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At least 865 records · Page 48Linked to original sources

PubMed1991

Muscarinic receptors in diabetic rat prostate.

To investigate the effects of experimentally-induced diabetes on prostatic muscarinic cholinergic receptors, the binding characteristics of [3H]quinuclidinyl benzilate ([3H]QNB) to prostatic membrane particulates were examined in four groups of rats: control, diabetic, diabetic insulin treated, and diabetic myo-inositol treated. Diabetes was induced by i.v. injection of streptozotocin (STZ), 65 mg/kg. Diabetic and diabetic myo-inositol-treated rats had hyperglycemia, hypoinsulinemia, glucosuria, polydipsia, and polyuria as well as significantly smaller prostates and lower body weights compared to control and diabetic insulin-treated animals. The densities of muscarinic receptors (Bmax) as determined by saturation studies with [3H]QNB in the prostatic plasma membranes of control, diabetic, diabetic insulin-treated and diabetic myo-inositol-treated rats were 80 +/- 8, 51 +/- 5, 78 +/- 3, and 47 +/- 7 fmol/mg of protein, respectively. [3H]QNB binding to muscarinic receptors was inhibited by muscarinic antagonists with the following rank order of Ki values: atropine much less than pirenzepine less than AF-DX 116. The pharmacological profile of the muscarinic receptors was similar in all groups examined and was consistent with the predominance of the M3 muscarinic receptor subtype in prostatic membrane particulates. Our data indicate that STZ-induced diabetes caused a variety of abnormalities including a down-regulation in the density of M3 muscarinic receptors in the rat prostate and that insulin, but not myo-inositol could prevent the development of these abnormalities.

Animals↗

PubMed1990

A possible role of hippocampal dysfunction in schizophrenic symptomatology.

The author proposes a pathogenesis for the bizarre, repetitive behaviors frequently seen in deteriorated schizophrenics, i.e., polydipsia, hoarding, pacing, etc. It is argued that such behaviors may have a neurobiology similar to schedule-induced behaviors or incentive-conditioned behaviors described in animal models, which involve the hippocampus, nucleus accumbens, and the neurotransmitter dopamine. Such behaviors are augmented by hippocampal lesions, stress, increased drive state, or dopaminergic agents, and reduced by 6-OH dopamine lesions to nucleus accumbens or antipsychotic agents. These repetitive behaviors may reflect the failure of hippocampus to modulate the impact of mesolimbic dopaminergic activity on the nucleus accumbens and thus on motor behavior. Such a hypothesis is consistent with a growing body of neuropathological and brain imaging results demonstrating hippocampal lesions in chronic schizophrenics.

Animals↗

PubMed1992

Dietary calcium blocks lithium toxicity in hamsters without affecting circadian rhythms.

Lithium can be toxic to rodents at plasma concentrations (0.6-1.2 mmol/L) that also phase delay circadian rhythms. In hamsters, raising the concentration of calcium in the diet from 0.1%-3% reduced weight loss and polydipsia caused by 0.4% lithium carbonate. Calcium ingestion did not affect plasma lithium concentration or the phase of the circadian wheel-running rhythm in lithium-treated animals. Calcium ingestion did not alter weight gain, salt or water intake, or circadian rhythms in hamsters not receiving lithium. Dietary calcium supplementation may prevent some toxic effects of lithium without interfering with other central nervous system actions.

Animals↗

PubMed1985

Individual differences in non-regulatory ingestive behavior and catecholamine systems.

Animals that eat and/or drink in response to electrical stimulation of the lateral hypothalamus (ESLH-pos) are more responsive to both schedule-induced polydipsia (SIP) tests and a series of amphetamine (AMPH) injections than animals that do not exhibit these behaviors (ESLH-neg). Moreover, prior exposure to the behaviorally activating SIP experience, or to AMPH, permanently transformed the ESLH-neg animals into animals that reliably ate or drank during ESLH. Prior treatment with AMPH also increases the water consumed during subsequent SIP tests. Thus, initial of induced differences in sensitivity to activating experiences can determine behavioral propensities.

Animals↗

PubMed1986

Regulatory changes following kainic acid-induced striatal lesions.

