PubMed Health⌕ Search

Biomedical subjects

R M Quock

Publications and source records attributed to R M Quock.

At least 73 records · Page 4Linked to original sources
PubMed1984

Pharmacological characterization of apomorphine-induced hypothermia in the spontaneously hypertensive rat.

The dopamine agonist apomorphine was more potent in eliciting hypothermia in spontaneously hypertensive rats (SHRs) than in normotensive Wistar rats (NWRs), while normotensive Wistar-Kyoto rats (WKYs) were intermediate in response. Various drug interventions were attempted in an effort to explain the greater sensitivity of SHRs to apomorphine. Haloperidol produced abolition of apomorphine-induced hypothermia in SHRs but at greater doses than required for antagonism of the drug effect in WKYs and NWRs. Chronic hydralazine treatment that reduced the high blood pressure of SHRs failed to appreciably influence the magnitude of apomorphine-induced hypothermia, compared to the response in control SHRs that received no hydralazine. These findings suggested to us that the enhanced hypothermic effect of apomorphine in SHRs was entirely dopamine receptor-mediated and that it was also independent of the high blood pressure. We also found that chronic lithium treatment that had no influence upon apomorphine-induced hypothermia in WKYs and NWRs significantly reduced the drug effect in SHRs. Based on this finding, we suggest that the greater hypothermic effect induced by apomorphine in SHRs might be due to a supersensitivity of hypothermia-mediating dopamine receptors in the hypertensive strain.

Animals↗
PubMed1984

Influence of chronic naloxone treatment on development of hypertension in the spontaneously hypertensive rat.

Chronic administration of naloxone by means of miniosmotic pumps retarded the development of hypertension in young spontaneously hypertensive rats (SHRs) in a dose-related manner. Abrupt termination of naloxone treatment resulted in acceleration in the rate of the blood pressure increase, while increasing the naloxone concentration further slowed the development of hypertension in SHRs. The heart rates of SHRs undergoing chronic naloxone treatment were generally lower than those of control SHRs. Naloxone had no influence upon the mean systolic blood pressures or heart rates of normotensive Wistar-Kyoto control rats. These findings indicate that chronic naloxone treatment can alter the development of hypertension in the SHR.

Aging↗
PubMed1984

Pipradrol-induced hyperthermia in the rabbit.

Intravenous administration of the stimulant drug pipradrol evoked a dose-dependent hyperthermic response in rabbits. This drug effect was significantly reduced by pretreatment with chlorpromazine, phenoxybenzamine, intravenous BE-2254 or intracerebroventricular BE-2254. In animals pretreated with cyproheptadine or atropine, the hyperthermic effect was significantly potentiated. However, haloperidol, pimozide, diphenhydramine and pentobarbital failed to appreciably influence the drug response. These findings suggest that pipradrol-induced hyperthermia in the rabbit involves activation of central alpha-adrenergic receptors and is apparently enhanced by blockade of serotonergic or cholinergic receptors.

Animals↗
PubMed1984

Possible noradrenergic involvement in naloxone potentiation of apomorphine-induced stereotypic climbing in mice.

Apomorphine-induced stereotypic climbing behavior in mice was significantly potentiated by pretreatment with the opiate receptor blocker naloxone. In animals additionally pretreated with alpha-methyl-p-tyrosine, brain levels of norepinephrine (NE) and dopamine (DA) were markedly reduced and naloxone potentiation of apomorphine-induced stereotypic climbing was blocked. In mice pretreated with diethyldithiocarbamic acid, brain NE was slightly reduced, brain DA was slightly elevated but naloxone potentiation of apomorphine-induced stereotypic climbing was unaltered. In animals pretreated with reserpine, both brain NE and DA were significantly reduced by naloxone potentiation of apomorphine-induced stereotypic climbing was not affected. In other experiments, pretreatment with low doses of the alpha-adrenergic receptor blocker BE-2254 failed to suppress climbing activity induced by apomorphine alone but did successfully prevent naloxone potentiation of apomorphine-induced stereotypic climbing. These findings suggest the possibility that NE and alpha-adrenergic receptors might play a role in the potentiating influence of naloxone upon apomorphine-induced stereotypic climbing activity in mice.

Animals↗
PubMed1984

Differential effects of 5-hydroxytryptaminergic antagonists upon apomorphine- and lergotrile-induced hypothermia and stereotyped behaviour in rats.

