Plasma Catecholamines and Cardiovascular Responses to Hypoglycemia in Hyperthyroidism before and during Treatment with Metoprolol or Propranolol*

Hypoglycemia normally promotes increases in plasma epinephrine (E) and norepinephrine (NE), tachycardia, and a widened pulse pressure; these responses can be modified by β-adrenoceptor-blocking agents. We assessed the catechola-mine and cardiovascular responses to a standard insulin tolerance test in 18 hyperthyroid patients before and during treatment with selective β-l (metoprolol; n = 9) or nonselective (propranolol; n = 9) β-blocking agents. During hypoglycemia, metoprolol as well as propranolol treatment caused an augmented increase in plasma E, while the increase in NE remained unaltered during β-blockade compared to pretreatment changes. Treatment with metoprolol reduced the supine basal heart rate (HR), although the HR rose significantly during hypoglycemia. Blood pressure (BP) changes were similar to pretreatment values. Propranolol not only lowered basal HR but also totally blocked hypoglycemia-induced tachycardia. Compared to pre-treatment, an increase in diastolic BP and a further rise in systolic BP were recorded. Eleven subjects were reexamined when they were made eu-thyroid by conventional antithyroid therapy. During hypogly-cemia, NE concentrations reached a similar maximum value in the hyperthyroid and euthyroid states, although basal concentrations were lower during hyperthyroidism. No differences were seen between plasma levels of E, and the cardiovascular changes were similar in hyper- and euthyroidism, except for lower basal diastolic BP in hyperthyroidism. Our data demonstrate that stress-induced increases in plasma catecholamines are not suppressed in hyperthyroidism. During β-adrenoceptor blockade, hypoglycemia provokes an enhanced response in plasma E. This increment in plasma E induces changes in the cardiovascular response which are quite different during selective β-l or nonselective β-blockade. The difference is probably due to a coexisting and unopposed change in the a-adrenergic tone during nonselective β-blockade. (J Clin Endo-crinol Metab50: 906, 1980)