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Biomedical subjects

K Gulati

Publications and source records attributed to K Gulati.

26 records · Page 2Linked to original sources
PubMed1991

Effects of baclofen and nitrendipine on ethanol withdrawal responses in the rat.

Withdrawal of rats from 5 weeks of a liquid ethanol diet (10%), resulted in anxiogenic responses in the social interaction and elevated plus-maze tests of anxiety. The rats withdrawn from ethanol also showed increased aggression, tremor and rearing. Baclofen (1.25 and 2.5 mg/kg), but not nitrendipine (25-100 mg/kg), reversed the anxiogenic withdrawal responses, without having any effect in control animals and without having significant sedative effects. Baclofen reduced the enhanced aggression during withdrawal of ethanol, but this may have reflected a more general anti-aggressive action. Baclofen (2.5 mg/kg) reduced the withdrawal tremor. Nitrendipine (100 mg/kg) significantly reduced withdrawal tremor, but this dose was sedative, so this was likely to be a non-specific effect. It is proposed that the anxiogenic response during withdrawal of ethanol is due to a reduced GABA function, involving both GABAA and GABAB receptors.

Aggression↗
PubMed1991

Role of diurnal variation and receptor specificity in the opioidergic regulation of food intake in free-fed and food-deprived rats.

The effects of opioid agonists, morphine (MOR) and ketocyclazocine (KCZ), and antagonists, naltrexone (NALTX) and Mr2266, were investigated on food intake under various conditions, i.e., during light and dark phases of diurnal cycle and free-fed and fasting states in rats. NALTX showed a greater anorexic effect during dark phase, whereas Mr2266 produced such effect during light phase. This suggests that mu-receptors play a major role during dark phase while kappa-receptors are more important in light phase. The comparison of effects of different opioidergic drugs in fasted and free-fed rats showed that NALTX and Mr2266 reduced the elevated basal food intake in 18-h fasted rats to free-fed control levels. Therefore, it appears that enhanced endogenous mu- and kappa-directed neural mechanisms are one of the factors responsible for enhancing food intake in fasted rats. Differential role of MOR and KCZ on food intake in free-fed and fasted rats is also indicated in our study. Both agonists produced a biphasic response in fasted rats, i.e., hyperphagia (0-1 h) followed by hypophagia (1-6 h). However, a generalized hyperphagic effect is observed in free-fed rats (except during 3-6 h by MOR). The initial hyperphagic effect is more prominent in fasted rats which may be due to additive effects of endopioid mechanisms. Specificity of the response at various intervals is confirmed by blockade with NALTX and Mr2266. NALTX appears more potent than Mr2266 in antagonising the effects of MOR but markedly less potent than Mr2266 in inhibiting the effects of KCZ. This suggests that both MOR and KCZ have a mu as well as kappa component in food intake response.

Animals↗
PubMed1991

Effects of acute and chronic morphine on food intake in rats: modulation by oxytocin and vasopressin.

The effects of acute and chronic morphine administration and the interaction with oxytocin and vasopressin on food intake response were investigated at various intervals during a 24-h schedule in rats. Acute morphine (5 mg/kg, IP) produced a generalized hyperphagic effect in both light (0-6 h) and dark (6-24 h) phases, the most marked effects being at 0-1 h, 1-3 h and 6-24 h. Chronic morphine (7 days) in an escalating dose schedule (5-35 mg/kg/day) produced (a) an enhancement of the hyperphagic effect in the light phase and (b) an attenuation of the food intake response during the dark phase. Neither oxytocin nor vasopressin had any significant influence on food intake, per se, after either acute or chronic administrations. However, both OXY and AVP reduced the hyperphagic response to acute morphine throughout the 24-h observation period. Further, on chronic administration, both neurohypophyseal peptides blocked the enhancements of morphine-induced hyperphagia (reverse tolerance) during light phase, whereas only vasopressin was effective in attenuating the reduction of hyperphagia (tolerance) during dark phase. These results are discussed in light of complex opiate-oxytocin/vasopressin interactions in the regulation of food intake.

Animals↗
PubMed1977

On the mechanism of central hypotensive action of clonidine.

The hypotensive effect of clonidine in anaesthetised (pentobarbitone) cat has been analysed with the help of pharmacological tools. Application of clonidine (0.1%) to the exposed ventral surface of medulla oblongata produced hypotension (28.6%) and bradycardia (18%). Similar application of glycine (5%) and GABA (10%) also lowered the blood pressure of cat by 20.3% and 29.3%, respectively. The hypotension as well as the bradycardia owing to clonidine were significantly (p less than 0.01) blocked by similar prior application of atropine methylnitrate (1%) and hemicholinium-3 (HC3, 1%), whereas HC3 pretreatment only insignificantly blocked the hypotension produced by glycine (p greater than 0.80) and GABA (p less than 0.70). Topical application of atropine (1%) also blocked (p less than 0.05) the hypotensive effect of clonidine. Intravenous administration of clonidine (50 microgram/kg) produced hypotension (34.6%) after an initial hypertensive response and bradycardia (38.8%). The hypotension was significantly (p less than 0.01) blocked by pretreatment of the cat with intracerebroventricular atropine (4 mg) or HC3 (0.5 mg). Topical application of atropine (1%) to the ventral surface of medulla also significantly (p less than 0.05) reduced the hypotension and bradycardia resulting from intravenous administration of clonidine. It is concluded that an intact cholinergic link in the brainstem is essential for the hypotensive effect of clonidine.

Acetylcholine↗
PubMedDate not supplied

Pharmacological studies on 2-(2-(4-(3-methylphenyl)-1-piperazinyl)ethyl) quinoline (centhaquin). I. Hypotensive activity.

Hypotensive activity of 2-(2-(4-(3-methylphenyl)-1-piperazinyl)ethyl) quinoline (compound 71/73; centhaquin) was studied in cat and rat. The compound lowered the blood pressure and reduced the heart rate of anaesthetized and unanaesthetized (decerebrate) cat in a dose-dependent manner (0.01-1.0 mg/kg i.v. or 1.0-2.5 mg/kg intraduodenally). The hypotensive effect was insignificant in spinal transected cat but more marked in deafferented and vagotomized animals. Localization of centhaquin to brain by intravertebral arterial injection (5-10 micrograms) or by topical application to the exposed ventral surface of medulla or floor of the fourth ventricle caused hypotension and bradycardia as well as reduced the excitability of the vasomotor loci. It was also effective in rats after single as well as multiple dosing. The compound seems to act centrally to reduce the blood pressure.

Administration, Oral↗
PubMedDate not supplied

On the mechanisms of hypotensive action of indoramin.

Effect of indoramin in small doses on the central vasomotor loci has been studied in chloralose anesthetized cats by localizing it to the central sites. An intracerebroventricular dose of 100 micrograms or intra-vertebral arterial injection of 50 micrograms significantly inhibited the excitability of hypothalamic and medullary vasomotor loci and produced hypotension. Similarly, topical application of indoramin (0.5%) to the floor of the IV ventricle inhibited the medullary and the hypothalamic vasomotor responses but a similar application to the ventral surface of the medulla had no effect. An intrathecal dose of 100 micrograms did not inhibit the spinal compression vasmotor response. Administration of higher amounts led to inhibition of the adrenaline pressor response also, indicating a peripheral leak of the drug. Indoramin has a definite inhibitory effect on the medullary vasomotor loci which contributes to the hypotension produced by this drug.

Administration, Topical↗