Disease relevance of Drinking

• Therefore, there are specific impairments of water intake in response to hypertonicity and hypovolemia in aged MW rats, but Ang-related drinking is not reduced [1].
• While DHEA treatments did not block either the direct cytotoxic action of SZ on beta-cells or the development of insulitis, the steroid significantly moderated the severity of the ensuing diabetes (reduced hyperglycemia and water consumption, and increased plasma insulin and numbers of residual, granulated beta-cells [2].
• Body weight, water intake, urine output, solute and urea excretion, serum and urine osmolality, serum creatinine, 24-h creatinine clearance, and fractional excretion of sodium were comparable among the three groups [3].
• DOCA-salt rats failed to gain weight with markedly increased water intake and decreased food intake; drug treatment did not alter these parameters [4].
• 2. These studies show that cumulative sodium balance and aldosterone secretion rates in patients with SIADH are negatively correlated with water intake [5].

Psychiatry related information on Drinking

• We conclude that after 24 hours of water deprivation, there is a deficit in thirst and water intake in healthy elderly men, as compared with younger men, although vasopressin osmoreceptor responsiveness is maintained or even increased [6].
• There were no significant differences in any of the regulatory behaviors (food/water intake or locomotor activity), prostate weight, or testosterone levels between the treatment groups [7].
• Peripheral and central administration of the AT1 receptor blocker significantly lengthened the onset of drinking behavior and reduced the cumulative water intake observed after intracerebroventricular injection of renin [8].
• The antagonist haloperidol decreased alcohol consumption but only at doses that also reduced water consumption [9].
• The water intake of rats maintained through food deprivation at 70, 80, 90, and 100% of free-feeding body weights was examined under conditions where a small amount of sweetened condensed milk containing 8% sodium chloride was presented at one-minute intervals [10].

High impact information on Drinking

• Demeclocycline (600 to 1200 mg daily) restored serum sodium concentration to 139 +/- 1.1 meq per liter within five to 14 days, permitting unrestricted water intake in all patients [11].
• Pairing lithium chloride with stimulation of the amygdala had no effect on subsequent water intake in the absence of brain stimulation [12].
• Subjects receiving this pairing greatly reduced their water intake in a retention test, in a similar manner to a group in which saccharin was paired with poisoning [12].
• Cerebroventricular infusion of P-113, the blocking agent of angiotensin II, into rats for 75 minutes prior to their being allowed to drink, significantly attenuated their water intake when they had been deprived of water for 30 hours [13].
• Neither intravenous D-glucose nor water intake enhanced MSA [14].

Chemical compound and disease context of Drinking

• There was a significant increase in the plasma norepinephrine concentration after insulin infusion, whereas no significant changes in plasma triglyceride and glucose concentrations, water intake, urine flow, sodium excretion, sodium gain, and body weight gain were observed [15].
• Hypercapnia did not alter sheep behavior, food and water intake, arterial pressures, core temperature, or brain lactate release [16].
• The effects of the peptides on body weight gain, food and water intake, glucose homeostasis, and thermoregulation were assessed [17].
• Body weight and temperature, food and water intake, and plasma TSH, T4, free T4 (FT4), T3, and corticosterone levels were measured daily, and hypothalamic pro-TRH messenger RNA (mRNA) and hypophysial TSH beta mRNA were determined after termination of the experiments [18].
• Body weight, water intake, urine output, solute and urea excretion, and serum and urine osmolality were comparable among the three groups at the conclusion of the 10-wk treatment period [19].

Biological context of Drinking

• The initial response to constriction was a reduction in blood pressure, a rise in plasma renin activity, plasma aldosterone, and water intake, and nearly complete sodium retention [20].
• NPY (24, 78, 235, 783, and 2351 pmol/0.3 mul) produced a large, dose-dependent increase in food intake as well as small increase in water intake [21].
• There was a twofold increase in diuresis and water intake in enalapril-treated rats throughout the study course [22].
• The doubly labeled water method was compared with indirect calorimetry and a nutrient-balance study for simultaneous determination of rates of CO2 production, energy expenditure, and water intake over 5 days in four preterm infants [23].
• Studies in Sprague-Dawley rats showed that restriction of water intake for 3 days results in upregulation of urea transporter (UT) mRNA in the inner stripe of outer medulla of the kidney (2.9-kb UT2) but not in the inner medulla (4.0-kb UT1) [24].

