Endogenous opioid peptides: do they mediate the acute antihypertensive action of clonidine in humans?
The involvement of endogenous opioid peptides in the antihypertensive action of acutely administered clonidine, a centrally acting adrenergic agonist, was studied in humans. Eight hypertensive subjects received clonidine 0.2 mg orally, naloxone 8 mg i.v. followed by a 0.13 mg/min infusion, and both drugs together on separate days. Clonidine resulted in a significant decrease in mean blood pressure, which was not affected by concomitant treatment with naloxone. Naloxone alone or with clonidine caused significant elevations in plasma aldosterone, not mediated by increased plasma renin activity. Plasma beta-endorphin was not increased after clonidine administration. In humans, the antihypertensive effects of acute clonidine administration do not appear to be mediated by the release or action of endogenous opioids.
D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects; D003000:Clonidine / Q000494:pharmacology* / Q000627:therapeutic use; D004723:Endorphins / Q000097:blood / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009270:Naloxone / Q000494:pharmacology; D012083:Renin / Q000097:blood; D001615:beta-Endorphin
D004723:Endorphins; D009270:Naloxone; D000450:Aldosterone; D001615:beta-Endorphin; D012083:Renin; D003000:Clonidine