Kainic acid-induced lesions (KAL) of the striatum produce body weight and regulatory deficits in the rat. Unlike lateral hypothalamic rats. KAL rats drink more during food deprivation and eat more afterwards as compared to both baseline conditions and control rats. The present study investigated these effects further. As in previous studies, food deprivation was found to cause polydipsia and increased postdeprivational food intake in the KAL animal. Urination and defecation, often used as an index of emotionality, were also found to increase under these conditions. When the antidiuretic hormone vasopressin was injected, all of these differences remained with the exception of postdeprivational feeding--KAL rats no longer ate more than controls. These findings suggest that psychogenic factors--but not hormonal influences--may play a primary role in the regulatory peculiarities seen in the KAL rat.

Animals↗

PubMed1990

Sensitivity to angiotensin II of neurons in the circumventricular organs of polydipsic inbred mice.

The polydipsic inbred mice, STR/N, are known to possess an extremely strong appetite for drinking but no abnormality in the vasopressin system and renal functions. In brain slice preparations the sensitivity of neurons in the anteroventral region of the third ventricle (AV3V) and the subfornical organ (SFO) to angiotensin II (ANG II) was investigated using extracellular recordings in the STR/N and its control, Swiss/Webster (S/W) mice. In the AV3V, less proportion of neurons (15 out of 168; 9%) of the STR/N than that in the S/W (49/206; 24%) was excited by ANG II added to the medium. In the SFO, a proportion of neurons excited by ANG II was again lower in the STR/N (27/104; 26%) than in the S/W mice (64/118; 54%). The threshold concentration of ANG II for excitation of the AV3V and SFO neurons was, however, similar for both strains, 10(-9) M or less. Only one neuron in the SFO of a S/W mouse was inhibited by ANG II application. The excitatory effect of ANG II on AV3V and SFO neurons of both strains of mice persisted under synaptic blockade and was reversibly antagonized by an ANG II antagonist, saralasin. Such differences in sensitivity to ANG II of neurons in the SFO and AV3V, the regions thought to be involved in drinking behavior, suggest the involvement, at least in part, of the central angiotensin system in the polydipsia of the STR/N mice.

Angiotensin II↗

PubMed1991

Characterization of opioid-sensitive neurons in the anteroventral third ventricle region of polydipsic inbred mice in vitro.

In previous studies we found that in the extremely polydipsic special strain of mice, STR/N, spontaneous drinking was greatly attenuated by injection of the opioid antagonists given intracerebroventricularly as well as subcutaneously. Therefore, we investigated, using hypothalamic slice preparations, responses of neurons in the anteroventral third ventricle region (AV3V) of the STR/N and its control, Swiss/Webster (S/W) mice to morphine and opiate peptides. An application of morphine at 10(-6) M to the circulating medium inhibited activities of 44% of AV3V neurons (45 of 102) in the STR/N, and 59% (76/129) in the S/W, demonstrating that morphine affected a smaller proportion of neurons of the polydipsic mice than that of controls. Opioid agonists for 3 receptor types, mu, delta and kappa, at 10(-6) to 10(-5) M inhibited AV3V neurons in both the STR/N and S/W mice, but to a different degree. No cell of either strain was excited by morphine or any of the opioids. The mu-receptor agonist, [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAGO), was the most potent inhibitor of AV3V neurons; in the STR/N 53% (25/47), and in the S/W 77% (34/44) were inhibited. The kappa-agonist, dynorphin A-(1-13) (DYN), inhibited fewer cells in the STR/N (9%, 4/47), compared with the S/W (36%, 16/44). Only a few cells responded to the delta-agonist, [D-Pen2,5]enkephalin (DPDPE), in both strains. The inhibitory actions of the opiates were reversibly blocked by naloxone, and persisted under synaptic blockade. The threshold concentration of morphine or DAGO for inhibition of AV3V neurons was higher in the STR/N (approximately 10(-8) M for both morphine and DAGO) than in S/W mice (approximately 10(-9) M for morphine and less than 10(-9) M for DAGO). Although the AV3V also contains angiotensin II-sensitive neurons, they were not affected by morphine (10(-6) M). Similarly neurons inhibited by morphine were not excited by angiotensin II (10(-7) M); some neurons were unresponsive to both chemicals. We conclude that morphine and opiate peptides directly inhibit the AV3V neurons of both the STR/N and S/W strains of mice and the sensitivity of these neurons to the opiates is lower in the polydipsic inbred mice compared to their controls. The results, together with our behavioral studies, suggest involvement of the central opioid system in the polydipsia of the STR/N mice.

