1 The hypokalaemic effect of salbutamol after more than 30 min of administration has been well described. A hyper-and-hypokalaemic effect for adrenaline has been reported, but no such hyperkalaemic effect for salbutamol. 2 The possible hyper-and-hypokalaemic effects of salbutamol with the concomitant potential for pro-arrhythmia were assessed in the baboon (Papio ursinus). 3 Male and femal baboons were anaesthetized with ketamine (15 mg kg-') and maintained with 6% pentobarbitone as spontaneously breathing animals. Six baboons in each group received either 10, 100 or 500 jg kg-' salbutamol i.v. Lead II of the ECG and femoral i.a. blood pressure were recorded continuously for 10 min. Arterial blood samples were collected at 0 min and then after 3 and 10 min of salbutamol administration. 4 All the animals developed sinus tachycardia (above 200 beatsmin-') within 30s of each dose of salbutamol administration and the high heart rate persisted throughout the experiment. All the animals were hyperkalaemic after 3 min and hypokalaemic after O min for each dose of salbutamol. Left ventricular conduction defects were seen in 3 animals during the hyperkalaemic phase. No arrhythmia was seen during the hypokalaemic phase. 5 Salbutamol has a transient hyperkalaemic and a more prolonged hypokalaemic effect in the baboon. The hypokalaemia could not be associated with arrhythmia although conduction defects were associated with the hyperkalaemia. 6 Since salbutamol is used as a bronchodilator in asthmatic patients and to treat acute hyperkalaemia, it is suggested that caution should be exercised when using salbutamol in high doses to treat acute asthma especially during the first few minutes of administration. The finding of hyperkalaemia with salbutamol questions its use in the treatment of hyperkalaemia.

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Angiotensin I was infused into 16 healthy volunteers, 8 blacks and 8 whites with diastolic blood pressures below 75 mm Hg and the infusion rate increased at 3 min intervals until a diastolic blood pressure of equal to or greater than 95 mm Hg was achieved. Blacks exhibited a significantly greater angiotensin I sensitivity needing 1.8 micrograms/min as opposed to 3.9 micrograms/min in whites to achieve the target blood pressure. Plasma renin activities were similar in the two groups, but blacks had significantly higher urinary sodium values than whites, 223 mmol per 24 h as compared to 121 mmol per 24 h. It is concluded that the differences in response could be largely due to differences in dietary sodium intake. These factors need to be carefully considered when using angiotensin I infusion as a pharmacodynamic model for studying the effects of ACE inhibitors.

The effect of electrical stimulation of the cut cervical vagal nerves in dogs on airway resistance and circulating catecholamine concentrations was determined before and after propranolol. Airway resistance increased after 1 min of stimulation and decreased after 9 min of stimulation. The circulating catecholamine levels increased significantly in the pulmonary artery after 1 min of stimulation. After 9 min of stimulation the increase in the femoral artery was relatively more than in the pulmonary artery. This late increase most probably represents catecholamine supply from lung structures.

Submaximal histamine dose-response curves were obtained on 34 dogs divided into six groups. These groups were: A (n=6) untreated; B (n=6) after atropine (1 mg/kg); C (n=5) after verapamil inhalation (10 mg total dose); D (n=5) after verapamil inhalation (100 mg total dose); E and F (n=6) as for C and D but pre-treated with atropine (1 mg/kg). Total lung resistance (Rl) was measured in each case at increasing delivered concentrations of inhaled histamine and expressed as a ratio of baseline valve. For each group a composite mean curve was obtained and the maximal recorded responses (mean maximal resistance ratios) for the various groups were compared. It appears that the combination of verapamil inhalation (low dose) and atropine reduced the anticholinergic effect of atropine causing marked bronchoconstriction. This unexpected result depends on the verapamil dose since it was not present at the higher dose (group F).