Use of corticotropin-induced potassium changes in the diagnosis of both hypo- and hyperkalemic periodic paralysis.

Both hypo- and hyperkalemic periodic paralysis may be difficult to diagnose conclusively when patients are not seen during attacks. Since paralysis of both types can be induced with ACTH, we have determined the frequency of this response in small groups of patients. Weakness or paralysis with appropriate changes in serum K concentration resulted from ACTH gel administration, in 4 of 5 patients with known hypokalemic periodic paralysis and in 3 of 3 patients with hyperkalemic paralysis. No adverse effects of the test were observed, but hospitalization and careful monitoring were necessary. The response to ACTH appears to be a sensitive, useful aid to the diagnosis of both hypo- and hyperkalemic periodic paralysis.

Primary hyperepinephrinemia in patients without pheochromocytoma.

Clinical features of epinephrine release led to the finding of spontaneously elevated plasma epinephrine concentrations in five patients, in four of whom plasma norepinephrine concentrations were normal. Adrenal medullary hyperplasia was suspected in one patient, whose first cousin had multiple endocrine neoplasia type IIa, and in two others, all of whom have experienced relief from symptoms during propranolol or atenolol administration. The other two patients had unilateral adrenal cysts, with negative metaiodobenzylguanidine scans and no histological evidence of pheochromocytoma, but complete relief of symptoms by excision of the cysts. In one patient, Cushing's syndrome and associated hypertension, diabetes, and ischemic finger-tip ulceration all disappeared after surgery. It is concluded that spontaneous hyperepinephrinemic manifestations can be received by beta-blockers or, when an adrenal mass is present, by unilateral adrenalectomy even when the metalodobenzylguanidine test result is negative.

Action of L-epinephrine on the renin-aldosterone system and on urinary electrolyte excretion in man.

The effect of L-epinephrine infusions (0.5-6.5 micrograms/min for up to 24 hr) in recumbency, on the renin-aldosterone system was studied in normal volunteers on diets containing 200 mEq sodium. Urinary sodium excretion was increased, potassium excretion was decreased, aldosterone excretion was suppressed while blood pressure and heart rate were minimally affected by epinephrine (1 microgram/min). Inulin and para-aminohippurate clearances changed transiently and slightly during epinephrine infusions over 10 hr in normal subjects. In separate experiments, epinephrine lowered serum K, raised serum Na, raised plasma renin activity and, usually lowered plasma aldosterone concentrations. There was an excellent correlation between epinephrine-induced changes in serum K and plasma aldosterone concentrations (r = +0.85, p less than 0.001). Significant dose-response relationships were found between L-epinephrine infusion rates of 0.5-6.5 micrograms/min and observed serum K concentrations. We conclude that L-epinephrine infusions at rates probably well within the physiological range, induce hypokalemia (by increased cellular uptake of K) which lowers aldosterone secretion depsite concomitant elevation of PRA and causes natriuresis for up to 24 hr.