Anatomical context of Drinking

• Now, roles have been established for the apelin system in lowering blood pressure, as a potent cardiac inotrope, in modulating pituitary hormone release and food and water intake, in stress activation, and as a novel adipokine that is excreted from fat cells and regulates insulin [25].
• Intracerebroventricular (third ventricle) infusion of 1.0 or 2.0 nmol of ANF in conscious, overnight-dehydrated rats significantly inhibited subsequent water intake over a 2-hr test period [26].
• These results indicate a possible physiologic role for ANF in the hypothalamic control of water intake and reveal that the cardiac peptides can act centrally, as well as peripherally, to assist in the normalization of extracellular fluid volume [26].
• The activation of neurons in the subfornical organ (SFO) by angiotensin II (AngII) is well established and is widely regarded as the basis for the AngII-induced increase in water intake [27].
• OBJECTIVE: To determine whether discontinuation of insulin therapy and glucose monitoring and instructions to increase dietary salt and water intake after pancreas transplantation (PTX) resulted in changes in food choices [28].

Associations of Drinking with chemical compounds

• Normal or increased durations of PS were observed after intravenous (i.v.) administration of vasopressin but also when the normal daily water intake (240 ml) was infused i.v. These results provide direct evidence that PS deficits in the HODI rat are not due to the absence of vasopressin [29].
• While on ad lib. water intake, the urine flow, urine osmolality, urinary excretion of Na +, K +, creatinine, or total solute excretion did not change [30].
• In the control rats only water intake was stimulated in response to the induced hyperosmolality, but in the rAOT-treated rats hypertonic mannitol caused a robust salt appetite as well as thirst [31].
• Chronically, this can be accomplished with increased salt and water intake in conjunction with fludrocortisone [32].
• NE had no effect on water intake at any age [33].

Gene context of Drinking

• GLP-1 is produced in the brain, and intracerebroventricular GLP-1 in rodents is a potent inhibitor of food and water intake [34].
• In the present study, a 7-day intracerebroventricular infusion to male rats of either the MC receptor antagonist SHU9119 or porcine NPY (10 nmol/day) was shown to strongly stimulate food and water intake and to markedly increase fat pad mass [35].
• After 17 days of whisky consumption, serum capacity to induce ABCA1-dependent cholesterol efflux from J774 mouse macrophages was increased by 17.5% (P = 0.027) compared with water consumption [36].
• Neither IGF-1, nor IGFBP-1 levels changed significantly after water intake [37].
• The IGF-1 : IGFBP-1 ratio declined markedly after ethanol (from 15.7 +/- 3.9 to 3.9 +/- 0.6; P < 0.01), but not after water intake [37].

Analytical, diagnostic and therapeutic context of Drinking

• Intravenous infusion of 2.0 nmol, but not 1.0 nmol, of ANF resulted in a similar inhibitory action, suggesting that ANF released from the heart might act centrally to inhibit water intake by an action at one or more of the circumventricular organs [26].
• CA was either reduced by increasing water intake (mixing the food with a gel bringing 1.6 mL water per g food) (Low-CA), or increased by chronic intraperitoneal infusion of 1-desamino 8-D-arginine vasopressin (200 ng/day) (High-CA) [38].
• AB-ANP reduced water intake induced by overnight deprivation but not by icv microinjection of AII, while AB-AII reduced water intake in both situations [39].
• In Experiment I, three groups of female rats were water deprived and conditioned to avoid a 0.025 M Polycose, a 0.1 M sucrose, or a 0.1 M maltose solution by pairing solution consumption with a lithium chloride (LiCl) injection; in a control group water consumption was paired with the LiCl injection [40].
• In rats with a pre-existing increase in sodium appetite caused by adrenalectomy, low dosage of captopril augmented intake of both water and 2.7% NaCl whereas high dosage inhibited intake of both fluids after an initial increase in water intake [41].

References