Carotid sinus reflexes in rats given small doses of lead.

The effect of low level lead poisoning on the carotid sinus reflex in rats was studied. The reflex was evoked by carotid artery clamping, in control and lead-poisoned animals. Wistar rats were given lead acetate trihydrate (50 mg/kg) via stomach tube once weekly for 5 weeks; control animals were given equimolar amounts of sodium acetate. Both groups were fed a regular animal food diet. At the end of the 6th week, and under urethane anesthesia, mean arterial blood pressure and heart rate were continuously recorded for both groups, before and after clamping, and after unclamping the left common carotid artery. In other experiments, some animals were pre-treated with dopamine, 0.040 mg/kg; practolol, 3 mg/kg; propranolol, 0.1 mg/kg; or atropine, 0.1 mg/kg. In animals not given drugs, lead produced a less pronounced rise in mean arterial blood pressure after clamping, and a more pronounced decrease in heart rate after unclamping, compared to control animals. Some drugs altered this response pattern. Atropine led to a more pronounced tachycardia in the lead-poisoned rats, whereas practolol led to a more pronounced bradycardia in the lead-poisoned rats. Propranolol pretreatment led to a less pronounced decrease in heart rate for lead-poisoned rats, again as compared to the controls. Atropine and beta-adrenergic receptor blocking agents produced similar carotid sinus reflex responses in control and lead-poisoned animals.