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M R Zarrindast

Publications and source records attributed to M R Zarrindast.

124 records · Page 7Linked to original sources
PubMed1977

Cyclic AMP and cyclic GMP levels in glandular stomach of restrained rats.

Cyclic AMP and cyclic GMP were measured in glandular stomach of rats subjected to saline administration, cold (4 degrees C), restraint and restraint+cold after 15, 30, 60, 90 and 120 minutes. All animals subjected to restraint+cold had gastric ulceration after 2 hours. A significant but transient decrease in cAMP was observed 15 minutes after restraint+cold. A marked, sustained and significant decrease of cGMP was observed in the same group of animals. It is concluded that it seems unlikely to be a correlation between cAMP and cGMP changes of the stomach and the restraint-induced gastric ulceration.

Animals↗
PubMed1976

Mazindol anorexia is mediated by activation of dopaminergic mechanisms.

1 Anorexia in rats following injections of mazindol (0.1-8 mg/kg i.p.) could be antagonized by pretreatment with a dopamine receptor blocker (primozide) but not by pretreatment with an alpha-adrenoceptor blocker (phenoxybenzamine), a beta-adrenoceptor blocker ((-)-propranolol), or a 5-hydroxytryptamine receptor blocker (methergoline). 2 In rats with a unilateral lesion in the substantia nigra made by stereotaxic injection of 6-hydroxydopamine, mazindol caused a dose-dependent turning towards the lesioned side, indicating an indirect mechanism of action. This effect could be antagonized by pretreatment with a dopamine receptor blocker. 3 In rats pretreated with reserpine and alpha-methyl-p-tyrosine, mazindol did not have any motor stimulant action. 4 In vitro studies with synaptosomes prepared from rat brain, indicated that mazindol blocks uptake and causes release of dopamine. 5 It is concluded that the anorectic action of mazindol is mediated by a dopaminergic mechanism.

Animals↗
PubMed1975

Synthesis and pharmacological activity of 5-substituted 2-(N,N-dialkylaminoethyl)amino- and 2-N-methylpiperazinyl-1,3,4-thiadiazoles.

5-Substituted 2-amino-1,3,4-thiadiazoles were transformed to their corresponding 2-bromo derivatives. The reaction of the 5-substituted 2-bromo-1,3,4-thiadiazoles with N,N-dialkylaminoethylamines or N-methylpiperazine afforded the corresponding amino-1,3,4-thiadiazole derivatives. All prepared compounds displayed antihistaminic, anticholinergic, and norepinephrine-potentiating activities.

Animals↗
PubMed1974

The effect of ethacrynic acid on the guinea-pig and rat isolated vas deferens.

1 The effect of ethacrynic acid (EA) was studied on guinea-pig and rat vas deferens in vitro.2 EA contracted the guinea-pig but not the rat vas deferens in a dose-dependent manner (50-800 mug/ml). Tyramine caused contraction in 10 out of 18 guinea-pig vas deferens; EA caused contraction in 17 of the preparations which did not respond to tyramine. Repeated doses of EA produced tachyphylaxis, but there was no cross tachyphylaxis to tyramine.3 The contractions produced by EA were prevented by phentolamine or reserpine pretreatment and potentiated by cocaine. A low concentration of desipramine (3 ng/ml) potentiated and higher concentrations (0.6 and 3.0 mug/ml) inhibited the response of vas deferens to EA.4 Hexamethonium (100 mug/ml) or atropine (0.1 mug/ml) did not inhibit the effect of EA, excluding the nicotinic and muscarinic receptors as the sites of action.5 The effect of noradrenaline (NA) on the guinea-pig and rat vas deferens was enhanced by EA pretreatment, which may be due to inhibition of NA uptake.6 It is concluded that EA releases NA from guinea-pig vas deferens. The mechanism of release seems to be different from that of tyramine.

Animals↗
PubMedDate not supplied

On the mechanism of tolerance to morphine-induced Straub tail reaction in mice.

