Effect of osmotic pressure, Na+-K+ ratio and medium concentration on the enzyme activity and growth of L cells in suspension culture.
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Animals↗
Biomedical subjects
J M Elliott
Publications and source records attributed to J M Elliott.
Slow wave sleep in humans: role of 5-HT2A and 5-HT2C receptors.
We studied the effects of the 5-HT2 receptor antagonists, ritanserin and ketanserin, on the sleep of healthy volunteers in order to clarify the role of 5-HT2A and 5-HT2C receptors in the regulation of slow wave sleep (SWS) in humans. Ritanserin, 5 mg, produced a substantially larger increase in SWS (51.4%) than either ketanserin, 20 mg (17.2%) or ketanserin, 40 mg (24.4%). Ritanserin has a significantly higher affinity than ketanserin for 5-HT2C receptor binding sites in the human brain and, based on estimates of per cent occupancy by the two compounds at brain 5-HT2A and 5-HT2C receptors, we conclude that SWS in humans is primarily regulated by 5-HT2C receptors.
Adult↗
Dieting and weight loss in volunteers increases the number of alpha 2-adrenoceptors and 5-HT receptors on blood platelets without effect on [3H]imipramine binding.
Platelet monoamine receptor binding was determined in normal male and female subjects before and at the end of a 2- to 3-week weight reducing diet (1200 kcal daily). Dieting was associated with an increase in platelet binding sites for both [3H]yohimbine and [125I]iodolysergic acid diethylamide (iodoLSD). The affinity at the platelet [125I]iodoLSD binding site was reduced. In contrast, [3H]imipramine binding was unchanged. These results have important implications for studies that employ platelet binding as a peripheral marker of neurotransmitter function in psychiatric illness.
Adult↗
Platelet 5-HT receptor binding during depressive illness and tricyclic antidepressant treatment.
5-Hydroxytryptamine (5-HT) receptor binding was determined in intact human platelets using 125I-iodolysergic acid diethylamide (125I-iodoLSD). The assay revealed that platelets possess a single population of specific binding sites for 125I-iodoLSD which have a high affinity for the 5-HT2 receptor antagonists, ketanserin and spiperone. There was no difference in platelet 125I-iodoLSD receptor binding between depressed patients and controls. However, treatment with tricyclic antidepressants increased the number of 125I-iodoLSD receptor binding sites without significantly altering their affinity.
Adult↗
Cardiovascular effects of intracisternal 6-hydroxydopamine and of subsequent lesions of the ventrolateral medulla coinciding with the Al group of noradrenaline cells in the rabbit.
The acute cardiovascular effects of intracisternal injections of 6-hydroxydopamine (6-OHDA), 5,6-dihydroxytryptamine and 5,7-dihydroxytryptamine and the degree of neurotransmitter depletion achieved by such injections were studied. The two different vehicles used--0.2% ascorbic acid in 0.9% NaCl, or 0.9% NaCl--had little effect on the cardiovascular response to 6-OHDA injections but had a striking effect on levels of noradrenaline (NA) subsequently measured in the thoracic spinal cord. 6-OHDA (600 micrograms kg-1 free base) dissolved in normal saline depleted spinal cord NA to less than 1% of control levels whereas the same dose of 6-OHDA dissolved in ascorbate saline only depleted spinal cord NA to 24% of control levels. The degree of depletion of NA in medulla, pons and hypothalamus was similar in the two groups. Ascorbic acid also appeared to contribute to the non-specific toxicity of intracisternal injections of 6-OHDA. The hypertension and bradycardia that followed lesions of the ventrolateral medulla coinciding with the A1 group of noradrenergic cells (Al lesions) were attenuated in animals in which spinal cord NA had been depleted to 2% of control using 6-OHDA in normal saline. However, pretreatment with 6-OHDA in ascorbate saline, which only reduced spinal cord NA to 23% of control, had no effect on the cardiovascular response to Al lesions. It seems likely that the effects of Al lesions are mediated, at least in part, by NA projections descending within the spinal cord.
5,6-Dihydroxytryptamine↗
Effects of vasopressin on heart rate in conscious rabbits.
The effects of vasopressin on heart rate and on the baroreceptor-heart period reflex were assessed during graded intravenous infusions of arginine vasopressin. Infusions which elevated plasma arginine vasopressin to 200 pg/ml had no effect on blood pressure, but induced a fall in heart rate and cardiac output and an increase in peripheral resistance. These effects were unaltered by vagal blockade with methylscopolamine and cardiac sympathetic blockade with propranolol but were prevented by pretreatment with a specific vascular antagonist to vasopressin, d(CH2)5Tyr(Me)AVP. Baroreflex control of heart rate was studied during vasopressin infusion by monitoring the heart period responses to graded changes in mean arterial blood pressure produced by inflation of balloon occluders around the abdominal aorta and thoracic vena cava. Elevation of plasma arginine vasopressin to 50 pg/ml and 200 pg/ml had no significant effect on the slope or sensitivity of the baroreceptor-heart period reflex but increased the maximum bradycardia elicited in response to large increases in blood pressure. We conclude that at physiological levels, arginine vasopressin has a direct cardiodepressant action that is not dependent on cardiac vagal or sympathetic activity. Our results indicate that arginine vasopressin increases the maximum bradycardia that can be elicited through baroreceptor reflexes but does not alter the slope relating change in heart rate to change in blood pressure.
Animals↗
The central noradrenergic control of blood pressure and heart rate.
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Anesthesia↗
In vivo and in vitro metabolism studies on a class III antiarrhythmic agent.
The metabolism of L-691,121 (I), a class III antiarrhythmic agent, was studied in vivo in rats and dogs and in vitro by using liver S9 or slices from these species and humans. After oral doses of [14C]I to rats (5 mg/kg) and dogs (1 mg/kg), urinary recoveries of label were, respectively, 6% and 28%. Biliary excretion (0-24 hr) accounted for 68% of a 5 mg/kg, po dose in rats and 19% of a 10 mg/kg dose, po in dogs. Metabolites were identified by application of FAB/MS, NMR, and diode-array UV spectroscopy. The major dog metabolites were the secondary alcohol (II) produced by carbonyl reduction and its glucuronide conjugate (III). It was estimated that II and III represented 24 and 36%, respectively, of the dog biliary radioactivity. After a 50 mg/kg dose of I, II represented approximately 50% of the dog urinary label. A minor metabolite (IV) in dog urine was produced by reduction and loss of N-substitution. There were species differences in that, relative to dogs, II represented a much smaller fraction of the excreted dose in rats and there was no evidence for excretion of III in rats. N-Dealkylated I (V) was excreted, along with IV in rat bile. Dog liver slices and S9 fractions were most efficient (relative to human and rat liver tissues) at reducing I to II. Metabolic reduction of I to II was highly stereoselective and yielded the (-)-antipode as determined by chiral chromatography.
Aged↗