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PubMed1990

Drinking and smoking at 3 months postpartum by lactation history.

A spontaneous decrease in maternal drinking and smoking often occurs during pregnancy. The present study was conducted to determine if these lower levels of maternal drinking and smoking during pregnancy persist into the postpartum period, and if so, to determine if they are related to breastfeeding. Drinking and smoking were estimated in three cohorts of postpartum women who had been followed since pregnancy. The first group never breastfed their infants; the second group breastfed for less than 1 month; the third group breastfed for more than three months. (Women who weaned between one and three months were not studied). Drinking and smoking in all three groups decreased sharply during pregnancy but rose again in the 3 months after delivery, though not to levels that were reported before conception. Usual drinking in the third month postpartum did not differ significantly among the three lactation groups. However, women who were still nursing were less likely to report occasional episodes of heavy drinking (binges) in this month than women who had weaned early or never breastfed. Women nursing in the third month postpartum were also significantly less likely to smoke during the month; if smoking, they were less likely to smoke heavily. These differences in postpartum drinking and smoking were not due entirely to habits before conception or to the influence of other potentially confounding variables.

Alcohol Drinking↗
PubMed2004

Alcohol drinking patterns and health care utilization in a managed care organization.

OBJECTIVE: To estimate the relationship between current drinking patterns and health care utilization over the previous two years in a managed care organization (MCO) among individuals who were screened for their alcohol use. STUDY DESIGN: Three primary care clinics at a large western MCO administered a short health and lifestyle questionnaire to all adult patients on their first visit to the clinic from March 1998 through December 1998. Patients who exceeded the National Institute on Alcohol Abuse and Alcoholism (NIAAA) guidelines for moderate drinking were given a more comprehensive alcohol screening using a modified version of the Alcohol Use Disorders Identification Test (AUDIT). Health care encounter data for two years preceding the screening visit were linked to the remaining individuals who responded to one or both instruments. Using both quantity-frequency and AUDIT-based drinking pattern variables, we estimated negative binomial models of the relationship between drinking patterns and days of health care use, controlling for demographic characteristics and other variables. PRINCIPAL FINDINGS: For both the quantity-frequency and AUDIT-based drinking pattern variables, current alcohol use is generally associated with less health care utilization relative to abstainers. This relationship holds even for heavier drinkers, although the differences are not always statistically significant. With some exceptions, the overall trend is that more extensive drinking patterns are associated with lower health care use. CONCLUSIONS: Based on our sample, we find little evidence that alcohol use is associated with increased health care utilization. On the contrary, we find that alcohol use is generally associated with decreased health care utilization regardless of drinking pattern.

Adult↗
PubMed1995

Hon v. Stroh Brewery Company: what do we mean by "moderate" and "heavy" drinking?

Although widely used, drinking terms such as "light,"' "moderate," and "heavy" are unstandardized and, as a result, public health messages using these terms may convey confusing information. As an initial attempt in providing such standardization, the present study surveyed public definitions for these terms. "Light" drinking was operationally defined as 1.4-2.4 drinks/day; "moderate" drinking was defined as 2.5-3.6 drinks/day; and "heavy" drinking was defined as 3.7 drinks/day and above. These ranges, however, were dependent on the respondent's gender, age, socioeconomic status, and especially the respondent's self-reported tolerance. Males had a higher threshold of consumption for "moderate" and "heavy" drinking than women. Older respondents likewise assigned a higher threshold for these terms than younger respondents. As respondent income increased, the threshold for "heavy" drinking decreased. The heaviest drinkers had a higher threshold for assigning the "heavy" label than did any other group. Ethnicity did not significantly affect these ranges, and religion only affected the threshold for "heavy" drinking. Because reseachers ultimately rely on terms such as "moderate" or ":heavy" to communicate their findings to colleagues and the public, it would seem apposite for them to agree on operational definitions for such terms. It would also seem appropriate to consider the operational definitions the public uses when referring to these terms to promote credibility of research findings and appropriate changes in behavior.

