Antihypertensive action of propranolol in man: lack of evidence for a neural depressive effect.
The hypothesis that a neural depressive action is related to the antihypertensive effects of beta blockers has been evaluated in 14 essential hypertensive male patients through the circulatory response to noxious stimuli. The pressor reaction to mental arithmetic was primarily mediated by cardiac stimulation (beta receptors activation), that to cold by vasoconstriction (alpha receptors activation). Arithmetic and cold were tested to separate the effects of peripheral beta blackade from possible neural and other influences. After propanolol (320 mg per day for 3 wk): (1) The baseline pressure was reduced; (2) appearance, peak, and disappearance time of the circulatory reaction to either stimulus was not altered; (3) the pressor effect of arithmetic was decreased in an extent proportional to the reduced rise of cardiac output; and (4) pressure during cold reached the pretreatment levels through an augmented increase of vascular resistance. Our findings indicate that propranolol depresses only the circulatory reactions mediated through beta receptors activation and provide no evidence of effects other than beta blockade.
D000319:Adrenergic beta-Antagonists; D000959:Antihypertensive Agents; D001341:Autonomic Nervous System / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D003864:Depression, Chemical; D006801:Humans; D008297:Male; D010919:Placebos; D011433:Propranolol / Q000494:pharmacology*; D011941:Receptors, Adrenergic / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects
D000319:Adrenergic beta-Antagonists; D000959:Antihypertensive Agents; D010919:Placebos; D011941:Receptors, Adrenergic; D011433:Propranolol