The effect of 5-HT and opioid receptor antagonists on morphine-induced Straub tail was studied in mice. Straub tail behavior was induced by subcutaneous administration of different doses (20, 30, and 40 mg/kg) of morphine hydrochloride to mice. The effect of morphine was dose-dependent. Maximum response was obtained with 40 mg/kg of the drug. The response induced by morphine (20 and 40 mg/kg) was decreased by different doses of intraperitoneal injection of naloxone (1 and 2 mg/kg) or methysergide, mianserin, and ritanserin (1 and 2 mg/kg). The effect of morphine (40 mg/kg) was also reduced by intracerebroventricular injection of naloxone (0.4-0.8 microg/animal) or mianserin (2 and 4 microg/animal). Different groups of mice received one daily dose (50 mg/kg sc) of morphine sulfate for 3 days to develop tolerance to morphine. The Straub tail reaction induced by morphine hydrochloride (40 mg/kg) was tested on the fourth day. Naloxone injection (1 and 2 mg/kg ip) on Day 3 (1 h after morphine sulfate injection) or on Day 4 (1 h before test dose of morphine hydrochloride), decreased tolerance induced to morphine. Methysergide, mianserin, or ritanserin (intraperitoneal) on Days 2 and 3 (1 h after morphine sulfate injection) or on Day 4 (1 h before test dose of morphine hydrochloride), also decreased tolerance induced to morphine. Intracerebroventricular injection of either naloxone or mianserin also reduced tolerance to morphine. It is concluded that 5-HT(2) and opioid receptor mechanisms are involved in morphine-induced Straub tail reaction and tolerance induced to morphine also may be mediated through these receptors.

Analgesics, Opioid↗
PubMedDate not supplied

Stress-induced antinociception and GABAergic mechanism.

The antinociceptive effects of GABAergic agents in presence or absence of swim-stress were investigated in mice, using the tail-flick test. Swim-stress, the GABAB agonist baclofen and the GABAA agonist muscimol raised the threshold of withdrawal reactions to nociceptive stimulation. The antinociception, induced by an interaction of stress and GABA agonists, was higher than that of stress or a GABA agonist alone. The GABAB antagonist phaclofen and the GABAA antagonists bicuculline and picrotoxin decreased the antinociceptive action induced by stress plus baclofen. Picrotoxin administration also decreased the response of baclofen. Picrotoxin and biculline, but not phaclofen, reduced the antinociceptive response induced by muscimol in stressed mice. Administration of picrotoxin, bicuculline or phaclofen alone did not decrease the stress-induced antinociception. The antagonists even increased the base line latencies in both normal and stressed mice. It is concluded that stimulation of both GABAA and GABAB receptor sites has an antinociceptive effect, but that the involvement of a GABAergic mechanism in stress-induced antinociception is unlikely.

Analgesics↗
PubMedDate not supplied

Influences of dopamine agonists and antagonists of baclofen antinociception in mice.

The effects of dopamine agonists and antagonists on baclofen antinociception were examined in mice using the tail-flick test. Injection of different doses of baclofen (5-10 mg/kg, i.p.) produced dose-related antinociception. This effect was decreased in animals treated with SKF 38393 (8 mg/kg, i.p.) or apomorphine (2 mg/kg, s.c.). The inhibitory responses of both SKF 38393 and apomorphine were decreased in animals pretreated with SCH 23390 (0.1 mg/kg, s.c.). Bromocriptine (1 mg/kg, i.p.), or lower doses of apomorphine (0.1 mg/kg, s.c.), did not alter the baclofen-induced antinociception. Antinociception induced by baclofen (5-10 mg/kg, i.p.) was decreased in animals pretreated with sulpiride (10 mg/kg, i.p.) but not by SCH 23390 (0.1 mg/kg, s.c.). Administration of apomorphine, SKF 38393, bromocriptine or sulpiride alone did not change the latency in the tail-flick test, but SCH 23390 induced a slight but significant antinociception. On the basis of the above findings, it may be concluded that D-1 receptor activation can decrease the baclofen antinociceptive effect.

