Captopril potentiates chronotropic baroreflex responses to carotid stimuli in humans.
Angiotensin II is a potent vasoconstrictor and has profound effects on autonomic neural mechanisms in experimental animals. Human carotid baroreflex control of arterial pressure and heart period was examined before and after acutely decreasing angiotensin II levels by administering 50 mg of oral captopril, an angiotensin converting enzyme inhibitor. Carotid baroreceptor stimuli were delivered by a neck chamber worn by 14 normotensive volunteers. Four subjects received placebo. Arterial pressure responses to carotid distention and tachycardia in response to carotid compression were not changed in captopril or placebo groups; however, there was an augmented bradycardic response to carotid stretch in captopril-treated subjects. These results indicate that captopril has an asymmetrical effect on carotid baroreflex function and suggest that enhanced baroreflex mediated bradycardia is due to a reduction in central nervous system angiotensin II levels by captopril, which augments vagal-cardiac responses to carotid stimuli.
D000328:Adult; D000804:Angiotensin II / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology*; D002346:Carotid Sinus / Q000294:innervation*; D004357:Drug Synergism; D006339:Heart Rate / Q000187:drug effects*; D006801:Humans; D008297:Male; D011311:Pressoreceptors / Q000502:physiology*; D011392:Proline / Q000031:analogs & derivatives*; D012018:Reflex / Q000187:drug effects*
D000804:Angiotensin II; D011392:Proline; D002216:Captopril