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At least 469 records · Page 26Linked to original sources
PubMed1992

The involvement of the hypothalamic preoptic area on the regulation of thirst in the rat.

Acute reversible lesion in the medial preoptic area (MPOA) by unilateral injection of the local anesthetic lidocaine chlorhydrate (1 microliter, 20 ng/microliters) causes a transient increase in water intake induced by water deprivation in rats. Since lidocaine suppresses the nervous activity, leaving intact fibers of passage and blood vessels, the results suggest an intrinsic inhibitory action of the MPOA on the regulation of water intake. Drinking elicited a return to volumes similar to those of control rats, 3-4 h after lidocaine administration. Lidocaine released into the lateral preoptic area (LPO) slightly decreased or did not change water intake, as compared with controls. The urinary excretion in the MPO group was higher than that of the controls and the LPO, while this last group excreted significantly less urine. The ablation of the POA with lidocaine suggests that the medial aspect of the POA has an intrinsic inhibitory factor influencing drinking, while the lateral aspect did not show a relevant effect.

Animals↗
PubMed1994

Antisense oligonucleotide to AT1 receptor mRNA inhibits central angiotensin induced thirst and vasopressin.

Antisense oligodeoxynucleotides (AS-ODN) to AT1 receptor mRNA inhibit high blood pressure in Spontaneously Hypertensive Rats (SHR) when injected into the brain. The effect is presumably through inhibition of the actions of brain angiotensin II (Ang II). Central injection of Ang II elicits several physiological responses including release of vasopressin and motivation to drink. The angiotensin II type-I (AT1) receptor is located in brain regions which have been implicated in mediating these effects. Therefore we hypothesized that AS-ODN to AT1 mRNA would inhibit the drinking and AVP response to central administration of Ang II in adult male SHR. AS-ODN were constructed to bases +63 to +77 (15-mer) of the AT1 receptor RNA. 24 h after AS-ODN treatment (50 micrograms/4 microliters) (intracerebroventricularly, i.c.v.), the drinking response to Ang II (50 ng, i.c.v.) was significantly reduced in the SHR (P < 0.05). The drinking response to Ang II (i.c.v.) was also reduced in the Sprague-Dawley rats (P < 0.05). There was no reduction of water intake in the control animals treated with scrambled ODN (SC-ODN). Repeated injection of AS-ODN did not produce a greater reduction in drinking response. Arginine vasopressin (AVP) release to central Ang II was significantly decreased after AS-ODN treatment when compared to vehicle (P < 0.05) and to SC-ODN injections (P < 0.05). Radioligand binding assays of the hypothalamic block after AS-ODN treatment showed a significant decrease of AT1 receptor binding (P < 0.05). The results show that the antisense inhibition of brain AT1 receptor gene expression decreases the Ang II induced drinking and AVP release responses.

Animals↗
PubMed1996

Increased sodium appetite and thirst in rat induced by the ingredients of liquorice, glycyrrhizic acid and glycyrrhetinic acid.

In the rat, blocking 11 beta-OHSD with the active ingredient of liquorice, glycyrrhizic acid (GZA) or its hydrolytic product, 18 beta-glycyrrhetinic acid (GTA), caused potassium loss, increased water intake and a primary increase in salt appetite that was specific for sodium and not secondary to sodium loss. Intracerebroventricular injection of angiotensin II enhanced the sodium appetite but carbachol did not. The stimulating effects of GZA or GTA on intakes of water and NaCl resembled those caused by the administration of excessive amounts of mineralocorticoid. The results suggest that GZA- or GTA-induced drinking behaviour is mediated by circulating glucocorticoids. After liquorice blockade of 11 beta-OHSD, the peripheral and central mineralocorticoid receptors are no longer protected from glucocorticoid action.

Angiotensin II↗
PubMed1985

Thirst and vasopressin secretion following central administration of angiotensin II in rats with lesions of the septal area and subfornical organ.

Various dipsogenic stimuli, including peripheral and central administration of angiotensin II, have been shown to be capable of releasing vasopressin from the neurohypophyseal system. Studies were carried out in the rat to investigate whether the septal area, which contains a high concentration of angiotensin-sensitive cells and has neural connections with hypothalamic vasopressin-secreting neurons, mediated the stimulatory effect produced by angiotensin II on vasopressin release. Rats with electrolytic lesions in the region of the septal area had increased daily water consumption and urine output when these lesions included the medioventral or lateral nuclei of the septal forebrain, but not when the lesion involved the subfornical organ. No difference was observed in drinking responses following water deprivation or intracerebroventricular injection of angiotensin II in all experimental groups. In addition, the impaired ability to maintain water homeostasis (polyuro-polydipsic syndrome) of septal-lesioned rats was associated septal-lesioned rats was associated with decreased levels of circulating radioimmunoassayable vasopressin. Furthermore, the vasopressin release which occurred in response to intracerebroventricular angiotensin II in normal controls, sham-lesioned and subfornical organ-lesioned rats was significantly attenuated in rats with electrolytic lesion of the medioventral or lateral septal area. Since cells in the lateral septal area are excited by iontophoretic application of angiotensin II, the present data might be consistent with the hypothesis that the stimulatory effect produced by central administration of angiotensin II on vasopressin release rests upon the integrity of the lateral septal area.

Angiotensin II↗
PubMed2004

Reduced thirst in old, thermally dehydrated rats.

Water intake and blood parameters of young (7-month) and old (23-month) male Brown Norway rats were assessed following a period of thermal dehydration. Rats of both ages were randomly assigned to one of three groups: (1) Unheated-blood sample, (2) Heated-blood sample, and (3) Heated-water intake. The colonic temperature of heated rats was raised at the rate of 0.05 degrees C/min for 1 h using an infrared heat lamp. Water intake was then measured over the following 2 h. The heating protocol resulted in a similar level of dehydration in both young and old rats; however, plasma osmolality and sodium concentration increased to a significant extent only in the young rats. Old rats drank significantly less water at all time points during the 2 h following the heat stress. While neither group replaced the water lost as a result of the thermal dehydration, the young rats did rehydrate to a greater extent. These results suggest that the diminished level of rehydration in aged rats, following a thermal dehydration, is due to an attenuated rise in plasma osmolality.

Aging↗
PubMed1997

[Morphological study of Organum cavum pre-lamina terminalis (OCPLT), implicated in thirst in rats].

It has been shown that micro-injections of angiotensin II in the Organum cavum pre-lamina terminalis (OCPLT) of the rat brain trigger water intake. Our anatomical study shows that the anterior, vertical extension of this Organum corresponds to the anterior inter-hemispheric fissure, and its posterior, horizontal extension to the Cavum septi pellucidi (CSP). Contrary to classical descriptions, the CSP persists in the adult rat, though reduced to one third of its initial antero-posterior extension. It appears rostrally as an opening into the anterior inter-hemispheric fissure. The absence of ependymal cells and of communication with the lateral ventricles points to the fact that this diverticulum is not a median cerebral ventricle. Its pial sheathing and the presence of leptomenix in the cavity confirm its inter-hemispheric origin. The pinocytotic vesicles of the meningeal capillaries suggest an active transfer of substances. Circumstantial evidence suggests circulating angiotensin could be one of them.

Angiotensin II↗