Hydrochlorothiazide-induced sympathetic hyperactivity in hypertensive patients.
Hydrochlorothiazide-induced diuresis and natriuresis is considered to be responsible for the antihypertensive effect of this drug. After short-term treatment there is decreased cardiac output and increased peripheral resistance which we have found to be attended by increased plasma norepinephrine (NE) levels. After longer treatment cardiac output returns to normal and peripheral resistance declines. At this time, plasma NE levels remain elevated, indicating that peripheral resistance reduction is not a consequence of a reduction of the elevated level of sympathetic activity. These results provide a rationale for the combined use of diuretics and drugs which diminish noradrenergic activity in the treatment of hypertension.
D000328:Adult; D001794:Blood Pressure / Q000187:drug effects; D004299:Dopamine beta-Hydroxylase / Q000097:blood; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006852:Hydrochlorothiazide / Q000494:pharmacology / Q000627:therapeutic use*; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood*; D011187:Posture; D011674:Pulse
D006852:Hydrochlorothiazide; D004299:Dopamine beta-Hydroxylase; D009638:Norepinephrine