The role of adrenergic receptors in mediating renin secretion was studied in normal subjects with the use of upright posture and administration of diazoxide, ethacrynic acid and theophylline to provoke renin release. Each of these stimuli produced the expected rise in plasma renin activity (PRA), despite marked differences in their effect on urinary sodium excretion. In each case the increase in PRA was markedly suppressed on retesting with an infusion of either phentolamine, an alpha-adrenergic blocking agent, or propranolol, a beta-adrenergic blocking agent, whereas adrenergic blockade had little or no affect on sodium excretion. Since the stimuli chosen for provoking renin release have diverse mechanisms of action, it is noteworthy that PRA was suppressed by adrenergic blockade, regardless of the stimulus used. These findings suggest that many, if not all, of the stimuli for renin release are mediated by a common pathway which may involve alpha-and beta-adrenergic receptors. Moreover, renin release may occur independently of changes in sodium excretion. (J Clin Endocr 29: 1168

Pyruvic carboxylase activated by acetyl coenzyme A is highly active in the mitochondria of rodent liver, and its activity is increased in fasting and alloxan diabetes. In conjunction with acyl carboxylase activated by di- and tricarboxylic acid, it forms a reciprocating control network. Analog models of similar networks tend to correct for perturbations, stabilizing the overall system.

A diabetes mellitus-like disease occurs in male DBA/2 mice infected with the M variant of the encephalomyocarditis virus. Female mice of this strain sustain systemic infection, but rarely exhibit hyperglycaemia. The diabetogenic effects of the virus were studied in 3 groups of adult DBA/2 males-castrates, castrates treated with testosterone, and sham-operated controls. After infection, pancreatic insulin concentrations decreased precipitously to approximately 10% of control values in intact males and castrates treated with testosterone; hyperglycaemia occurred concomitantly in both groups. In contrast, untreated castrates failed to develop hyperglycaemia and the effect on the insulin content of the pancreas was less striking.

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