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Biomedical subjects

K J Rogers

Publications and source records attributed to K J Rogers.

At least 37 records · Page 2Linked to original sources
PubMed1975

Characterisation of the adrenoceptor mediating changes in cyclic adenosine 3'-5' monophosphate in chick cerebral hemispheres.

Noradrenaline, adrenaline, isoprenaline and salbutamol induced marked accumulations of cyclic AMP in incubated slices of chick cerebral hemispheres. Isoprenaline was both more potent and more powerful than adrenaline or noradrenaline and the increase in cyclic AMP elicited by the catecholamines was powerfully antagonized by the beta-adrenoceptor antagonist propranolol but not by the alphapadrenoceptor blocker phentolamine. The order of potency of the catecholamines isoprenaline greater than adrenaline greater than noradrenaline and the ability of the non-catechol salbutamol to stimulate cyclic AMP accumulation in chick cerebral slices suggests that the beta-adrenoceptro may resemble that found in the lung (beta2) rather than that in the heart (beta1). Propranolol proved to be a very potent antagonist of the cyclic AMP response induced by isoprenaline in vivo. Beta-adrenoceptor blockade was still evident 12 hrs after a single injection of the durg although only negligible amounts of 3H-propranolol could be detected in cerebral tissue after 2 hrs.

Albuterol↗
PubMed1973

Role of brain monoamines in the fatal hyperthermia induced by pethidine or imipramine in rabbits pretreated with a monoamine oxidase inhibitor.

1. The intravenous infusion of pethidine or imipramine, in doses of 5 mg/kg, caused fatal hyperpyrexia in rabbits premedicated with pargyline.2. The drug interaction was not antagonized when either reserpine or alpha-methyl-p-tyrosine were administered with pargyline. Neither reserpine nor alpha-methyl-p-tyrosine prevented the rise in brain stem 5-hydroxytryptamine content following monoamine oxidase inhibition, although the increase in catecholamines normally produced by pargyline was prevented.3. The development of fatal hyperthermia was completely prevented when rabbits were treated with p-chlorophenylalanine prior to pargyline premedication. In these animals, the concentration of brain stem catecholamines, but not 5-hydroxytryptamine, was increased.4. The results indicate that the hyperthermia evoked by pethidine or imipramine in combination with monoamine oxidase inhibitors can take place only in the presence of raised concentrations of 5-hydroxytryptamine in the brain stem.

Amines↗
PubMed1973

Effect of depletion of cerebral monoamines on the concentration of glycogen and on amphetamine-induced glycogenolysis in the brain.

1. An increase in the concentration of glycogen occurs in the mouse brain after depletion of cerebral catecholamines by alpha methyl-p-tyrosine methylester (H44/68), diethyldithiocarbamate, or reserpine.2. Depletion of cerebral 5-hydroxytryptamine with parachlorophenylalanine (PCPA) does not result in a change in the concentration of brain glycogen.3. When H44/68 is administered together with reserpine to inhibit the synthesis and storage of cerebral catecholamines, and thus bring about their total depletion from the brain, the cerebral glycogenolytic effect of amphetamine is abolished.4. Amphetamine-inducing glycogenolysis is only partially antagonized if only one of the catecholamine-depleting agents H44/68, diethyldithiocarbamate, or reserpine is injected prior to the amphetamine. The persistence of this glycogenolytic effect of amphetamine is possibly due to the presence of residual stores of catecholamines available for release by the stimulant drug.5. Depletion of cerebral 5-hydroxytryptamine by PCPA does not result in any antagonism of amphetamine-induced glycogenolysis.6. The results suggest that amphetamine depletes brain glycogen by the release of central catecholamines rather than by a direct action at receptors.

Amphetamine↗