Biomedical subjects

F S Kraly

Publications and source records attributed to F S Kraly.

At least 19 recordsLinked to original sources

PubMed1999

Histaminergic activation of endogenous angiotensin II fails to inhibit alcohol intake in rats.

Demonstrations that alcohol intake can be inhibited by pharmacological activation of the renal renin-angiotensin system (RRA) or injection of angiotensin II (ANG II) in rats led to this study of a role for endogenous ANG II in inhibition of alcohol intake in rats. Relatively small doses of histamine, above threshold for eliciting drinking of water and activation of the RRA, were injected SC in adult male Sprague-Dawley rats with access to 3.0% alcohol in 45-min one-bottle alcohol tests and in two-bottle tests in which alcohol and water were available at the midpoint of the 12-h dark phase. The 0.312 and 1.25 mg/kg doses of SC histamine elevated plasma renin activity to levels similar to those in rats that had just eaten food. Neither dose of histamine affected alcohol intake in one-bottle tests. A relatively large 10 mg/kg dose of histamine increased alcohol intake in a one-bottle test, but decreased alcohol intake and increased water intake in two-bottle tests. The inhibitory effect of the 10 mg/kg dose of histamine on alcohol intake was completely blocked by SC 10 mg/kg losartan, a selective AT1 angiotensin receptor antagonist. This 10 mg/kg dose of losartan given alone, however, failed to increase alcohol intake in one- or two-bottle tests. These results generally do not support a role for endogenous ANG II as an inhibitory physiological signal in the control of alcohol ingestion in rats, because histaminergic activation of RRA, using small but physiologically meaningful doses of histamine, failed to inhibit alcohol intake.

Alcohol Drinking↗

PubMed1998

H2 histaminergic control of inhibition of eating induced by intragastric NaCl in rats.

A role for endogenous histamine and histamine receptor subtypes in mediating the inhibition of eating induced by intragastric (i.g.) hypertonic NaCl was examined in adult male Sprague-Dawley rats surgically equipped with a chronic gastric catheter. The i.g. infusion of 2 mL 900 or 1,800 mOsm/kg of NaCl inhibited: 1) ingestion of pellets in rats eating after 24-h food deprivation; and 2) ingestion of cookies in rats eating without prior deprivation. The H1 receptor antagonists dexbrompheniramine (DXB; 1 mg/kg) and pyrilamine (PYR; 4 mg/kg) did not attenuate the inhibitory effects of i.g. 900 or 1,800 mOsm/kg of NaCl for rats eating pellets and for rats eating cookies. The H2 antagonists cimetidine (CIM; 16 mg/kg) and metiamide (MET; 16 mg/kg) attenuated the inhibitory effects of i.g. 1,800 mOsm/kg of NaCl upon ingestion of cookies, but intracerebroventricular (i.c.v.) infusion (through a chronic indwelling cannula) of 100 microg of CIM did not mimic this effect of intraperitoneal (i.p.) CIM. The i.p. CIM failed to attenuate the inhibition of eating cookies produced by i.p. octapeptide of cholecystokinin (CCK-8; 3 microg/kg). The H3 antagonist thioperamide (TH; 10 mg/kg i.p.) and the H3 agonist R-alpha-methylhistamine (RAM; 3 mg/kg i.p.) did not alter the inhibitory effect of i.g. 1,800 mOsm/kg of NaCl for rats eating cookies. Combined treatments of systemic DXB plus CIM, and DXB plus CIM plus thioperamide (TH) did not reverse the inhibitory effects of i.g. 1,800 mOsm/kg of NaCl upon ingestion of cookies. Finally, i.p. DXB, but not CIM, attenuated the ability of i.g. 900 mOsm/kg of NaCl to increase water intake; conversely, i.p. CIM, but not DXB, attenuated the ability of i.g. 900 mOsm/kg of NaCl to inhibit eating of cookies. These findings demonstrate a double dissociation of effects upon ingestive behavior: H1, but not H2, antagonism attenuates the effect of i.g. hypertonic NaCl on water intake, whereas H2, but not H1, antagonism attenuates the inhibition of eating produced by i.g. hypertonic NaCl. These results demonstrate that different subtypes of peripheral and/or central histamine receptors contribute to different behavioral consequences of postprandial gastrointestinal osmotic loads in rats.

