Dispersed luteal cells were prepared both from samples of human corpora lutea obtained during normal menstrual cycles and from luteinized rat ovaries of animals pretreated with pregnant mare's serum gonadotrophin and human chorionic gonadotrophin (hCG). Addition of the long-acting analogue, D-Ala6-des-Gly10-LH releasing hormone ethylamide (D-Ala6-LHRH), to rat luteal cells caused a small but significant increase in progesterone production. An inhibitory action of the analogue on hCG-stimulated steroidogenesis by rat luteal cells was confirmed. Addition of D-Ala6-LHRH to suspensions of human luteal cells had no effect on either basal or hCG-stimulated progesterone production. Studies on the interaction of 125I-labelled D-Ala6-LHRH with the dispersed cell preparations, while confirming the presence of displaceable binding to rat luteal cells, failed to detect any equivalent binding to human luteal cells. Low levels of displaceable binding observed using homogenates of human corpora lutea are interpreted as being of doubtful physiological significance in view of the negative findings obtained with the intact cell system.

1 The polymorphism of phenformin oxidation has been investigated in 103 non-insulindependent (Type II) diabetics. The frequency distribution was clearly bimodal and 14 poor metabolisers were identified. The frequency of the recessive allele (0.369) was not significantly different from that found previously in non-diabetics. 2 Six of the extensive metabolisers of phenformin were matched for age, sex and oxidiser phenotype with non-diabetic controls. All subjects underwent a standard 3-min exercise test, using a bicycle ergometer, after which plasma lactate concentration was monitored for 90 min. There was no significant difference between groups in lactate accumulation or elimination. 3 Ten extensive metabolisers, ten poor metabolisers and seven non-diabetics (matched for age, sex and phenotype with seven of the diabetic extensive metabolisers) were challenged with a fasting oral dose of phenformin (50 mg), after which plasma lactate, and blood pyruvate and glucose concentrations were monitored for 4 h. A further ten diabetics (five extensive and five poor metabolisers of phenformin) received a single dose of metformin (1 g) following an identical protocol. No significant changes were observed in any group.

1 Osmotic water movement across toad isolated hemibladders was measured by a gravimetric method. 2 The influence of carbamazepine, chlorpropamide and demeclocycline on the antidiuretic hormone (ADH)-induced water flow rate was examined.3 No antidiuretic activity due to carbamazepine alone was observed but a slight inhibition due to ADHinduced water flow was observed in the presence of carbamazepine over a selected dose-range. This was unexpected and is inconsistent with data from in vivo studies in man. 4 Chlorpropamide potentiated ADH-induced water flow, in keeping with the hypothesis that chlorpropamide sensitizes the renal tubules to ADH-induced water flow. 5 Demeclocycline inhibited ADH-induced water flow. The mechanism of action remains unclear.

The concentration of phenytoin in saliva has been measured in 8 healthy volunteers at intervals after an intravenous dose and after single oral doses of five formulations commercially available in the United Kingdom. The six doses (all 300 mg) were given in random order and at least one week apart. There were no significant differences in the mean values of the peak saliva concentration, the time-to-peak and the area under the saliva concentration-time curve between the five oral formulations. The absolute bioavailability of phenytoin varied between 68 and 74%.

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