Polyuria and imparied ADH release following medial preoptic lesioning in the rat.
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.
D000818:Animals; D001769:Blood; D004326:Drinking; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D007031:Hypothalamus / Q000502:physiology*; D007671:Kidney Concentrating Ability; D008297:Male; D009994:Osmolar Concentration; D010902:Pituitary Gland / Q000032:analysis; D011141:Polyuria / Q000209:etiology*; D011301:Preoptic Area / Q000502:physiology* / Q000601:surgery; D011863:Radioimmunoassay; D051381:Rats; D014667:Vasopressins / Q000032:analysis / Q000378:metabolism* / Q000652:urine; D014882:Water-Electrolyte Balance
D014667:Vasopressins