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PubMed1979

Role of central catecholamines in the control of blood pressure and drinking behavior.

The role of central nervous system (CNS) catecholamines in the development of hypertension and the control of drinking behavior was assessed in rats by depleting these amines with 6-hydroxydopamine (6-OHDA). Intraventricular administration of 6-OHDA completely prevented the development of one-kidney renal hypertension and abolished the associated increase in water consumption. 6-OHDA-treated rats showed deficits in drinking behavior when challenged with subcutaneous injections of angiotensin II (AII) and hypertonic sodium chloride. The acute pressor responses produced by intraventricular injections of AII and carbachol were virtually abolished by central catecholamine depletion. However, drinking produced by central cholinergic stimulation remained intact while AII drinking was significantly reduced. These data demonstrate that the integrity of CNS catecholamines is required for the development of one-kidney renal hypertension and the increased drinking which accompanies it. In addition, destruction of central catecholamine-containing neurons allows for a specific dissociation of the pressor and drinking responses produced by central cholinergic but not AII stimulation.

Animals↗
PubMed1979

Pharmacologic independence of subfornical organ receptors mediating drinking.

In rats with chronically implanted cannulae in the subfornical organ (SFO), the relationship between cholinergic- and angiotensin (AII)-induced drinking was investigated pharmacologically. All substances were injected via SFO cannulae which did not rupture ventricular ependyma. Pretreatment with low doses of the muscarinic antagonist atropine abolished carbachol-induced drinking, while nicotinic antagonists had no effect. Nonetheless, pretreatment with much larger doses of atropine had no effect on AII-induced drinking. Similarly, relatively small doses of the AII antagonist, saralasin, blocked AII-induced drinking, yet a much larger dose of saralasin had no effect on carbachol-induced drinking. The receptors mediating cholinergic- and AII-induced drinking therefore cannot be in series and must be in parallel. A hypothesis is proposed to account for this independence and for the significance of the SFO cholinergic innervation.

Angiotensin II↗
PubMed1984

Clonidine antagonism of angiotensin-related drinking: a central site of action.

Administration of either isoproterenol (25 micrograms/kg, s.c.) or angiotensin II (200 micrograms/kg, s.c.) induces drinking in rats within 0.5-1 h. This drinking was inhibited by prior administration of the presynaptic alpha-adrenergic agonist clonidine (12 micrograms/kg, i.p.). Urine output was enhanced by clonidine in the angiotensin II-, but not the isoproterenol-treated group. Drinking in response to peripheral administration of either angiotensin II or isoproterenol was also inhibited by intracerebroventricular (i.v.t.) administration of clonidine (8 micrograms/kg). This dose of clonidine also enhanced the urine output after angiotensin II. Further, the drinking induced by i.v.t. administration of angiotensin II, at 4 but not 20 ng/kg was inhibited by peripheral administration of clonidine (12 micrograms/kg, i.p.). When clonidine was administered i.v.t. prior to i.v.t. injection of either angiotensin II (20 ng/kg) or carbachol (1.2 micrograms/kg), the drinking response to these dipsogens was attenuated. These results suggest that clonidine may act centrally to attenuate drinking at a site, possibly in the nucleus tractus solitarius, that may be considered a final common pathway for this response.

Angiotensin II↗
PubMed1987

Intracerebroventricular dopamine attenuates sodium-induced but not angiotensin-induced drinking in minipigs.

Drinking in response to dopamine (100 micrograms) injected into the lateral cerebral ventricles (i.c.v.), alone, or together with angiotensin II (AII, 300 ng) or hypertonic NaCl (1.4 Osm) was studied in water-replete minipigs trained to obtain their water under operant conditions. Dopamine itself was ineffective at producing drinking and it did not affect AII-induced drinking. Drinking in response to hypertonic NaCl was significantly attenuated by dopamine. Therefore in minipigs angiotensin-induced drinking does not appear to operate through a dopaminergic mechanism whereas sodium-induced drinking does.

Angiotensin II↗
PubMed1989

Contribution of nucleus medianus to the drinking and pressor responses to angiotensin II acting at subfornical organ.