Adult↗
PubMed1995

Development and initial validation of a measure of drinking urges in abstinent alcoholics.

Although drinking urges and cravings are commonly reported by alcoholics, prospective studies have found inconsistent associations between such urges and drinking relapses. Previous studies have measured drinking urges by use of single-item ratings of alcohol craving or other measures of unknown reliability and validity. To permit improved evaluation of hypotheses regarding alcohol craving, a 49-item questionnaire that reflects several urge-related domains was developed and pretested. Items assessed subjects' desire for a drink, expectations of positive effects following drinking, relief of withdrawal and negative affect following drinking, and intention to drink. Exploratory and confirmatory factor analyses of the responses of 351 abstinent, treatment-seeking alcoholics indicated that alcohol urges are best described by a single factor. Based on these analyses, an internally consistent, reliable, and psychometrically valid 8-item scale, the Alcohol Urge Questionnaire (AUQ), was developed. Data indicated that AUQ scores were strongly related to alcohol dependence severity and to cognitive preoccupation with alcohol, and that they declined with prolonged abstinence. The AUQ may be useful in alcoholism treatment research and in laboratory studies of reactivity to alcohol or other manipulations.

Adult↗
PubMed2004

Ethnic variation in drinking, drug use, and sexual behavior among adolescents in Hawaii.

This study examined ethnic differences in substance use and sexual behavior and whether drinking and drug use constitute risk factors for unsafe sexual practices among Native Hawaiian (NH), Caucasian, and Asian/Pacific Islander (API) high school students in Hawaii. A secondary data analysis of the Youth Risk Behavior Survey (1997 and 1999) using a representative sample of 2,657 students in 9-12 grades was performed. Chi-square tests for bivariate associations and multivariate regression analyses were conducted to identify predictors. NHs were more sexually active, initiated sex earlier, and tended to have multiple partners. Alcohol lifetime use was higher in NH, Caucasians, and males. NHs were more likely to initiate drinking by age 12 and engage more in episodic drinking. Non-episodic or episodic drinkers and students who use drugs were at risk to engage in sexual activity, have multiple partners, and use alcohol/drugs during sex. Risk was two times higher for substance use during sex if drinking was initiated at age 10 or younger compared to 15 years or older. Compared to abstainers, the risk doubled for lifetime multiple partners if drinking was initiated at ages 13-14. Overall, females were more sexually active. Because drinking was associated with sexual initiation and risky behavior, adverse effects of alcohol must be addressed in programs targeting underage drinking, thus helping youth delay or minimize sexual activity and prevent other associated problems. Intervention efforts should enhance life skills that endorse abstinence from alcohol and drug use.

Adolescent↗
PubMed1974

Drinking induced by injections of angiotensin into forebrain and mid-brain sites of the monkey.

