Changes in glucose tolerance and development of gall stones during high dose treatment with octreotide for acromegaly.

Our results confirm a previous case report in which a sharp rise in plasma atrial natriuretic factor was recorded immediately after pericardiocentesis.3 A similar twofold to threefold increase was also described after pericardiectomy in a patient with chronic constrictive pericarditis.4 These findings are in strong contrast to other conditions, such as left ventricular failure, in which cardiac filling pressures are correlated with circulating concentrations of atrial natriuretic factor.5 Clinical deterioration is associated with a further increase in peptide concentrations, while treatments which lower cardiac filling pressures also lower plasma atrial natriuretic factor values.' Our findings suggest that raised atrial pressure does not directly stimulate the release of atrial natriuretic factor. Rather, raised filling pressures increase atrial distension, which in turn increases secretion of the peptide. Further support for this hypothesis has come from a definitive experiment, conducted in anaesthetised dogs, in which the induction of cardiac tamponade did not increase plasma concentrations of atrial natriuretic factor despite a considerable increase in atrial pressures. In contrast there was a threefold rise in peptide values when atrial pressures were raised to a similar degree by constriction of the great arteries. We conclude that in humans, as in this animal model, the primary stimulus for the release of atrial natriuretic factor is atrial distension.