Animals↗

PubMed1996

H1, H2, and H3 receptors contribute to drinking elicited by exogenous histamine and eating in rats.

Roles for H1, H2, and H3 receptor subtypes for drinking elicited by exogenous histamine and drinking elicited by eating was examined in adult male Sprague-Dawley rats. Drinking elicited by SC 5 mg/kg histamine was: (a) inhibited approximately 30% by H1 antagonism using IP 1 mg/kg dexbrompheniramine (DXB); (b) inhibited approximately 30% by H2 antagonism using IP 16 mg/kg cimetidine (C); (c) inhibited approximately 40% by H3 antagonism using SC 10 mg/kg thioperamide (Th); (d) inhibited approximately 80% by combined H1 and H2 antagonism using IP DXB plus IP C; (e) inhibited approximately 85% by combined H1 and H3 antagonism using IP DXB plus SC Th; (f) inhibited approximately 70% by combined H2 and H3 antagonism using IP C plus SC Th; and (g) abolished by combined H1, H2, and H3 antagonism using IP DXB plus IP C plus SC Th. For rats eating pellets and drinking after 24-h food deprivation: (a) systemic injections of DXB, C, and Th, sufficient to abolish drinking elicited by SC histamine, inhibited water/food ratio (W/F) by approximately 20%; (b) ICV injections (through a chronic cannula in a lateral ventricle) of 50 micrograms DXB plus 100 micrograms C plus 60 micrograms Th inhibited W/F by approximately 20%. For rats drinking after IG infusion (through a chronic gastric catheter) of 2 ml 1,800 mOsm/kg NaCl: (a) systemic injections of DXB, C, and Th, sufficient to abolish drinking elicited by SC histamine, inhibited water intake by approximately 70%; (b) IP DXB alone and IP C alone failed to inhibit water intake; (c) IP Th alone inhibited water intake by approximately 20%; (d) IP DXB combined with IP C inhibited water intake by approximately 55%. The results demonstrate the involvement of H1, H2, and H3 receptors for drinking elicited by exogenous histamine, and our findings extend the evidence for a role for endogenous histamine and H1, H2, and H3 receptor subtypes for drinking elicited by eating, including drinking elicited by gastrointestinal osmotic consequences of eating that can increase systemic plasma osmolality.

Animals↗

PubMed1995

Histamine H3 receptors contribute to drinking elicited by eating in rats.

A role for endogenous histamine and its H3 receptor subtype for mediating drinking elicited by eating was examined in adult male Sprague-Dawley rats. The i.p. injection of the H3 agonist R-alpha-methylhistamine (Ramh, 2.5 mg/kg) shortened the latency to initiate drinking and increased 1-h water intake in nondeprived rats freely eating pellets and drinking water. The ICV injection (through a surgically implanted chronic cannula) of 10 micrograms Ramh increased water intake; this Ramh-induced drinking was abolished by previous ICV injection of the H3 antagonist thioperamide (Th, 60 micrograms). For rats drinking and eating after 24-h food deprivation, s.c. Th inhibited drinking behavior: for example, 10 mg/kg Th s.c. delayed the latency to initiate drinking and inhibited 1-h water intake without inhibition of food intake. In contrast, 60 micrograms Th ICV failed to inhibit food-related drinking in rats eating after food deprivation. For nondeprived rats eating a small cracker, 10 mg/kg Th s.c. delayed the latency to initiate drinking and abolished water intake without effect of eating, and 60 micrograms Th ICV had similar effects upon drinking elicited by ingestion of cracker. The IG infusion (through a surgically implanted gastric catheter) of 2 ml 600 or 900 mOsm/kg NaCl, a treatment that is subthreshold for increase in systemic plasma osmolality at the initiation of drinking, elicited drinking that was abolished by 10 mg/kg Th s.c. and attenuated by 60 micrograms Th ICV. The IG infusion of 2 ml 1800 mOsm/kg NaCl, a treatment that is above threshold for increase in systemic plasma osmolality, elicited drinking that was attenuated by 10 mg/kg s.c. or 60 micrograms Th ICV. These results demonstrate that peripheral and central H3 receptors for histamine have a role in drinking elicited by eating and the postprandial gastrointestinal osmotic consequences of eating. These findings extend the evidence demonstrating a histaminergic contribution to food-related drinking in rats.