1. Unilateral and bilateral injections of 1.0 mul. solutions of angiotensin II into specific brain sites produced copious drinking of water in the water-replete rhesus monkey (Macaca mulatta).2. Of six brain regions in seven monkeys into which a total of 368 microinjections of angiotensin II were made, three were sensitive to angiotensin II. In decreasing order of sensitivity, they were (i) a rostral zone that included the septum, the anterior hypothalamus and the preoptic region, (ii) a caudal zone consisting of the mesencephalic central grey, and (iii) the lateral and third ventricles near the foramen of Monro. Of the regions tested, those that were relatively inactive included (i) the mid line thalmus, (ii) the mid-brain reticular formation, and (iii) metencephalic points in the cerebellum, the 4th ventricle and the dorsal aspect of the pons.3. Bilateral microinjections of angiotensin II into the sensitive regions in doses as low as 0.75-6 ng were dipsogenic and, with increasing doses, drinking occurred in a dose-dependent fashion up to 500 ng, after which the amount drunk levelled off or was reduced. The dose-response curve for unilateral microinjections began at 12.5 ng, and at doses higher than 50 ng unilateral and bilateral microinjections were equipotent.4. The onset of drinking (without eating) averaged 2.1-3.2 min following the end of microinjections for all sensitive tissue sites. Injections into the ventricles produced significantly longer drinking latencies.5. Angiotensin I elicited drinking in amounts comparable to angiotensin II at a dose of 100 ng whereas analogues of angiotensin II were weak dipsogens. Of the three analogues tested, Phe(4), Tyr(8)-angiotensin II was the most potent dipsogen, followed by Ile(8)-angiotensin II. The 1-7 heptapeptide, des-Phe(8)-angiotensin II was an ineffective dipsogen. Carbachol microinjected into the most sensitive angiotensin drinking sites had no dipsogenic action in the water-replete monkey.6. Tachyphylaxis to angiotensin II was demonstrated as a reduction in mean water intake of 55 and 74 per cent on the second and third microinjections, respectively. This reduction appeared to be due to dilutional inhibition or signals from the amount of water ingested on the first microinjection of angiotensin II.7. Monkeys drank an amount equal to a normal daily intake following two to three microinjections of angiotensin II in doses of 100-250 ng into sensitive regions. This extra water load caused no reductions in normal daily water intake either for the remainder of the experimental day or 24 hr later.8. Pre-treatments with microinjections of an angiotensin-converting enzyme inhibitor, SQ 20,881, did not reduce the dipsogenic action of angiotensin I, suggesting that this and perhaps other peptide precursors act directly on receptor mechanisms to produce drinking. Attempts to change the polydipsic effects of angiotensin II were unsuccessful with pre-treatments of intracranial microinjections of either haloperidol, Ile(8)-angiotensin II or carbachol.9. Microinjections of angiotensin II dissolved in hypertonic saline solutions had no influence on water intake when compared with the same dose dissolved in distilled water or isotonic saline.10. Yawning was the only other response that appeared to be related directly to intracranial injections of angiotensin II. In some instances, a hyperactive state of the animal followed intraventricular injections of angiotensin II. In other instances, intracranial microinjections of angiotensin II were followed by quietude or e.e.g. and behavioural signs of light sleep.11. This work further confirms the findings of previous research which showed that angiotensin II is the most potent dipsogen in all species tested to date. This endogenous peptide appears to participate in natural thirst by acting on central mechanisms of extracellular thirst.

Angiotensin II↗
PubMed1975

Drinking behaviour in the cat induced by renin, angiotensin I, II and isoprenaline.

1. Angiotensin I, II and hog renin, infused into the lateral cerebral ventricles (I.C.V.) of water replete cats, each induced water drinking behaviour. 2. Intravenous infusion of high doses of angiotensin I or II also elicited a drinking response. The dipsogenic effect of I.V. renin was not marked. 3. Drinking in response to I.C.V. angiotensin II was abolished after autonomic ganglion blockade with I.V. hexamethonium or pempidine and was significantly reduced after I.V. atropine methonitrate. 4. The dipsogenic response to I.C.V. angiotensin II was unaffected by either peripheral adrenergic neurone blockade with I.V. bethanidine, alpha-adrenoceptor blockade with phentolamine or beta-adrenoceptor blockade with sotalol. 5. Atropine, atropine methonitrate, hexamethonium and pempidine given I.C.V did not inhibit the diposgenic response to I.C.V. angiotensin II. 6. Bethanidine I.C.V. produced a dose related reduction in the dipsogenic response to I.C.V. angiotensin II. 7. The alpha-adrenoceptor blocking agents tolazoline and phenoxybenzamine given I.C.V did not affect angiotensin induced drinking but the response was regularly inhibited by phentolamine I.C.V. 8. The beta-adrenoceptor blocking agents propranolol and practolol given I.C.V. each inhibited angiotensin induced drinking. The L-isomer of propranolol was a more effective blocker than the D-isomer. 9. Isoprenaline given I.C.V induced drinking in ten of sixteen cats. Subcutaneous administration of isoprenaline also elicited drinking but the onset of the response was delayed and the amount consumed slightly less than after I.C.V infusion.

Angiotensin II↗
PubMed1979

The role of circulating renin in drinking in response to isoprenaline.