Analgesics↗
PubMedDate not supplied

Bromocriptine-induced hypothermia: D-2 receptor involvement.

Bromocriptine (2-16 mg/kg, i.p.) caused a dose-dependent fall in core body temperature of mice. The hypothermic effect of bromocriptine was decreased by pretreatment of the animals with sulpiride, but SCH 23390, methergoline, phenoxybenzamine, propranolol and atropine did not decrease the response. Administration of reserpine plus alpha-methyl-p-tyrosine prior to bromocriptine injection abolished hypothermia in mice. It is concluded that D-2 dopamine receptors may be involved in bromocriptine-induced hypothermia.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Opposing influences of D-1 and D-2 dopamine receptors activation on morphine-induced antinociception.

Subcutaneous (s.c.) injection of morphine (3-9 mg/kg) to mice induces a dose-related antinociceptive effect in the tail-flick test. In animals treated with different doses of apomorphine (0.1-3 mg/kg, s.c.) the antinociceptive effect of morphine changed; low doses of apomorphine were found to potentiate, whereas higher doses of the drug decreased the antinociception induced by morphine. Intraperitoneal (i.p.) injection of the D-2 agonist bromocriptine (0.5-2 mg/kg) increased the antinociceptive action of morphine dose-dependently. This potentiation was decreased in animals pretreated with sulpiride. The D-1 agonist SKF 38393 (4-12 mg/kg, i.p.) caused a reduction of morphine antinociception in a dose-dependent manner. The inhibitory effect of SKF 38393 was decreased in animals pretreated with SCH 23390. Theophylline (12.5-50 mg/kg, i.p.) pretreatment of animals decreased the morphine antinociception. Single administration of SCH 23390 increased the base line latency, while bromocriptine, SKF 38393, sulpiride, theophylline or apomorphine did not change the latency in the tail-flick test. It may be postulated that D-1 receptor activation decreases, while D-2 receptor stimulation increases the antinociceptive effects of morphine. Whether the effects of D-1 and D-2 receptors are mediated through the changes in cAMP levels remains to be clarified.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMedDate not supplied

Effects of drugs active at adenosine receptors on stress-induced analgesia in mice.

Mice were stressed by swimming for 3 min in water at 20 degrees C and antinociception was assessed by the tail-flick test. The stress-induced antinociception was potentiated by intraperitoneal administration of different doses of theophylline. The effect of the drug was dose-dependent. 5'-N-Ethylcarboxamidoadenosine administration also increased the stress response dose-dependently. N6-Phenyl-isopropyladenosine decreased the antinociception induced by swim-stress as well as after stress plus theophylline. Administration of dipyridamole caused a decrease of antinociception induced by stress or stress plus theophylline. It may be concluded that activation of A2 adenosine receptors increased whereas activation of A1 adenosine sites decreased the stress-induced antinociception. The responses of A2 or A1 activation may be irrelevant to changes in cAMP levels. Because the adenosine agonists and antagonists employed were not selective at the receptor level, other possibilities are not excluded.

Adenosine↗
PubMedDate not supplied

Antinociception: interaction between adenosine and GABA systems.

The interaction of GABA agonists and antagonists with the antinociceptive effects of drugs active on adenosine receptors, was examined in mice using the tail-flick test. Baclofen, but not muscimol (in the doses used), induced antinociception. The adenosine agonist NECA (5'-N-ethylcarboxamidoadenosine) produced a greater degree of antinociception than did PIA (N6-phenylisopropyladenosine). The antinociceptive effect of NECA and PIA was decreased by the GABA antagonists bicuculline, picrotoxin and phaclophen. Combination of theophylline with baclofen, but not with muscimol, induced a high antinociceptive response. Muscimol decreased the antinociceptive effect of NECA, and baclofen increased the antinociceptive action of PIA. It is concluded that there may be an interaction between antinociception induced by GABA and that induced by (an) adenosine mechanism(s).

Adenosine↗