Angiotensin II↗

PubMed1990

The effect of lithium therapy on arginine vasopressin secretion and thirst in man.

Lithium therapy is known to reduce the renal responsiveness to arginine vasopressin (AVP: the antidiuretic hormone in man) and a proportion of treated patients develop polyuria and polydipsia. In this study seven nonpolyuric female patients receiving lithium treatment for an affective disorder (lithium group) were age-matched with seven healthy females (control group). The mean response of plasma AVP to osmotic stimulation was significantly enhanced in the lithium group but the mean osmotic threshold for AVP release was unchanged. Thirst appreciation in the lithium group commenced and increased overall at an osmotic stimulus 5 mmol/kg less than the control group. It is suggested that primary thirst does play a role in the expression of lithium-induced polyuria.

Adult↗

PubMed1981

Suppression of drinking by naloxone in the rat: a further characterization.

The effects of naloxone, an opiate antagonist, were examined on drinking induced by various dipsogenic stimuli. In rats deprived of water for 24 h, naloxone (0.1-10 mg/kg) produced a dose-related suppression of drinking immediately following water presentation but did not alter the latency to begin drinking. Naloxone also produced a dose-related suppression of water consumption induced by isoproterenol and angiotensin II, agents simulating conditions of extracellular dehydration. Naltrexone, a congener of naloxone, was more potent than naloxone in reducing isoproterenol-induced water intake. Schedule-induced polydipsia, which occurs in the absence of body fluid deficits, was not altered by either naloxone or naltrexone at doses attenuating drinking induced by the other methods. These data suggest that the suppressant effects of naloxone on water consumption are not a manifestation of an increased latency to drink or an impairment in the motor components of drinking activity. Furthermore, narcotic antagonists appear to attenuate regulatory, but not adjunctive drinking.

Angiotensin II↗

PubMed1984

Effects of kainic acid injections in the striatum on physiologic and behavioral functions in conscious rats.

Alterations in both physiologic and behavioral functions were assessed in unanesthetized rats after a unilateral injection of kainic acid (KA) in the striatum. The immediate behavioral effects were dyskinesias, head swaying, circling, tail elevation, hyperpnea and marked salivation. The induced behavioral responses lasted for about 14 to 18 h. Rats with intrastriatal KA injection, although showing no thermoregulatory deficit at both moderate (22 degrees C) and hot (30 degrees C) environmental temperatures, displayed a lower metabolism and a lower rectal temperature than the preinjection controls in the cold (8 degrees C) environment. In addition, the hypothermia induced by intrastriatal administration of apomorphine (dopamine agonist) was greatly antagonized by pretreatment with intrastriatal injection of KA. Furthermore, intrastriatal infusions of KA (1 microgram in 0.5 microliter) also caused a decrease in pain threshold (or in the latency to the hind-paw lick on the hot plate test), hypophagia, polydipsia, and weight loss. The induced alterations in thermoregulation, pain reflex, and ingestive behavior lasted for about 7 days. These data indicate that striatal neurons are involved in the central control of motor activity, thermoregulation, the pain reflex, and ingestive behavior.

Animals↗

PubMed1986

Neurogenic diabetes insipidus in a sheep.

A 7-month-old Suffolk-cross ram was examined because of polydipsia and polyuria of 2 months" duration. Neurogenic diabetes insipidus was diagnosed on the basis of failure to concentrate urine of low specific gravity in response to water deprivation and a positive response to antidiuretic hormone administration. Post-mortem examination of the brain revealed degeneration in the cerebral peduncles, an absence of pituitary neural tissue and evidence suggesting external pressure as the cause.

Animals↗

PubMed1982

Similarities and differences between effects of testosterone and 19-nortestosterone in rats, with particular reference to hypertensogenic potency.

