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The effect of insulin-induced hypoglycemia upon plasma renin activity (PRA) was assessed in 4 normal volunteers, 4 adrenalectomized patients and 10 patients with various pituitary hormone deficiences. Significant increases in PRA were observed in all three groups. The PRA responses to hypoglcemia could be blocked by propranolol, and appeared to be potentiated by theophyline. It is concluded that sympathetic reflex stimulation, not adrenal-dependent and not pituitary-dependent, is the major mechanism for this phenomenon in man and that this adrenergic effect may be mediated by cyclic AMP.

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SUMMARY Insulin-induced hypoglycemia previously has been shown to provoke a /S-adrenergic response that normally results in an increase in plasma renin activity (PRA). In our study, hypoglycemia induced definite increases in PRA in a group of five patients with normal renin essential hypertension but failed to do so in a group of six patients with low renin essential hypertension. In both groups, plasma cyclic adenosine 3',S'-monophosphate (cyclic AMP; cAMP) increased more than 2-fold during hypoglycemia, but the response in the low renin group was significantly less than that previously observed in normal subjects under the same conditions. Plasma cortisol increased to an equal extent in both groups of hypertensive patients during hypoglycemia. Infusion of the phosphodiesterase inhibitor, theophylline, resulted in definite increases of PRA in patients with normal renin hypertension but not in patients with low renin hypertension. Because changes in the level of plasma cAMP during hypoglycemia have been thought to reflect adrenal catecholamine release, our finding of a blunted increase in plasma cAMP during hypoglycemia in patients with low renin hypertension may suggest that there is a generalized alteration in adrenergic responsiveness in this condition.INSULIN-INDUCED hypoglycemia has been shown to promote an increase in plasma renin activity (PRA) in dogs 1 and in normal human subjects. 2 This response in PRA is inhibited by /?-adrenergic blockade; 2 -3 insulin-induced hypoglycemia thus appears to provide an endogenous /3-adrenergic stimulus to renin release.The change in PRA is abnormally low in response to various stimuli in a distinct subgroup of the population with essential hypertension, 4 " 6 and this group has been referred to as having low renin essential hypertension. In an effort to gain insight into the mechanism(s) under which renin release is dampened in low renin essential hypertension, we have evaluated PRA responsiveness to the endogenous ^-adrenergic stimulus which results from hypoglycemia in patients with normal renin and low renin essential hypertension. Moreover, since it has been suggested that adrenergic responsiveness may be impaired in low renin essential hypertension, 7 -8 and since changes in extracellular cyclic adenosine 3',5'-monophosphate (cyclic AMP; cAMP) during hypoglycemia have been thought to reflect adrenal catecholamine release, 9 we also have measured plasma cAMP in our low renin and normal renin essential hypertension patients during hypoglycemia.Finally, because infusion of the phosphodiesterase inhibitor, theophylline, has been associated with an increase in cAMP levels of some tissues 1013 as well as with increases in PRA, 2 -14 and because intracellular cAMP has been implicated in the mediation of renin release, 2 -15 " 17 we also examined the PRA responses to theophylline infusion in these two groups of hypertensive subjects. MethodsEleven hypertensive patients, studied as outpatients, were separated into two groups on the basis of their PRA responses to the dual...

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