic‐anterior hypothalamic area stimulation of the excitability of mediobasal hypothalamic neurones in the rat.

“…The medial preoptic area is concerned functionally with thermoregulation (Hammel, 1968;Hayward & Baker, 1968), water balance (Hayward & Baker, 1968;Fitzsimons, 1972;van Gemert, Miller, Carey & Moses, 1975), sexual behaviour (Numan, 1974;Pfaff, Daikow, Zigmond & Kow, 1974) and endocrine function, in particular the regulation of pituitary gonadotropin secretion (Halasz, 1969;Cramer & Barraclough, 1973). Until recently there was relatively little data on neuronal connexions between MPOA-AHA and MBH.…”

Vasopressin and Water Metabolism

“…Conversely, the vasopressin response to prolonged fluid deprivation can be prevented in rats by producing small lesions in the medial preoptic area of the hypothalamus that do not involve the neurohypophysis. 6 These conclusions are further supported by studies performed about the same time in several patients with hypothalamic pathology and the rare clinical syndrome of adipsic hypernatremia. As originally suggested by indirect studies/, and confirmed recently by direct assay of plasma vasopressin,8.9 some of these patients have a total lack of osmotically mediated vasopressin secretion, but continue to exhibit a normal response to hemodynamic stimuli.…”

The Awareness of Thirst: Proposed Neural Correlates

“…In rats, bilateral N-methyl-D-aspartate lesions produce long-lasting insomnia and increased locomotor activity, but no change in water or food intake (John & Kumar, 1998). Reversible lesions of medial preoptic area, using the anaesthetic agent lidocaine chlorhydrate, cause a transient increase in water intake (Cambiasso & Chiaraviglio, 1992), and radiofrequency electrocoagulative lesions also increase water intake (Van Gemert, Miller, Carey, & Moses, 1975). There are two possible explanations for the discrepancy between the stimulation and lesion data: (a) in the stimulation experiments, AII may have leaked into the third ventricle (although the authors of these studies were fairly certain that this was not the case) or into the median preoptic nucleus, which means that the medial preoptic area is not involved in the thirst system, and the median preoptic nucleus is the essential structure in which signals from the circumventricular organs are integrated; or (b) the lesions did not entirely destroy the subarea of the medial preoptic area that is involved in the generation of thirst.…”