The dopaminergic stimulants apomorphine and lergotrile both evoked hypothermia and stereotyped behaviour in rats. These drug effects were sensitive to antagonism by haloperidol, a dopaminergic receptor blocker. In rats pretreated with 5-hydroxytryptaminergic receptor blockers, cinanserin reduced apomorphine-induced hypothermia but cyproheptadine did not. Both cinanserin and cyproheptadine significantly potentiated lergotrile-induced hypothermia. Similarly, the stereotypic effects of apomorphine were partly reduced by cyproheptadine, although higher doses of cyproheptadine did potentiate lergotrile-induced stereotyped behaviour. These findings of different influences of 5-HT antagonists upon the effects of apomorphine and lergotrile indicate that these two dopaminergic stimulants may not work in identical manner to produce outwardly similar drug effects.

5-Hydroxytryptophan↗
PubMed1984

Dynorphin-(1-13)-like immunoreactivity in central nervous system and pituitary gland of spontaneously hypertensive rats.

We determined by radioimmunoassay concentration of dynorphin-(1-13)-like immunoreactivity in the central nervous system and pituitary gland of spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto rats (WKYs). Compared to WKYs, SHRs had significantly lower levels of dynorphin-(1-13)-like immunoreactivity in the hypothalamus and pituitary gland. However, such immunoreactivity in the cerebral cortex, caudate nucleus, diencephalon, brainstem and spinal cord of SHRs and WKYs were similar.

Animals↗
PubMed1983

Potentiation by naloxone of the anti-oxotremorine effect of L-DOPA.

Pretreatment with the catecholamine precursor L-DOPA but not the narcotic antagonist naloxone suppressed the tremorigenic effect of oxotremorine in mice. However, when animals were pretreated with both L-DOPA and several different doses of naloxone, there was a dose-related potentiation of the antitremor effect of L-DOPA. Naloxone also produced dose-dependent potentiation of the antitremor activity of lower doses of L-DOPA in the presence of the peripheral decarboxylase inhibitor carbidopa. These findings suggest a possible therapeutic application for naloxone in treatment of dopamine dysfunction disorders.

Animals↗
PubMed1983

Potentiation of apomorphine-induced stereotypies by naloxone and L-prolyl-L-leucyl-glycinamide.

We compared the influences of pretreatment with the narcotic antagonist drug naloxone and the neuropeptide L-prolyl-L-leucyl-glycinamide (PLG) upon apomorphine-induced stereotypic climbing activity in mice and apomorphine-induced contralateral rotational behavior in rats with unilateral 6-hydroxydopamine lesions of the substantia nigra. Naloxone produced dose-related potentiation in the mouse climbing model, while PLG was without effect. On the other hand, PLG produced dose-related potentiation in the rat rotational paradigm, while naloxone was without appreciable influence. These findings show an asymmetrical potentiation of apomorphine by naloxone and PLG in these two standard experimental models of striatal dopaminergic activity.

Animals↗
PubMed1979

p-Chloroamphetamine-induced hyperthermia pharmacologically distinct from fenfluramine-induced hyperthermia.

The influence of various drug pretreatments upon the responses of rabbits to the putative indirect 5-hydroxytryptaminergic agonists p-chloroamphetamine (PCA) and fenfluramine were examined. In naive rabbits PCA evoked hyperthermia, behavioural excitation and prominent forepaw clonic activity, while fenfluramine produced only hyperthermia and behavioural stimulation. The hyperthermic and behavioural responses of both agents were reduced by the 5-hydroxytryptamine (5-HT) uptake inhibitor, fluoxetine, potentiated by the monoamine oxidase inhibitor, pheniprazine, and unaltered by the dopaminergic antagonist, haloperidol. Pretreatment with the 5-hydroxytryptaminergic receptor blockers cinanserin, cyproheptadine or D-2-bromolysergic acid diethylamide markedly attenuated the effects of fenfluramine but only slightly influenced the responses to PCA. Depeletion of central 5-HT stores with p-chlorophenylalanine also affected responses to fenfluramine more than responses to PCA. The tryptaminergic receptor blocker methergoline abolished both PCA-induced hyperthermia and forepaw clonus--but not behavioural stimulation--while the effects of flenfluramine were only partly reduced. We interpret these data to mean that PCA- and fenfluramine-induced drug effects have different underlying mechanisms, the PCA responses relying possibly upon tryptamine while the fenfluramine responses are 5-hydroxytryptaminergic.

Amphetamines↗