Hypertension in hyperthyroidism: is there an epinephrine connection?
Since hypertension seen in euthyroid subjects with depressed conjugated epinephrine and moderately elevated free epinephrine in plasma is strikingly similar to the beta-hyperadrenergic, high-output hypertension seen in some hyperthyroid patients, the possibility is discussed that thyroid action on sulfoconjugation could affect the biodisposability of endogenous free E and so indirectly the manifestation of sympathetic hyperactivity. There is only circumstantial evidence for such a possibility at present. Differences in the conjugation system may be operative in dealing with endogenous as well as exogenous catecholamines. If the latter are used in evaluating the adrenergic receptor reactivity, this may result in incorrect dose-response curves if the concentrations of catecholamines remaining free following infusion are not monitored. The conjugation of catecholamines, E in particular, is a variable which has to be taken account of in the investigation of catecholamine-like manifestation of T3 and T4 excess and in the evaluation of adrenergic influences on thyroid function.
D001794:Blood Pressure; D004298:Dopamine / Q000097:blood; D004837:Epinephrine / Q000097:blood*; D006339:Heart Rate; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000503:physiopathology; D006980:Hyperthyroidism / Q000150:complications* / Q000503:physiopathology
D004298:Dopamine; D004837:Epinephrine