Animals↗

PubMed1995

Angiotensin AT1 and AT2 receptors contribute to drinking elicited by eating in rats.

A role for endogenous angiotensin II and its AT1 and AT2 receptor subtypes for mediating drinking elicited by eating was examined in adult male Sprague-Dawley rats. The ability of pharmacological antagonism of AT1 and/or AT2 receptors to abolish drinking elicited by exogenous angiotensin II was established first. The s.c. injection of the AT1 antagonist losartan (DuP 753) was sufficient to abolish drinking elicited by s.c. angiotensin II. The ICV injection (through a surgically implanted chronic cannula) of losartan inhibited drinking elicited by ICV angiotensin II; the combined ICV injection of losartan plus the AT2 antagonist PD123319 was sufficient to abolish drinking elicited by ICV angiotensin II. For rats drinking and eating after 24-h food deprivation, s.c. losartan plus PD123319 inhibited water to food ratio, but ICV losartan and/or PD123319 failed to inhibit food-related drinking. For nondeprived rats eating a small cracker, s.c. losartan and/or PD123319 attenuated water intake, but only ICV losartan produced statistically significant inhibition of drinking elicited by ingestion of cracker. The IG infusion (through a surgically implanted gastric catheter) of 2 ml 600 or 900 mOsm/kg NaCl, a treatment that is subthreshold for increase in systemic plasma osmolality at the initiation of drinking, elicited drinking that was attenuated by s.c. losartan and/or PD123319 and attenuated by ICV losartan only. The IG infusion of 2 ml 1800 mOsm/kg NaCl, a treatment that is above threshold for increase in systemic plasma osmolality at the initiation of drinking, elicited drinking that was not inhibited by S or ICV losartan and/or PD123319. These results demonstrate that peripheral AT1 and AT2 and central AT1 receptors for angiotensin II contribute to drinking elicited by eating and the gastrointestinal osmotic consequences of eating. These findings extend the evidence demonstrating a renal renin-angiotensin contribution to food-related drinking in rats.

Angiotensin II↗

PubMed1995

Renal nerve transection inhibits drinking elicited by eating and by intragastric osmotic loads in rats.

Adult Sprague-Dawley male rats surgically equipped with a chronic gastric catheter were tested for drinking after 2 ml intragastric infusions of 290, 600, 900, 1200, or 1800 mOsm/kg Nacl. Rats with bilateral transection of renal nerves (RD) drank less than neurologically intact rats (S) after 600 and 900 mOsm/kg NaCl infusions. The RD rats were capable of a rapid and robust drinking response to relatively mild experimental challenges, because they drank appropriately in response to s.c. angiotensin II and to dose of histamine that is a threshold dose for increasing water intake. The RD rats ate less than S rats, but RD rats drank appropriate amounts of water when eating and drinking after 24-h food deprivation. When nondeprived and ingesting one, two, or four small (0.57 g) salted crackers, the RD rats drank significantly less water than S rats. At the time drinking was initiated after ingestion of one salted cracker, plasma osmolality, sodium, protein, and packed cell volume were not changed from baseline conditions (i.e., no eating) in neurologically intact rats; plasma renin activity was significantly elevated at the time drinking was initiated following the ingestion of one or two small crackers. These findings (a) demonstrate a role for renal nerves in drinking behavior in rats, and (b) suggest the working hypothesis that the ingestion of a small meal, and the subsequent delivery of a relatively small osmotic load to the gastrointestinal tract and/or hepatic-portal vein, activates mechanisms for drinking that include a change in activity of renal nerves to increase plasma renin activity without cellular dehydration or hypovolemia. Such mechanisms may be activated to mobilize drinking behavior in advance of postprandial fluid deficit.