The contribution of neurons in the nucleus medianus (NM) in mediating the drinking and pressor responses elicited by administration of angiotensin II (AII) either directly into the subfornical organ (SFO) or intravenously was investigated in conscious, unrestrained rats. Microinjection of AII into the SFO elicited a robust drinking (7.9 +/- 0.8 ml in 15 min; n = 24) and pressor (peak rise in mean arterial pressure (MAP), 15 +/- 1 mm Hg; n = 20) response. On the other hand, intravenous infusion of AII elicited an increase in MAP (36 +/- 3 mm Hg; n = 14) accompanied by a marked reflex bradycardia (134 +/- 18 beats/min), but not a significant drinking response. Lesions of NM cells, dorsal to the anterior commissure and between the fornical columns, with the neurotoxin kainic acid significantly (P less than 0.05) attenuated the drinking response (prelesion volume, 8.3 +/- 0.8 ml in 15 min; postlesion volume, 1.9 +/- 1.4 ml in 15 min; n = 7), but did not alter the pressor response to AII injected directly into the SFO. Similarly, kainic acid lesions of NM cells did not significantly effect the pressor response or the associated reflex bradycardia to intravenous administration of AII. Sham lesions of NM cells or control kainic acid lesions of adjacent structures did not alter the AII-induced drinking or pressor responses. These data suggest that neurons in the dorsal NM are part of a forebrain neuronal circuit that is involved in the drinking, but not the pressor responses to AII acting at the SFO in the conscious rat.

Angiotensin II↗
PubMed1989

Decreased norepinephrine in the ventral lamina terminalis region is associated with angiotensin II drinking response deficits following local 6-hydroxydopamine injections.

Previous studies have demonstrated that punctate injections of 6-hydroxydopamine (6-OHDA) into structures along the ventral lamina terminalis reduce drinking responses elicited by angiotensin II (ANG II). The purpose of the present study was to extend these findings by quantifying the catecholamine depletions that are associated with the drinking response deficits. Male Sprague-Dawley rats were given injections of 6-OHDA into the median preoptic nucleus (MnPO) and the organum vasculosum of the lamina terminalis (OVLT) after pretreatment with pargyline. Controls were injected with vehicle and a third group received 6-OHDA after pretreatment with desmethylimipramine (DMI). All subjects were tested for drinking responses to centrally injected ANG II and carbachol. Changes in catecholamine content of the MnPO, OVLT, supraoptic nucleus, paraventricular nucleus, caudate and cortex were determined using HPLC with electrochemical detection after behavioral testing. Only rats injected with 6-OHDA without DMI pretreatment showed a significant reduction in ANG II-induced drinking responses. This behavioral deficit was associated with a significant norepinephrine decrease in the ventral lamina terminalis region. All 3 groups showed comparable drinking responses to carbachol. These data support the hypothesis that noradrenergic innervation of the ventral lamina terminalis region is necessary for ANG II-induced drinking responses.

Angiotensin II↗
PubMed1983

Effects of systemic and intracranial inhibition of angiotensin-converting enzyme on isoproterenol-induced drinking in the rat.

We have investigated the effects of separate and combined s.c. and intracerebroventricular (i.c.v.) injections of captopril, an inhibitor of angiotensin I-converting enzyme, on isoproterenol-induced thirst. Whereas s.c. injections of captopril (0.5 mg/kg) increased drinking, combined s.c. and i.c.v. (20 micrograms) injections of captopril nearly abolished drinking to isoproterenol (0.1 mg/kg s.c.). This inhibition was not caused by general debility of the rats since the same treatment did not reduce drinking to 12h water deprivation. Intracerebroventricular injection of 20 micrograms captopril alone also greatly reduced isoproterenol-induced drinking, perhaps because it leaked into the circulation; captopril i.c.v. also reduced the pressor response to i.v. injection of hog renin (0.1 Goldblatt Unit) by about 65%. These results support the hypotheses that the renin-angiotensin system participates in the stimulation of drinking by isoproterenol and that the enhancement of drinking caused by inhibition of CE only in the circulation is the result of increased synthesis of angiotensin II in the brain.

Angiotensin II↗
PubMed1992

Drinking induced by subcutaneous injection of angiotensin II in the rat is blocked by the selective AT1 receptor antagonist DuP 753 but not by the selective AT2 receptor antagonist WL 19.

