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PubMed1976

Intracerebroventricular glycerol: a potent inhibitor of ADH-release and thirst.

Infusions of isotonic or hypertonic (0.3 or 0.5 M) glycerol into the lateral cerebral ventricle (60 min, 0.02 ml/min) of non-hydrated goats invariably induced a conspicuous and sustained water diuresis. Corresponding infusions of 0.3 M glycerol/0.16 M NaCl were almost equally efficient in this respect. A more short-lasting and less pronounced water diuresis was obtained in response to equivalent infusions of pure d-glucose, and the response to 0.3 M glucose/0.16 M NaCl was variable. Intravenous injections of vasopressin blocked the glucose-induced diuresis, but only postponed the glycerol-induced diuresis. Intracerebroventricular (IVT) infusions of 0.5 M glycerol caused a sustained, complete inhibition of the urge to drink in the 48 h dehydrated goat, whereas IVT glucose only attenuated dehydrative drinking. Twenty min after the infusions of glycerol the CSF [Na+] in the lateral ventricle was about 15% below normal. About 10% reduction of CSF [Na+] was obtained 20 min after the IVT infusion of glycerol/NaCl. The corresponding infusion of pure d-glucose reduced the CSF [Na+] by less than 5%. The glycerol and glycerol/NaCl infusions caused a moderate reduction of renal Na+ + K+ excretion. The possibility is discussed that the observed effects of IVT glycerol is a manifestation of its efficiency to inhibit choroidal and/or juxtaventricular (Na+-K+)-ATPase activity.

Animals↗
PubMed1992

Intracerebroventricular angiotensin II-induced thirst and sodium appetite in rat are blocked by the AT1 receptor antagonist, Losartan (DuP 753), but not by the AT2 antagonist, CGP 42112B.

In the rat, intakes of water and 1.8% NaCl induced by I.C.V. angiotensin II were inhibited by prior I.C.V. injection of the angiotensin subtype 1 receptor antagonist, Losartan, but not by the subtype 2 receptor antagonist, CGP 42112B. Drinking induced by I.C.V. carbachol was unaffected by either antagonist.

Angiotensin II↗
PubMed1975

Some central mechanisms of thirst in the dog.

Measurements of water intake were made on a population of trained conscious dogs of both sexes prepared with chronic third ventricle cannulae. 2. Injection of 100 ng angiotensin II into the third ventricle lead to a prompt stimulation of drinking, the mean water intake over a 5 min period being 503 +/- 89 ml. (n=6) compared with controls. This dipsogenic effect of angiotensin II was abolished by prior central administration of 10 mug saralasin acetate or 100 ng atropine. 3. Injection of 1 mug carbachol into the third ventricle produced a small, variable increase in drinking. 4. Injection of 0-2 ml. 5% NaCl into the third ventricle stimulated drinking, a response that was not affected by prior administration of 10 mug saralasin acetate or 100 ng atropine. 5. Following a 24 hr period of water deprivation there was an increase in plasma osmolality and plasma-renin activity. The drinking following this period of water deprivation was not affected by prior control administration of either 10 mug saralasin acetate or 100 ng atropine. 6. In two acute dogs, intracarotid infusion of 125I angiotensin II was not followed by significant appearance of radioactivity in the third ventricle or cisterna magna c.s.f. 7. The relevance of these results to the control of water intake is discussed.

Angiotensin II↗
PubMed1983

Effects of chronic hyperprolactinaemia on experimentally induced thirsts in male rats.

Chronic hyperprolactinaemia was induced in ten male Wistar rats by subcutaneous injection of tissue fragments of the MtTW 15 prolactin-secreting adenoma. Serum prolactin was elevated significantly by 3 weeks after adenoma inoculation and increased progressively thereafter. An additional ten Wister-Furth rats were inoculated with the MtTW 15 adenoma and an equal number of age-matched controls were used to evaluate the drinking response to several dipsogenic agents. The hyperprolactinaemic rats consumed twice as much water as did control rats over a 24 hr period. Administration of the beta-adrenergic agonist, isoprenaline (25 micrograms/kg, s.c.), resulted in a similar increase in water intake in both groups prior to an elevation in serum prolactin. However, as serum prolactin increased there was a corresponding significantly attenuated dipsogenic response to isoprenaline. Chronic hyperprolactinaemia did not alter the drinking response to angiotensin II (200 micrograms/kg, s.c.), to 24 hr of dehydration or to administration of hypertonic (1 M) saline. These results indicate that chronic hyperprolactinaemia selectively attenuates the dipsogenic response to beta-adrenergic stimulation and support an involvement of prolactin in modifying the responsiveness of the beta-adrenergic system.

Adenoma↗