Varying additive effects of bromocriptine with two somatostatin analogs in cultures of GH-secreting adenomas.

In this study, we have investigated the effect of combined treatment using two somatostatin analogs, lanreotide or octreotide, with bromocriptine on GH release in cultures of GH-secreting pituitary tumors. Sixteen acromegalic patients were included in the study. All patients had been treated with lanreotide prior to the surgery. Five patients (31.2 %) reached GH levels below 2.0 microg/l and normal IGF-I levels according to age and sex after lanreotide treatment. A positive correlation was observed between the lanreotide-induced inhibition of GH release in vitro and serum GH decrease after lanreotide treatment (r = 0.52; p = 0.03). Combined treatment significantly inhibited GH release in vitro in 8 of the 16 tumors (50 %). However, only 5 (31.2 %) of the respective patients had been resistant to presurgical treatment with lanreotide. Three of these 5 patients (18.7 %) responded to a BC concentration similar to that achieved with therapeutic doses, and in 2 patients only when a pharmacological dose of BC was used in the combined treatment. The additive effect was observed with the combination of lanreotide and BC in 6 tumors and with octreotide and BC in 3. Only one tumor showed simultaneous response to both types of combination. These results suggest that the additive effect under the combined treatment might be found between 18 and 30 % of patients who are resistant to these drugs, and that different combinations of somatostatin analogs and dopamine agonists should be tested in resistant patients.

Epidemiology of high blood pressure and obesity.

The relationship between bodyweight and arterial pressure was first discovered early this century. More recently, epidemiological studies have confirmed the correlation between bodyweight and blood pressure in both adults and children. Serum cholesterol levels, blood glucose levels, uric acid levels and blood pressure increase with increasing bodyweight. In the presence of androgens, upper body obesity, caused by excessive intake of calories, increases cardiovascular risk factors, probably as a result of hyperinsulinaemia. The activity of Na+/K(+)-ATPase in the cells of obese subjects is reduced in a way that may be genetically determined, or may be mediated by changes in plasma insulin levels or a natural inhibitor of Na+/K(+)-ATPase. In vitro studies have shown that the potency of a non-ouabain inhibitor of Na+/K(+)-ATPase is enhanced by the presence of insulin. This may result in vascular smooth muscle having increased reactivity to pressor agents. A knowledge of cellular membrane transport may lead to a better understanding of the epidemiology of obesity-related hypertension.