1. In nephrectomized rats, S.C. (0.12 mg. kg body wt.(-1)) or intracerebroventricular (I.C.V.: 0.03 mg. kg(-1)), isoprenaline failed to elicit drinking. However, when preceded (5-20 min) by a non-dipsogenic dose of I.V. pig renin, S.C. isoprenaline induced a marked, and I.C.V. isoprenaline a smaller drinking response. 2 hr after I.V. renin, S.C. isoprenaline no longer caused drinking.2. Pig renin did not enhance drinking in response to 0.12 mg. kg(-1) isoprenaline S.C. in intact or sham-operated rats.3. Isoprenaline (0.12 mg. kg body wt.(-1), S.C.) caused a larger fall of blood pressure in unanaesthetized nephrectomized than in intact unanaesthetized rats, but it was not the resulting hypotension that interfered with the nephrectomized rats' ability to drink, since intact rats with similar falls in blood pressure drank avidly in response to large doses of isoprenaline.4. Since the rate of inactivation of pig renin in nephrectomized rats was not modified by isoprenaline, drinking in nephrectomized animals in response to renin+isoprenaline was not attributable to increased plasma renin levels.5. Since isoprenaline induces drinking in the presence of circulating renin, but in the absence of renin release from kidneys, renin plays a permissive role in isoprenaline-induced drinking. Angiotensin and isoprenaline may interact at the level of intracranial receptors.

Animals↗
PubMed1982

The effects of changes in osmolality and sodium concentration on angiotensin-induced drinking and excretion in the pigeon.

1. The pigeon drank copiously after a short latency in response to intracerebro-ventricular (I.C.V.) infusion of angiotensin II dissolved in isotonic NaCl. There were small, insignificant increases in urinary excertion so that the increased water intake caused the pigeon to go into positive fluid balance. Water was chosen in preference to 0.3 M-NaCl, which was also available to drink in these experiments.2. I.C.V. infusion of angiotensin dissolved in water, or in isotonic or hypertonic solutions of non-eletrolytes, or in KCl or CaCl(2) resulted in about half the water intake produced by angiotensin dissolved in isotonic NaCl.3. I.C.V. infusion of hypertonic NaCl alone caused drinking. I.C.V. infusion of angiotensin dissolved in hypertonic NaCl caused an amount of water to be drunk that was a simple addition of the amounts drunk in response to angiotensin dissolved in isotonic NaCl and to the extra amount of NaCl.4. Drinking in response to I.C.V. infusion of two other dipsogenic peptides, eledoisin and physalaemin, was similarly affected by the composition of the solutions in which they were dissolved.5. The pigeon also drank in response to intravenous (I.V.) infusion of angiotensin II dissolved in isotonic NaCl. Urine flow and sodium excretion increased markedly so that the pigeons just maintained fluid balance.6. In contrast to the reduction in intake when angiotensin was infused I.C.V. dissolved in hypertonic non-electrolytes, I.V. infusions of angiotensin dissolved in hypertonic non-electrolytes caused enhanced drinking, compared with the corresponding infusions of angiotensin dissolved in isotonic NaCl.7. Drinking induced by I.V. infusion of angiotensin was little affected by simultaneous I.C.V. infusion of isotonic or hypertonic sucrose, or water, but it was increased by simultaneous I.C.V. infusion of hypertonic NaCl.8. Drinking responses were partly additive when angiotensin was given by simultaneous I.C.V. and I.V. infusion.9. The increased urine flow and electrolyte excretion in response to I.V. infusion of angiotensin were little affected by simultaneous I.C.V. infusion of angiotensin.10. These experiments suggest that in the pigeon there may be separate sets of receptors in the cerebral ventricles for initiating drinking, one set responding to angiotensin, another to hypertonic NaCl. Outside the blood-brain barrier, and accessible to blood-borne substances, there may also be separate sets of receptors, one set responding to angiotensin, another to increases in effective osmolality of the blood.

