Hypoxia-induced cardiovascular changes and plasma electrolytes before and after beta-adrenoceptor blockade.
The forearm blood flow responses to hypoxia obtained from ten subjects (ages 26-37 years) before and after propranolol showed no relation with either plasma osmolality or plasma concentrations of K+, Na+, Ca2+, Pi and Cl-. The average oral dose of 3.3 mg of propranolol/kg body weight decreased the overall mean flow response to hypoxia by 42.2% (P less than 0.025). This reflects some beta-adrenoceptor involvement. The residual vasodilatation observed after beta-blockade by propranolol could be attributed to activation of cholinergic vasodilator fibres by hypoxic stress. The mean heart rate during acute hypoxia before and after propranolol administration was 95 and 89 beats/min respectively. The residual tachycardia could be due to reduction of vagal tone during the hypoxic stress. The response of arterial blood pressure to the hypoxic stress before and after propranolol administration, on the other hand, was found to be negligible in most subjects. This lack of response during emotional stress is in agreement with previous findings. In the present circumstances the possible increase in baroreceptor activity is probably masked by the general peripheral vasodilatation.
D000320:Adrenergic Fibers / Q000503:physiopathology; D000328:Adult; D001794:Blood Pressure / Q000187:drug effects; D002319:Cardiovascular System / Q000503:physiopathology*; D004573:Electrolytes / Q000097:blood; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D009994:Osmolar Concentration; D011433:Propranolol / Q000494:pharmacology*; D014664:Vasodilation / Q000187:drug effects
D004573:Electrolytes; D011433:Propranolol