The role of AT1 and AT2 receptors in mediating the drinking response induced by angiotensin II in the rat was examined. Angiotensin II (0.1-1.0 mg/kg s.c.) caused a dose-dependent increase in drinking in water-replete rats. The angiotensin Il-induced drinking response was dose dependently blocked by the selective AT1 receptor antagonist DuP 753 (1-30 mg/kg s.c.). In contrast, the selective AT2 receptor antagonist WL 19 failed to block angiotensin II-induced drinking up to doses of 100 mg/kg s.c. and significantly enhanced the response at 3 and 100 mg/kg. These data suggest that drinking induced by angiotensin II is mediated by AT1 receptors and that AT2 receptor activation may inhibit the drinking response.

Angiotensin II↗
PubMed1983

The renin-angiotensin system and drinking in the euryhaline flounder, Platichthys flesus.

Drinking behaviour and its possible regulation by the renin-angiotensin system (RAS) has been examined in the euryhaline flounder. Fluid intake was greater in seawater (SW)-adapted than freshwater (FW)-adapted fish, the latter having significantly lower plasma sodium, chloride, and osmotic concentrations. Oesophageal cannulation in SW-adapted fish resulted in further elevation of drinking rates, which increased proportionally with progressive body water loss as measured by the fall in body weight and rise in plasma tonicity. The influence of the RAS on drinking in SW-adapted fish was examined in animals with an intact gastrointestinal tract. Fluid intake fell markedly following administration of the converting enzyme inhibitor, Captopril. Infusions of angiotensin I (AI) and angiotensin II (AII) induced dose-related increments in the rate of drinking. The increased drinking in response to AI was inhibited, however, by the simultaneous administration of Captopril. The results are consistent with the presence in the flounder of the major elements of the RAS, including AI, AII, and a converting enzyme-like substance. The RAS appears to play an important regulatory role in the adaptative drinking behaviour associated with migration of euryhaline teleosts between FW and SW.

Adaptation, Physiological↗
PubMed1982

Entrainment and masking of circadian drinking rhythms in primates: influence of light intensity.

The entrained drinking rhythms of squirrel monkeys were studied during exposure to 24 hr illumination cycles of three different intensities (60:0, 66:6, 76:16 lux). Increasing the intensity of ambient illumination significantly delayed the offset of drinking but had no effect on either the onset or the total amount of daily drinking behavior. Comparison of drinking behavior under an alternating schedule of LD 66:6 lux and constant light of 6 lux indicated that the twice daily light transitions consistently altered the temporal distribution of drinking behavior. The daily timing of squirrel monkey drinking behavior thus, depends not only o the mechanisms of circadian entrainment to the LD cycle, but also on the ability of the LD cycle to directly influence, or "mask" behavior.

Animals↗
PubMed1982

Histamine-elicited drinking is dependent upon gastric vagal afferents and peripheral angiotensin II in the rat.

While transection of either the anterior (including hepatic) or posterior (including coeliac) vagal trunk failed to alter drinking in response to subcutaneous histamine (0.312--20 mg/kg), selective gastric vagotomy severely attenuated drinking after systemic histamine (1.25--40 mg/kg) in male Sprague-Dawley rats. The dose-response curve for rats with gastric vagotomy was shifted to the right. Vagotomy increased the threshold dose nearly tenfold and more than doubled the ED50. Because the effect of vagotomy on histamine-elicited drinking was not mimicked by cholinergic blockade of vagal efferents using atropine methyl nitrate (10 mg/kg), these results demonstrate that gastric vagal afferents are necessary for a normal drinking response to systemic histamine. When gastric vagotomy was combined with intragastric SQ14,225 (to inhibit the conversion of peripheral angiotensin I to angiotensin II) drinking after systemic histamine was abolished. These results suggest that gastric vagal afferents and angiotensin II are necessary for systemic histamine to elicit drinking in the rat.

Angiotensin II↗
PubMed1986

Operant drinking in pigs following intracerebroventricular injections of hypertonic solutions and angiotensin II.