Angiotensin II↗

PubMed1995

Endogenous histamine contributes to drinking initiated without postprandial challenges to fluid homeostasis in rats.

A role for endogenous histamine and its receptor subtypes for mediating drinking elicited by eating was examined in adult male Sprague-Dawley rats in two experimental paradigms in which drinking was initiated without accompanying change in systemic fluid balance: (a) nondeprived rats eating a small (0.57 g) salted cracker; (b) nondeprived rats receiving IG infusion (through a chronic gastric catheter) of 2 ml 900 mOsm/kg NaCl. The ability of i.p., s.c., or ICV (through a surgically implanted chronic cannula in a lateral ventricle) injections of antagonists to H1, H2, or H3 receptors for histamine to inhibit drinking was examined. For rats ingesting a small cracker: systemic injection of H1 antagonists dexbrompheniramine (DXB) or pyrilamine (PYR) delayed the latency to initiate drinking. Systemic injection of H1 antagonists DXB, PYR, or terfenadine (TER; which fails to penetrate the blood-brain barrier) and ICV injection of DXB or PYR inhibited water intake. The H2 antagonist cimetidine (C) given i.p. or ICV failed to affect drinking. The H3 antagonist thioperamide (Th) given s.c. or ICV delayed the latency to drink and inhibited water intake. For rats receiving IG NaCl: systemic injection of H1 antagonists DXB or PYR or the H3 antagonist Th inhibited water intake, but the H2 antagonist C failed to inhibit drinking. Our findings extend the evidence for the involvement of endogenous histamine in drinking elicited by eating in rats by suggesting roles for peripheral and brain H1 and H3 receptors for drinking initiated by postprandial gastrointestinal osmotic consequences that are subthreshold for changes in systemic fluid balance.

Animals↗

PubMed1995

Drinking after intragastric NaCl without increase in systemic plasma osmolality in rats.

Drinking after intragastric hypertonic solutions was examined to determine whether increased plasma osmolality always accompanied initiation of drinking. A 2-ml infusion through a gastric catheter was the beginning of tests in Sprague-Dawley male rats. Latency to drink was shorter and 1-h water intake was greater for increasing concentrations of NaCl (600, 1,200, and 1,800 mosmol/kg) compared with baseline (290 mosmol/kg). Although 600, 900, or 1,200 mosmol/kg NaCl elicited drinking, such infusions failed to change systemic plasma osmolality, and 900 mosmol/kg also failed to change plasma sodium, protein, renin activity, or packed cell volume at the initiation of drinking. Intragastric 900 mosmol/kg sodium bicarbonate, sodium isethionate, potassium chloride, lithium chloride, and mannitol differentially increased water intake. Total subdiaphragmatic vagotomy abolished drinking elicited by intragastric NaCl; selective gastric or hepatic vagotomy attenuated intake under some conditions. These results support the hypothesis of a vagally mediated, gastrointestinal and/or hepatic-portal, osmosensitive mechanism for initiation of drinking in advance of postprandial increases in systemic osmolality.

Animals↗

PubMed1991

Separate controls for conditioned cephalic phases of acid secretion and drinking in the rat.

