Bay K 8644‐induced changes in the ECG pattern of the rat and their inhibition by antianginal drugs

1 The effects of intracarotid administration of Bay K 8644 on the ECG pattern along with their reversal by antianginal drugs were investigated in anaesthetized rats. 2 Intracarotid injections of Bay K 8644 (0.5–50.0 μg kg−1) produced a dose‐related transient increase in systemic blood pressure. 3 The pressor response was accompanied by ST segment elevation (0.5–10.0 μgkg−1), ST segment depression concomitant with the occurrence of arrhythmias (20.0 μgkg−1), or A‐V block (50.0 μgkg−1). 4 ST segment elevation reached its maximal value within 15 s and could be observed for 30–240 s. 5 The increase in blood pressure was immediate (within 5 s) and short lasting (30–120 s). After the initial increase it returned to control levels (0.5–20.0 μgkg−1) or dropped below (50.0 μgkg−1). 6 The ST segment elevation caused by 5.0 μgkg−1 Bay K 8644 (submaximal dose) was blocked by antianginal drugs (e.g. nitroglycerin, nifedipine and diltiazem) and by the peripheral benzodiazepine receptor antagonist PK 11195. However, the pressor response was not blocked by any of the drugs used. 7 ST segment elevation (or depression) induced by intracarotid administration of Bay K 8644 provides a useful tool for the evaluation of potential antianginal drugs.