The effect on operant drinking of intracerebroventricular injections of the following solutions has been investigated; hypertonic saline, hypertonic sugars, angiotensin II (Ang II) dissolved in water or dextrose, and Ang II dissolved in saline. Hypertonic (0.85 M) NaCl caused drinking in all pigs tested, but hypertonic (1.7 M) xylose, glucose or sucrose were less effective, indicating involvement of a cerebrospinal fluid sodium receptor mechanism as well as an osmoreceptor mechanism in the drinking responses. Angiotensin II in 0.15 M NaCl caused drinking in all pigs but when dissolved in water or dextrose it was ineffective. Injection of Ang II with hypertonic NaCl produced drinking similar in volume to the sum of the amount drunk in response to the individual stimuli. These results indicate that, in the pig, drinking in response to Ang II requires the presence of sodium ions.

Angiotensin II↗
PubMed1986

Influences of feeding and drinking on circadian rhythms of opioid peptides in plasma, hypothalamus and pituitary gland in rats.

Changes of plasma, hypothalamic and pituitary immunoreactive beta-endorphin (IR-beta-end), methionine-enkephalin (IR-Met-enk) and ACTH (IR-ACTH) were studied under various conditions of feeding and watering in rats. When rats were fed from 17:00 to 09:00 hr and water was given ad lib, plasma IR-beta-end and IR-ACTH had parallel circadian rhythms with a peak before feeding and drinking. In the hypothalamus, IR-beta-end and IR-Met-enk showed parallel circadian rhythms with a decrease before these behaviors. When rats were fed from 09:00 to 17:00 hr, the peaks of plasma IR-beta-end and IR-ACTH shifted to one hour before the onset of feeding and drinking. When feeding and watering were restricted to 17:00-09:00 hr and 09:00-12:00 hr respectively, plasma IR-beta-end and IR-ACTH exhibited parallel circadian rhythms with two separate peaks at one hour before drinking and feeding, respectively. In the hypothalamus, IR-beta-end, IR-Met-enk and IR-ACTH showed parallel circadian rhythms with a decrease before feeding but not before drinking. When rats were fed from 17:00 to 20:00 hr, plasma IR-beta-end increased and neurohypophysial IR-beta-end and IR-Met-enk decreased at 16:00 hr, one hour before feeding. It was observed that locomotor activities increased at the time of transition from light to dark and at one hour before the onset of feeding and drinking. The present results suggest that endogenous opioid peptides may have some physiological roles in feeding and drinking behaviors.

Adrenocorticotropic Hormone↗
PubMed1987

Central and peripheral injection of quaternary antagonist, SR58002C, reduces drinking.

Earlier research has demonstrated that opioid involvement in drinking is primarily mediated centrally [8,10]. Drinking is attenuated by the centrally and peripherally active opioid antagonists naloxone and naltrexone in doses as low as 1.0 mg/kg, but not by the quaternary forms of these antagonists [4]. Peripherally administered quaternary forms of these antagonists fail to suppress drinking in doses as high as 10 mg/kg. We generated dose-response curves for centrally and peripherally administered SR58002C, a "newer" quaternary opioid antagonist purported to have high peripheral selectivity, on drinking in 23.5 hr water deprived rats. SR58002C was administered both intracerebroventricularly (ICV, 0, 10, 40 and 80 micrograms/rat) and intraperitoneally (IP, 0, 10, 40 and 80 mg/kg). Doses of SR58002C above 10 mg/kg IP or 10 micrograms ICV significantly reduced drinking in comparison to controls. However, SR58002C appears to be less potent than quaternary naltrexone in suppressing drinking after ICV administration.

Animals↗
PubMed1988

Augmentation of isoproterenol-induced drinking by acute treatment with certain dopaminergic agonists.

