SUMMARY1. The present study examines the modulation, by parathyroid hormone, of the changes in myocardial contractile force induced by isoprenaline, propranolol isomers, verapamil, and nadolol.2. Cardiac contractile force was estimated by the use of guinea‐pig isolated auricles. Synthetic bovine 1‐34 parathyroid hormone (sPTH) alone did not modify contractile force; conversely, sPTH significantly inhibited the cardiode‐pressant effect ofl‐propranolol,d, l‐propranolol,d‐propranolol, and verapamil. These results suggested an action of sPTH independent of β‐adrenoceptors. Against an hypothesis of a single, non‐β‐adrenoceptor mechanism of sPTH action on the heart are the following observations: (i) when β‐adrenoceptors were blocked with nadolol, sPTH no longer inhibited the cardiodepressant effect of propranolol, (ii) sPTH reduced the inotropic effects of isoprenaline. Our conclusion, therefore, is that sPTH probably affects cardiac muscle contraction by at least two mechanisms, one of which involves non‐adrenergic transmembrane calcium flux and the second β‐adrenoceptors.3. When these studies were extended into the clinical pharmacological field, it was found that plasma ultrafiltrates from severely hyperparathyroid patients in chronic renal failure inhibited like sPTH the cardiodepressant action of propranolol. No such effect was seen with ultrafiltrates from parathyroidectomized patients. Accordingly, high PTH levels may inhibit the action of cardiotropic drugs administered to hyperparathyroid patients, and may be one factor in the cardiomyo