&NA;To study the effects of myocardial hypertrophy resulting from chronic pressure overload on excitation‐contraction coupling, the cardiac transmembrane L‐type calcium current (ICa) was investigated in the Goldblatt renovascular hypertensive (HBP) rat. ICawas measured in single myocytes enzymatically isolated from control (CTRL) and HBP rat hearts using the whole‐cell, patch‐clamp method. The peak ICaand ICadensity (obtained by normalizing ICato the average cell capacitative surface area) were larger in HBP cells (n=15) than in CTRL cells (n=10) at membrane potentials of −20 to 50 mV (p<0.01). The maximal peak ICaincreased from 0.9±0.5 nA (mean±SD) in CTRL cells to 2.8±1.0 nA in HBP cells (p<0.001). The corresponding ICadensity increased from 5.3±2.7 to 16.2±6.0 &mgr;A/cm2(p<0.001). There was no shift in the current‐voltage relation between CTRL and HBP cells. The time course of decay of HBP ICain response to clamp steps to the plateau range of the action potential (membrane potential, Vm= −10 to 30 mV) was delayed when compared with that of CTRL ICa. The inactivation time constants (biexponential) for the maximal ICawere 6.9±1.9 and 36.0±9.3 msec for CTRL cells and 6.7±1.4 and 49.5±12.9 msec for HBP cells (p<0.05 for the slower component of the maximal ICa). There was no difference in the steady‐state inactivation of ICa(fœ) for the CTRL and HBP cells. From the maximal peak ICa, cytoplasmic free Ca2+was estimated to reach a pCa of 6.95±0.07 for CTRL cells and 6.64±0.13 for HBP cells. It is concluded that ICais increased with myocardial hypertrophy. The lengthening of the action potential in hypertrophied rat myocardium is due to an increase in peak current density and to the slower inactivation of the maximal ICa. The increased transmembrane flux of Ca2+via ICain HBP cells is inadequate to achieve a myoplasmic free Ca2+level sufficient for direct partial activation of the contractile myofilaments. However, in the scheme of the calcium‐triggered calcium release hypothesis such an increase could provide an increased amount of activator calcium and/or serve to amplify the release of Ca2+from sarcoplasmic reticulum, thereby contributing to preserved peak developed tension in hypertrophied rat myocardium. (Circulation Research1989;64:753‐763)