Angiotensin II↗
PubMed1986

Plasma expansion does not precipitate the fall in plasma vasopressin in humans drinking isotonic fluids.

In a group of healthy humans, plasma vasopressin (AVP) levels fell on drinking either Tyrode or mannitol solutions isosmotic with plasma. Both the timing and magnitude of the fall were appropriate to account for the transient diuresis which followed the drinking. Although plasma expansion follows drinking Tyrode solution it occurred too late to account for the fall in plasma AVP. It was also too small to inhibit AVP secretion. Even though plasma volume tended to contract on drinking isosmotic mannitol solution a fall in plasma AVP and a diuresis occurred, similar to those found after drinking Tyrode solution. These findings appear to eliminate plasma volume expansion as the stimulus for the fall in plasma AVP and the associated diuresis on drinking isotonic fluids. In a further group of human subjects, bypassing the oropharynx by intragastric infusion resulted in a slower onset of diuresis after a water load. We suggest that receptors, as yet undefined, in the upper gastrointestinal tract contribute to the early stages of a water diuresis and account for the apparently inappropriate transient diuresis which follows the drinking of isotonic fluids.

Adult↗
PubMed1981

Smoking and drinking by middle-aged British men: effects of social class and town of residence.

In 7735 men aged 40-59, selected at random from general practices in 24 towns throughout Britain, pronounced differences were noted in the prevalences of smoking and drinking between the social classes. Social class differences also existed for frequency and quantity of drinking, type of beverage, and several aspects of smoking behaviour. Increasing amounts of smoking were associated with higher prevalences of moderate to heavy drinking, particularly in daily rather than weekend drinkers. Between drinking groups, however, the relation with smoking was more U-shaped, with light and heavy drinkers smoking more than moderate drinkers. The lowest rates of moderate to heavy smoking were observed in frequent light drinkers, particularly in the nonmanual workers. The proportion of moderate to heavy drinkers was no higher among ex-cigarette smokers than among current smokers. When the data were examined by town of residence social class differences persisted. Controlling for social class still showed pronounced differences between towns in both smoking and drinking behaviour. These data confirm that town of residence and social class have independent effects on smoking and drinking. The established regional and social class differences in cardiovascular disease may be due in part to the independent influences of town and social class on smoking and drinking behaviour.

Adult↗
PubMed1988

Kainic acid lesions of the median preoptic nucleus: effects on angiotensin II induced drinking and pressor responses in the conscious rat.

Input to the nucleus medianus of the preoptic region has been suggested to be involved in both the drinking and pressor responses elicited by the central administration of angiotensin II. Evidence in support of this suggestion has been gained principally from electrical lesion experiments. This lesion procedure does not differentiate between the cells of the region and fibers coursing through the region. To test the hypothesis that cells in this region are involved in both the pressor and drinking responses elicited by central administration of angiotensin II, injections of kainic acid were made to induce lesions of the cells, while sparing fibers of passage. Drinking and blood pressure responses were determined pre- and post-lesion in the chronically instrumented awake rat. Injections of 50 ng angiotensin II in a 2-microL volume into a lateral cerebral ventricle of the conscious rat elicited pronounced drinking and pressor responses with a latency of 3-5 min. Lesions of the median preoptic region produced by injecting 1.0 microgram of kainic acid in 0.25 microL for 15 s attenuated or blocked the drinking response and increased the latency to drink induced by central injections of angiotensin II. However, kainic acid lesions did not significantly alter the pressor responses produced by angiotensin II administration. These results suggest that cells in the median preoptic region are involved in the drinking response but do not participate in the pressor response elicited by angiotensin II administration into a lateral cerebral ventricle of the conscious rat.

Angiotensin II↗
PubMed2002

Differential regulation of adrenal corticosteroids after restriction-induced drinking in rats.