Adult male Sprague-Dawley rats, surgically equipped with a stainless steel gastric cannula, were tested in a paradigm known to support conditioning of cephalic phase gastric acid secretion. Rats were tested first under (a) baseline conditions--prepared to sham feed, but no food was offered and none should have been expected; then (b) 5 conditioning trials--prepared and allowed to sham feed sweetened milk; and finally (c) extinction trials--prepared to sham feed milk, but milk was not offered. Combined antagonism of H1 and H2 histamine receptors (using intraperitoneal dexbrompheniramine plus cimetidine) prevented the acquisition of conditioned cephalic phase of acid secretion, but had no effect on acquisition of conditioned water intake. Such histaminergic antagonism also blocked the expression of an established conditioned acid secretory response without effect on conditioned water intake; peripheral cholinergic blockade using atropine methyl nitrate had virtually the same effect as did histaminergic antagonism. The converse was observed following blockade of angiotensin II synthesis using subcutaneous captopril: Established conditioned secretion was unaffected, but conditioned water intake was inhibited. These results dissociate the physiological controls for conditioned responses which occur simultaneously in rats anticipating eating: Peripheral histamine mediates the acquisition and expression of the conditioned cephalic phase of acid secretion, whereas angiotensin II appears to mediate at least the expression of conditioned water intake.

Angiotensin II↗

PubMed1990

Histamine in brain may have no role for histaminergic control of food-related drinking in the rat.

Adult male Sprague-Dawley rats surgically fitted with a cannula positioned in the third cerebral ventricle were tested for drinking after exogenous histamine or after eating with or without antagonism of H1 and/or H2 receptors for histamine using intracerebroventricular (ICV) dexbrompheniramine (DXB; 12.5-50 micrograms) or cimetidine (C; 25-100 micrograms). Histamine (0.06-16 micrograms) given ICV failed to elicit drinking. For rats drinking in response to subcutaneous (SC) histamine, ICV DXB alone did not affect drinking, whereas ICV DXB plus C, and ICV C given alone inhibited drinking. Such inhibition appeared to be relatively selective for drinking elicited by SC histamine, because ICV 50 micrograms DXB plus 100 micrograms C abolished drinking elicited by SC histamine, but failed to inhibit drinking after 12-hr water deprivation. When rats ate and drank after food deprivation, ICV DXB alone and ICV DXB plus C did not significantly inhibit food-related water intake. The inhibition of food-related drinking by ICV 100 micrograms C given alone was accompanied by inhibition of eating. In summary, histamine had unimpressive dipsogenic effects when given ICV, ICV DXB and C inhibited drinking elicited by SC histamine, but ICV DXB and C failed to inhibit food-related drinking in a manner parallel to the selective effects of intraperitoneal injection of these drugs on drinking elicited by eating. This suggests that it is histamine and histamine receptors in the periphery rather than in brain that have the predominant role for a histaminergic mechanism for drinking elicited by eating in the rat, but our findings do not rule out a role(s) for histamine in brain in the control of ingestive behavior.

Animals↗

PubMed1990

Pregastric food-contingent stimulation elicits drinking in the absence of systemic dehydration in the rat.

Adult male Sprague-Dawley rats surgically fitted with a stainless steel gastric cannula were prepared following 24-h food deprivation for sham feeding liquid diet with open gastric fistula. Sham feeding (pregastric food-contingent stimulation) of 5, 10, 20 or 40 ml of liquid diet elicited water intake that was not in proportion to volume of liquid diet sham fed. Rats sham feeding between 1 and 68 ml of sweetened milk showed no evidence of cellular or extracellular dehydration as measured by plasma osmolality and hematocrit, respectively. Subcutaneous injection of 100 mg/kg captopril, a dose sufficient to block conversion of angiotensin I to angiotensin II in brain and periphery, inhibited drinking elicited by sham feeding without effect on sham feeding. These results demonstrate that pregastric food-contingent stimulation elicits water intake that is not in proportion to amount of liquid diet sham fed and that occurs in the apparent absence of systemic dehydration. That such drinking could depend upon endogenous angiotensin II provokes consideration of a role for angiotensin II in the mediation of a pregastric (perhaps histaminergic) mechanism that initiates drinking in advance of postprandial dehydration.

Angiotensin II↗

PubMed1990

Angiotensin II mediates drinking elicited by eating in the rat.