Bromocriptine (1 mg/kg, IP), a dopaminergic agonist that crosses the blood-brain barrier, augmented the dipsogenic responsiveness of rats to acute administration of the beta-adrenergic agonist, isoproterenol (15 micrograms/kg, SC), when administered at the same time. When administered alone, it had no effect on either water intake or urine output. Dopamine (20 mg/kg IP), which does not cross the blood-brain barrier, also augmented the dipsogenic responsiveness to acute administration of isoproterenol. However, a major difference between the responses to bromocriptine and dopamine was that the latter augmented drinking only when administered 15 to 30 min prior to isoproterenol. During the 30 min between injection of dopamine and the injection of isoproterenol, output of urine and sodium increased approximately 6-fold above the level of controls such that the concentration of the urine excreted by the treated group was approximately isotonic. However, in spite of a 6-fold increase in output of urine by the treated, compared to the control group, dopamine-treated rats ingested water only to the same extent as untreated controls when access to water was allowed. This suggests that an isotonic contraction of extracellular fluid may not induce a dipsogenesis. It also suggests that the augmentation of isoproterenol-induced drinking by dopamine was not the result of a dehydration-induced drink superimposed on the isoproterenol-induced drink. The centrally and peripherally acting dopaminergic antagonist, spiroperidol (spiperone), inhibited the isoproterenol-induced drinking response in a dose-related fashion. However, the peripherally acting dopaminergic antagonist, domperidone,was without effect on isoproterenol induced drinking.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Food granules elicit heavy drinking in polydipsic rats independently of meal duration.

Excessive drinking, in rats made polydipsic on intermittent delivery of food pellets, is inversely related to the time the rat spends with its head in the feeder, early in the interfood interval. In a sensitization model, this explains why food textures that induce more oral activity, e.g., powder, do not elicit drinking. This hypothesis was examined by coding the behavior of polydipsic rats and varying the duration of the meal delivered in each interval, while holding texture constant. Polydipsic rats were presented with pellets, food granules, or food powder. The food granules were dispensed over periods lasting 1, 14, 21, and 28 s. All food deliveries were of the same mass. The food was delivered periodically at 60-s intervals in each condition. The 14 rats in the experiment served as their own controls by experiencing every condition. The food granule conditions induced the expected increases in feeding early in the interval. However, instead of progressively reducing drinking, the excessive drinking simply occurred later in the interval. By contrast, the powder condition resulted in the immediate elimination of polydipsia. The results suggest that food texture elicits excessive drinking independently of temporal factors and that elicitation of the sensitized drinking response must depend on other factors.

Animals↗
PubMed1994

Gastric pressures in pigs during eating and drinking.

Pressures were measured with miniature transducers positioned within the gastric lumen of six young pigs, 20-40 kg, eating and drinking operantly. The pigs were free to move about, lie down, sleep, eat, and drink without disturbance. 1) At the end of 4-5-h fasts (with no drinking), mean pressure within the stomach was 12 cm H2O, then rose during 22-min eating bouts to 22 cm H2O. 2) At the end of 16-18-h periods of food and water deprivation, intragastric pressure was 9 cm H2O. When water was drunk, pressures rose only to 13 cm H2O, then fell. When food was then eaten, pressures rose during 29-min meals to 22 cm H2O. 3) During spontaneous eating and drinking, intermeal pressures were maintained at 22-25 cm H2O, fell by 4-5 cm H2O just as eating or drinking began, then rose slowly, but only to the preingestive pressure level by the end of the bout. These results indicate that during spontaneous eating and drinking, gastric distention per se plays a smaller direct role in causing satiety than it does during meals ingested after a period of food deprivation.

Afferent Pathways↗
PubMed1983

One-year drinking history and mortality.

The one-year drinking history of 94 men was recorded by recurrent interviews (mean: 20 per person). The cohort was followed for 18.3 years; during that time, 13 men died. Cox's proportional hazards survival models including age and social class as confounders, indicated that mortality was significantly associated with total annual alcohol consumption, frequency of drinking, and frequency of intoxicating drinking. Estimates of risk of death for various consumption levels are presented: For having 10 drinks (each containing 12 grams of pure ethanol) a week vs one drink a week, the estimated relative risk of death (95% confidence limits in parentheses) was 2.3 (1.6-3.3). For being intoxicated once a week vs no intoxications at all during one year the respective risk was 2.1 (1.3-3.1). The risk estimates for the frequency of intoxication were found to be higher than those in an earlier study using single interview data on drinking. This suggests that more accurate measurement of alcohol consumption may yield higher risk of death estimates than found in studies based on single interview data on alcohol.

Adult↗