Water-restricted rats exhibit a rapid decrease in plasma corticosterone after drinking. The present study examined the effect of restriction-induced drinking on plasma aldosterone and plasma clearance of corticosterone. Rats were water restricted for 6-7 days and then killed before or 15 min after water administration; plasma and adrenal hormones were assayed. Plasma and adrenal corticosterone decreased after drinking without a change in plasma corticosteroid-binding globulin; plasma ACTH decreased or did not change. In contrast, plasma aldosterone did not change or increased after drinking; plasma renin activity was elevated by water restriction and increased further after drinking. In another experiment, rats were adrenalectomized, and corticosterone and aldosterone were replaced with pellets and osmotic minipumps, respectively. Rats were water restricted and killed. There was a small decrease in plasma corticosterone but no change in aldosterone after drinking in adrenalectomized animals. These data suggest that changes in plasma steroids after restriction-induced drinking result from zone-specific responses of the adrenal to known secretagogues, with minimal contribution from increased plasma clearance.

Adrenal Glands↗
PubMed2005

Cardiovascular responses to water drinking: does osmolality play a role?

Water drinking activates the autonomic nervous system and induces acute hemodynamic changes. The actual stimulus for these effects is undetermined but might be related to either gastric distension or to osmotic factors. In the present study, we tested whether the cardiovascular responses to water drinking are related to water's relative hypoosmolality. Therefore, we compared the cardiovascular effects of a water drink (7.5 ml/kg body wt) with an identical volume of a physiological (0.9%) saline solution in nine healthy subjects (6 male, 3 female, aged 26 +/- 2 years), while continuously monitoring beat-to-beat blood pressure (finger plethysmography), cardiac intervals (electrocardiography), and cardiac output (thoracic impedance). Total peripheral resistance was calculated as mean blood pressure/cardiac output. Cardiac interval variability (high-frequency power) was assessed by spectral analysis as an index of cardiac vagal tone. Baroreceptor sensitivity was evaluated using the sequence technique. Drinking water, but not saline, decreased heart rate (P = 0.01) and increased total peripheral resistance (P < 0.01), high-frequency cardiac interval variability (P = 0.03), and baroreceptor sensitivity (P = 0.01). Neither water nor saline substantially increased blood pressure. These responses suggest that water drinking simultaneously increases sympathetic vasoconstrictor activity and cardiac vagal tone. That these effects were absent after drinking physiological saline indicate that the cardiovascular responses to water drinking are influenced by its hypoosmotic properties.

Administration, Oral↗
PubMed1981

Separation of drinking and pressor responses to central angiotensin by monoamines.

This study investigated the neurotransmitters involved in the increase in blood pressure and drinking produced when angiotension II is injected intraventricularly (ivt). Using pharmacologic manipulations of the monoamines norepinephrine, dopamine, and serotonin it has been possible to separate the pressor response from dipsogenic responses to angiotension II. Alpha-adrenergic blockade with phentolamine restricted to the brain blocked the pressor response to angiotensin II in a dose-related manner, while drinking remained unaffected. Norepinephrine alone, injected into the ventricles elevated blood pressure, but did not produce drinking. The norepinephrine effect was also blocked by phentolamine by the same ventricular route. Other monoamines were not involved. Dopamine alone did not produce thirst. Cardiovascular effects with dopamine were observed only with large doses. The dopaminergic agonist apomorphine produced no change in blood pressure or drinking. Reduction of central serotonin stores by p-chlorophenylalanine intraperitoneally or 5,7-dihydroxytryptamine intraventricularly had no effect on the pressor or dipsogenic effects of angiotensin II. The serotonin agonist N,N-dimethyl-5-methoxytryptamine ivt did not produce a rise in blood pressure or drinking. It is concluded that the pressor effect of angiotensin II, but not the drinking effect is mediated by noradrenergic stimulation of alpha-receptors. The drinking response does not appear to be mediated by the monoamines.

Angiotensin II↗
PubMed1983

Influence of daily sodium intake on vasopressin secretion and drinking in dogs.