Captopril (CA) was used to block synthesis of endogenous angiotensin II (ANG II) in periphery and/or brain of adult male Sprague-Dawley rats in tests for drinking elicited by eating pelleted chow. Blockade of ANG II-converting enzyme (ACE) in periphery alone (using 0.5 mg/kg CA) increased drinking elicited by eating, whereas simultaneous blockade of ACE in periphery and brain (using subcutaneous 100 mg/kg CA or subcutaneous 0.5 mg/kg plus third ventricular 25 micrograms CA) decreased such drinking. The inhibitory effect of 100 mg/kg CA on water-to-food ratio was prevented by a dipsogenically subthreshold subcutaneous dose (5 micrograms/kg) of ANG II. Blockade of ACE in brain alone (third ventricular 25 micrograms CA) had no effect on food-related drinking. Pharmacological antagonism of ANG II (100 mg/kg CA) together with antagonism of histamine H1 and H2 receptors (using intraperitoneal dexbrompheniramine and cimetidine) were not additive in their inhibitory effects on drinking elicited by eating. Blockade of ACE (100 mg/kg CA) inhibited drinking elicited by subcutaneous histamine, but blockade of histamine receptors failed to inhibit drinking elicited by subcutaneous ANG II. These results support a role for endogenous ANG II under what appear to be physiological conditions for drinking behavior, i.e., when drinking is elicited by eating, and they suggest the working hypothesis of ANG II mediation of a histaminergic mechanism for food-related drinking in the rat.

Angiotensin II↗

PubMed1986

Specific postoperative syndromes after total and selective vagotomies in the rat.

Male Sprague-Dawley rats which survived bilateral subdiaphragmatic vagotomy (with hepatic branch intact) exhibited an acute syndrome of hypophagia, hypodipsia and severe loss of body weight when maintained on solid food and water for 14 days after vagotomy. This postvagotomy syndrome was attenuated when rats were maintained on a liquid diet (116EC) chosen to minimize postvagotomy dysphagia and abnormal gastric retention of food; vagotomized rats were hypophagic and lost body weight, but the degree of weight loss was not so severe as for vagotomized rats eating solid food. When rats with total subdiaphragramatic vagotomy were maintained on palatable sweet milk food, the acute postvagotomy syndrome was abolished; these vagotomized rats ate and drank as much as rats with sham vagotomy and they did not lose weight. When rats that underwent selective hepatic, gastric or coeliac vagotomy were maintained on the sweet milk diet, three different postoperative syndromes occurred: after selective hepatic vagotomy, rats were hyperphagic, hyperdipsic and gained body weight at a greater than normal rate; after selective gastric vagotomy, rats lost weight despite relatively normal food and water intakes; and after selective coeliac vagotomy, there was no change in food or water intakes or body weight. These results demonstrate that a sweet milk diet abolishes the anorexia, hypodipsia and weight loss that usually occur in vagotomized rats maintained on pellets and water. Use of this sweet milk diet revealed different acute syndromes after bilateral and selective vagotomies. The differences among the syndromes suggest that hepatic, gastric and coeliac vagal branches serve different functions in the control of food and water intake and body weight.

Animals↗

PubMed1985

Histamine and serotonin independently elicit drinking in the rat.

Drinking elicited by SC histamine or serotonin (5-HT) was studied in Sprague-Dawley male rats following 0.9% NaCl or combined antagonism of H1 and H2 histamine receptors using dexbrompheniramine (DXB) and cimetidine (C), or following antagonism of 5-HT receptors using methysergide (M). Histaminergic antagonism using IP 1 mg/kg DXB plus 16 mg/kg C abolished drinking elicited by SC 2.5 mg/kg histamine, but it failed to inhibit drinking elicited by the ED50 or by the ED100 for SC 5-HT in the same rats. Serotonergic antagonism using IP 3 mg/kg M abolished drinking elicited by SC 0.63 mg/kg 5-HT, but it failed to inhibit drinking elicited by the ED50 or by the ED100 for SC histamine in the same rats. These findings demonstrate that activation of peripheral 5-HT receptors is not necessary for SC histamine to elicit drinking and that activation of peripheral histamine receptors is not necessary for SC 5-HT to elicit drinking. This demonstrates that histamine and 5-HT activate different receptors to elicit drinking in the rat. The finding that the ED50 for histamine and the ED50 for 5-HT are not additive in their effects on drinking is consistent with the notion that a single mechanism mediates the dipsogenic effects of SC histamine and SC 5-HT in the rat.