Both 19-nordeoxycorticosterone and 19-norprogesterone are potent hypertensogens. This particularly interesting in the latter case, since the parent steroid is antimineralocorticoid and antihypertensive. The present experiment compared the ability of testosterone and 19-nortestosterone to cause hypertension in rats. Both steriods caused adrenal atrophy, nephromegaly, relative hypoproteinemia and increased hematocrit, but only testosterone provoked saline polydipsia, hypernatremia, hypertension, cardiomegaly and vascular lesions. It is evident that demethylation of testosterone at C10 completely destroys any effect on sodium metabolism or blood pressure, but leaves certain other pathophysiologic responses, including extreme adrenal atrophy, unimpaired. The hypertensogenic effect of testosterone has been attributed to its inhibitory effect on adrenal structure and function, the latter characterized by an induced enzymatic defect leading to increased secretion of deoxycorticosterone. This raises the intriguing question of whether, despite the comparable involution of the adrenal cortex, there are significant differences in adrenocortical enzymatic changes initiated by the respective androgens, which could account for their quiet different blood pressure effects.

Animals↗

PubMed1986

The effect of nivazol and cortivazol, novel synthetic steroids containing a phenylpyrazolo A-ring substitution, on blood pressure in sheep.

This study investigated the effect of 5 day infusions of two structurally novel synthetic steroids, nivazol and cortivazol on blood pressure and in vivo indices of "glucocorticoid" and "mineralocorticoid" activity. Cortivazol at 24 mg/day raised mean arterial pressure (MAP) by 16 mmHg (P less than 0.001). This was associated with increased cardiac rate, and increased fasting plasma [glucose], polyuria and polydipsia a trilogy characteristic of glucocorticoid effect. Cortivazol had no consistent action on plasma [Na] or [K], but caused an initial transient urinary Na retention and raised urinary excretion of Na and K on days 3 and 4 of treatment. Nivazol at 24 mg/day raised MAP 10 mmHg (P less than 0.001), but cardiac rate was unchanged. This infusion was also associated with the glucocorticoid effects of increased fasting plasma [glucose] and increased urine volume. Plasma [K] fell from a control of 4.4 +/- 0.1 to 4.0 +/- 0.1 mmol/l (P less than 0.01) after 5 days of infusion. There was no significant effect of nivazol on urinary Na or K excretion. This study demonstrates that replacement of the 3-keto group, by a bulky phenylpyrazolo group fused to the A ring at position 2 and 3, does not diminish either pressor or glucocorticoid activity of steroids containing the typical 4-pregnene-3,20-dione nucleus and confirms that the 3 keto group is not essential for optimal glucocorticoid activity. It is the first demonstration of the pressor effect of these novel steroids.

Animals↗

PubMed1990

Comparison of graft morphology and endocrine function after vascularized whole-pancrease transplantation in the rat by different surgical techniques.

Graft morphology and endocrine function following vascularized pancreas transplantation by different surgical techniques were determined in streptozotocin-diabetic rats. Eight different surgical techniques were studied. Intestinal drainage of exocrine secretion was accomplished by pancreaticoduodenal transplantation or by utilizing only a patch of the donor duodenum for duodenojejunostomy. Following pancreaticoureterostomy and pancreaticocystostomy, the graft's exocrine secretion was drained to the recipient's urinary tract. The exocrine secretion was allowed to drain freely into the recipient's peritoneal cavity following transverse or longitudinal incision of the common bile duct. Exocrine secretion was suppressed either by duct ligation or by retrograde ductal injection of prolamine. Following enteric or urinary exocrine graft drainage, the architecture of both the endocrine and exocrine pancreas was perfectly preserved. Pancreatic juice had remarkably few adverse effects on the recipient's urinary tract. Obstruction of the exocrine secretion induced atrophy of the acinar cells, proliferation of small pancreatic ducts, and a typical fragmentation of the islets of Langerhans. Prolamine was biologically degraded within 28 days. Following free intraperitoneal drainage, spontaneous suppression of the exocrine graft function occurred early after transplantation. Metabolic signs of diabetes mellitus including hypoinsulinemia, hyperglycemia, polydipsia, polyuria, and impaired glucose tolerance were completely normalized by pancreas transplantation irrespective of the surgical technique used. Despite fundamental differences in graft architecture no alteration of endocrine graft function was noted following vascularized pancreas transplantation by different surgical techniques.