Studies were carried out to determine the relationship between daily sodium intake, drinking, and vasopressin (AVP) secretion in normal conscious dogs. Chronic responses to 5-day elevations of daily sodium intake (200 meq/day) and 2-wk decreases in daily sodium intake (5 meq/day) were determined. Dogs were studied with ad libitum drinking and with water intake restricted to the amount drunk during the normal-sodium (30 meq/day) control period. Although acute elevations of plasma AVP occurred after a normal (40 meq Na) gastric load, chronic high-sodium intake resulted in no change of steady-state plasma AVP levels or daily AVP excretion (UAVP) with ad libitum drinking. Total water intake and frequency of drinking, however, increased nearly fourfold. In the absence of excess drinking, plasma AVP and UAVP both exhibited a nearly sixfold increase during the period of high-sodium intake. Despite elevations of plasma AVP, daily urine volume increased and urine osmolality rose only gradually during the 5 days of high-sodium intake. Chronic low-sodium intake also did not alter plasma AVP, but total water intake was reduced 20%. The data indicate that with water available, extracellular osmolality is controlled predominantly by drinking rather than by AVP secretion, that either osmolality or sodium concentration is the predominant controller of drinking and AVP secretion, and that daily water excretion need not be related directly to plasma AVP.

Animals↗
PubMed1990

Spontaneous drinking: is it stimulated by hypertonicity or hypovolemia?

Ten young female pigs were allowed to eat and drink whenever they wanted, and blood samples were taken without disturbance to the pig. Samples were divided into four categories: 1) base line, i.e., taken when not drinking and not eating; 2) preprandial, i.e., taken when starting to drink just before eating; 3) postcibal, i.e., taken when starting to drink after any eating; and 4) nonprandial, i.e., taken when starting to drink but not in association with eating. Osmolality (mosmol/kgH2O), plasma protein (g/dl), and packed cell volume (%) were, respectively, as follows (mean +/- SE): base line 294.9 +/- 1.8, 6.2 +/- 0.1, and 30.0 +/- 1.2; preprandial 295.1 +/- 1.7, 6.1 +/- 0.2, and 29.7 +/- 1.4; postcibal 295.0 +/- 3.3, 6.5 +/- 0.2, and 31.7 +/- 1.3; and nonprandial 295.2 +/- 1.4, 6.3 +/- 0.1, and 30.0 +/- 1.3. None of the parameters associated with drinking were significantly different from base-line parameters, except for the postcibal rise of packed cell volume. Calculated blood volume differences from base line were as follows: preprandial 0.7 +/- 1.2% fall; postcibal 0.2 +/- 1.7% increase; and nonprandial 0.8 +/- 0.9% fall. It is unlikely that either plasma hypertonicity or hypovolemia stimulates drinking under spontaneous conditions.

Animals↗
PubMed1990

Circulating angiotensin II and drinking behavior in rats.

This study was designed to investigate the effects on water drinking of acute and chronic increases in circulating angiotensin II (ANG II) concentrations in rats. Experiments were conducted in male Sprague-Dawley rats chronically instrumented with femoral arterial and venous catheters and permanently housed in metal metabolism cages. ANG II was infused intravenously either acutely (30 min-2 h) or chronically (3 days) in a dose range of 10-60 ng/min. In no instance did such infusions cause a statistically significant increase in water intake. Other experiments examined the influence of ANG II (10 ng/min iv) on drinking elicited by infusion of hypertonic sodium chloride (1.5 M at 3.5 microliters/min). ANG II administration did not increase drinking to a hypertonic saline stimulus or lower the osmotic threshold for drinking. Nitroprusside (12 micrograms/min) was infused for 30 min to produce hypotension and drinking. Water intake associated with this stimulus was not changed by blocking ANG II formation with enalapril (2 mg/kg iv) or by concomitant infusion of ANG II (10 ng/min iv). Finally, plasma ANG II concentrations were measured before and after 1-h intravenous infusion of saline or ANG II to determine the levels of circulating ANG II produced by the infusion rates used here. It is concluded that the range of circulating ANG II concentrations found under most physiological conditions in rats does not directly stimulate drinking or participate importantly in osmotic or hypotension-induced drinking.

Angiotensin II↗