Animals↗

PubMed1985

Histamine plays no part in schedule-induced polydipsia in the rat.

Twelve Sprague-Dawley male albino rats were tested with or without combined antagonism of peripheral H1 (using 2 mg/kg dexbrompheniramine IP) and H2 (using 32 mg/kg cimetidine IP) receptors for histamine prior to (a) drinking after 2.5 mg/kg histamine SC, (b) drinking after 24-hr water deprivation, and (c) drinking during the acquisition and maintenance of schedule-induced polydipsia (SIP) with a 45 mg Noyes pellet delivered every 90 sec. Such antagonism of histamine receptors abolished drinking elicited by exogenous histamine without inhibiting drinking after water deprivation. Moreover, histaminergic antagonism failed to prevent the acquisition and maintenance of SIP and failed to alter the distribution of contacts with the drinking spout during interpellet intervals. These findings demonstrate no role for endogenous systemic histamine in SIP.

Animals↗

PubMed1985

Histamine: a role in normal drinking.

Little is known about the physiological mechanisms that control normal drinking and, in particular, drinking around mealtime. This problem has recently been penetrated by experiments evaluating a role for histamine in drinking elicited by eating. This work supports the hypothesis of a preabsorptive, pregastric, vagally-mediated, histaminergic component of drinking elicited by eating in the rat.

Animals↗

PubMed1985

Disordered drinking in developing spontaneously hypertensive rats.

Eating and drinking in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were measured at 5-17 wk of life. The SHR drank significantly more water in 24 h than WKY as early as wk 9, spilled more dry food than did WKY, and exhibited an inverse relation between 24-h water intake and dry food spilled. When eating a meal of dry food after 12 h food deprivation, SHR drank earlier and drank more in a 1-h test than WKY rats. Moreover, SHR exhibited (as early as wk 7) a striking pattern of interrupting eating to drink. This pattern was not present when SHR ate liquid food, and it was attenuated by infusion of water through a cheek fistula. Adult SHR (22 wk) salivated less than WKY in response to intraperitoneal 3.25 mg/kg pilocarpine nitrate. When developing SHR and WKY were maintained on liquid and solid food, SHR gained disproportionately more weight than WKY during development. When young SHR were permitted to drink no more water than WKY rats, the development of hypertension was retarded, and body weight gain was slowed. Because restricted access to food, which produced an equivalent slowing of body weight gain as did restricted access to water, also retarded development of hypertension, it appears that restricted access to water retards development of hypertension due to delayed growth. These results demonstrate that hyperdipsia, apparently caused by deficient salivary function, is not necessary for the development of hypertension in SHR.

Animals↗

PubMed1984

Histamine plays a major role for drinking elicited by spontaneous eating in rats.

The effects of combined antagonism of H1 (using 1 mg/kg dexbrompheniramine IP) and H2 (using 16 mg/kg cimetidine IP) receptors for histamine prior to (a) drinking after 2.5 mg/kg histamine SC, (b) drinking after 1-hr water deprivation, and (c) drinking during spontaneous eating were examined at 1 hr into the dark phase of a 12:12'-hr light/dark cycle for 14 Sprague-Dawley male rats. Such antagonism of histamine receptors abolished drinking elicited by exogenous histamine without affecting drinking after water deprivation. Histaminergic antagonism did not affect spontaneous eating, but it appeared to abolish drinking prior to a meal (for only those 3 rats which exhibited such drinking), delayed the latency to initiate drinking after initiating a meal, and inhibited drinking which occurred during and after eating but prior to postprandial resting (i.e., satiety for food). Because antagonism of peripheral histamine receptors inhibited food-related drinking by over 60%, these results provide indirect support for the hypothesis that the preabsorptive food-contingent vagally-mediated release of gastric mucosal histamine plays a major role in spontaneous food-related drinking in the rat.

Animals↗