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Guanfacine, a central alpha-adrenoreceptor agonist, may increase growth hormone (GH) secretion. We have investigated the effect of guanfacine upon plasma GH levels in 16 hypertensive non-insulin-dependent diabetic (NIDD) patients. Guanfacine (1 to 2 mg/day/os) was administered for six months, and GH measured in basal plasma samples before and after treatment with this drug. Our results show an increase in GH plasma levels after guanfacine administration (2.88 +/- 2.05 ng/ml (X +/-SD) before, and 4.37 +/- 1.80 ng/ml (X +/- SD) after treatment). Since it is believed that GH levels plays a role in the course of diabetic retinopathy, caution should be taken with guanfacine antihypertensive treatment in patients affected with diabetes mellitus.

We show the autoradiograms of DNA from one child affected of familial isolated growth hormone deficiency type I-A. Restriction endonuclease analysis of DNA isolated from leukocytes was done using 32P-labeled human GH cDNA clone as a probe. DNA analysis using the restriction endonuclease Bam HI revealed that the 3.8 kb restriction fragment, which contain the normal hGH-N gene, was absent. Since these deletions preclude production of any GH-N protein, affected individuals tend to be immunologically intolerant to exogenous GH. The child was homozygote and after treatment with exogenous GH developed a high titre of antibodies to GH and growth arrest. This is the first case of this genetic disorder studied in Spain.

Insulin-induced hypoglycaemia, which stimulates gastric acid secretion, is associated with an increase in circulating somatostatin levels in man. In order to assess the mechanisms involved in this rise, six normal volunteers connected to a Biostator for continuous glucose monitoring were studied, on three separate occasions. On each occasion after basal blood sampling, 0.15 i.u./kg body weight of insulin was administered i.v. and further samples were obtained intermittently over 150 min. On one occasion, dextrose was infused by the Biostator to prevent hypoglycaemia, while on the other two, a constant infusion of either normal saline or the specific H2 antagonist cimetidine was administered. Insulin plus dextrose caused no significant changes in circulating somatostatin levels, whereas insulin plus saline was associated with a marked, sustained and significant rise in all subjects; insulin plus cimetidine also produced a rise but it was delayed; the area under the curve was significantly (P less than 0.05) greater with insulin plus saline than with insulin plus cimetidine. These results show that in man insulin itself does not stimulate somatostatin secretion directly, but indirectly via hypoglycaemia. Further, the inhibition of gastric acid secretion with cimetidine reduces somatostatin release during insulin-induced hypoglycaemia. This suggests that gastric acid may mediate somatostatin secretion associated with insulin-induced hypoglycaemia.