1. Isoprenaline (1 μmol/l) and glucagon (1 μmol/l) raised the levels of cyclic AMP in isolated adipose cells of the rat to a maximum after incubation for approximately 15 min. 2. The effect of glucagon was impaired by pretreatment of adipose cells with trypsin (0.2 mg/ml and 2.0 mg/ml) and N -ethylmaleimide (5 mmol/l). The β-adrenergic receptor was insensitive to such forms of treatment. 3. Insulin (430 μunits/ml) lowered the intracellular levels of cyclic AMP in adipose cells stimulated with isoprenaline (1 μmol/l) and glucagon (1 μmol/l). This effect was observed after incubation for 5 min. 4. Pretreatment of cells with trypsin (0.2 mg/ml and 2.0 mg/ml) and N -ethylmaleimide (0.5 and 5 mmol/l) abolished the effect of insulin in decreasing the intracellular levels of cyclic AMP. At the higher concentration of trypsin a rise in intracellular levels of cyclic AMP was observed in the presence of insulin. 5. Similar concentrations of trypsin and N -ethylmaleimide decreased the disappearance of unlabelled insulin from the incubation medium and also decreased the binding of 125 I-labelled insulin to isolated fat cells. 6. The effect of insulin on decreasing the intracellular levels of cyclic AMP in modified adipose cells significantly correlated with the disappearance of unlabelled insulin from the medium and with the percentage of total 125 I-labelled insulin bound to cells. 7. The possibility is discussed of using the disappearance of insulin or binding of 125 I-labelled insulin to adipose cells as a measure of insulin-receptor availability on the plasma membrane of fat-cells.
1. Measurements of urinary aldosterone excretion and of peripheral venous plasma concentrations of aldosterone, Cortisol and corticosterone have been made in hypertensive and normotensive patients after a sodium load and after dietary sodium restriction and ambulation. 2. Plasma concentrations of aldosterone, Cortisol and corticosterone did not differ significantly between the two groups of patients, but the rise in urinary aldosterone excretion was significantly greater in normotensive than in hypertensive patients after sodium restriction. 3. Division of the hypertensive patients into two groups according to the response in plasma renin on sodium restriction did not disclose any significant differences between responders and non-responders in respect of aldosterone or Cortisol, but the plasma corticosterone rose more in normotensive patients after sodium depletion than in the unresponsive hypertensive patients. 4. It is concluded that both the rise in plasma renin and in aldosterone excretion rate are blunted in hypertensive patients after sodium restriction. It is suggested that this may be due to a rise in total body sodium in hypertensive patients. 5. Differences in aldosterone excretion rate are not reflected in the values of peripheral venous concentrations, presumably because of the short-term rise in plasma aldosterone which results from ambulation.