Animals↗

PubMed1991

Seizure and acute osmotic change: clinical and neurophysiological aspects.

There are a number of clinical situations where overhydration may occur. If the reduction in plasma osmolality is acute, passive water influx swells brain cells, shrinking the extracellular space around them. It is during this time that susceptibility to generalized tonic-clonic seizure dramatically increases. Common clinical examples include hastened rehydration therapy, the dialysis disequilibrium syndrome, compulsive polydipsia, the syndrome of inappropriate ADH secretion (SIADH) and post-TURP syndrome. Treatments that tend to restore normal cellular volume (dehydration, mannitol infusion) help protect against this form of seizure. Support for a correlation between plasma osmolality and seizure susceptibility is scattered amongst the literature of several medical disciplines and spans almost 70 years. However a cellular basis to explain how overhydration might promote epileptiform activity has been examined only recently. The neocortical and hippocampal brain slice preparations permit an examination of how acute osmotic change alters cortical excitability independent of vascular damage, brain compression or other factors secondary to brain swelling. Electrophysiological evidence indicates that hyposmolality promotes epileptiform activity by strengthening both excitatory synaptic communication in neocortex and field effects among the entire cortical population. Moreover there is little evidence that associated hyponatremia in itself leads to increased CNS excitability. Such findings help in understanding how rapid lowering of plasma osmolality in clinical situations can promote the hyperexcitability associated with generalized tonic-clonic seizure.

Animals↗

PubMedDate not supplied

Increased immunoreactive dynorphin and leu-enkephalin in posterior pituitary of obese mice (ob/ob) and super-sensitivity to drugs that act at kappa receptors.

Posterior pituitaries of obese mice (ob/ob) contained significantly more immunoreactive dynorphin (P less than .01) and leu-enkephalin (P less than .01) than their lean littermates. Drinking in obese mice was stimulated by 0.3%, and feeding by 10%, of the dose of ethylketocyclazocine, a kappa receptor agonist, needed to produce extra feeding and drinking in lean mice. Obese mice also showed greater and longer lasting suppression of ingestion after MR-2266, a kappa antagonist, than did lean mice. MR-2266 was much more effective than naloxone in suppressing schedule-induced polydipsia in rats. These results indicate that kappa receptors are involved in feeding and drinking and that obesity is associated with changes in these receptors and their ligands.

Analgesics, Opioid↗

PubMed1984

Alloxan-induced diabetes in the rat - protective action of (-) epicatechin?

Administration of alloxan (150 mg/kg body weight, i.p.) to male Wistar rats induced a reproducible and persistent diabetes mellitus as evidenced by elevated serum glucose and low serum insulin concentrations. Administration of either (-)epicatechin or (+)catechin (250 mg/kg, i.p. on each occasion) at 36, 24, 12 and 1 hour before and at 12 and 24 hours after alloxan administration did not prevent the induction of the diabetes. Similarly, treatment of animals with (-)epicatechin or (+)catechin (125 mg/kg i.p. twice daily) for 21 days commencing 24 hours after alloxan administration did not reverse the persisting elevated serum glucose and low serum insulin concentrations. Moreover, administration of these compounds did not relieve any of the symptoms of the alloxan-induced diabetes such as poor weight gain, polyuria or polydipsia. Thus, this study does not confirm previous reports of prophylactic and curative effects of (-)epicatechin against alloxan-induced diabetes in rats, in spite of the high dosages of the compounds used in these experiments.

Animals↗

PubMed1986

Effect of pertussis toxin on water metabolism in the rat.

Pertussis toxin administered to rats resulted in a polyuric state that was due to enhanced renal water excretion. Pertussis toxin also induced a defect in renal water conservation. These abnormalities in renal water excretion could not be attributed to polydipsia, impaired synthesis and/or release of arginine vasopressin or renal tubular dysfunction with solute diuresis. No evidence of pertussis toxin-induced renal tubular damage was present. These results indicate that pertussis toxin induces nephrogenic diabetes insipidus and this defect occurs at the level of the renal collecting tubule.

Animals↗