EFFECTS OF CAPTOPRIL ON CALCIUM INFLUX IN VASCULAR SMOOTH-MUSCLE CELL

To evaluate whether captopril has a direct effect on the calcium homeo stasis in vascular smooth muscle cells (VSMC), cytosolic free calcium concentration ([Ca2+]i) was measured in cultured VSMC from Wistar-Kyot o rats using the fluorescent dye fura2. The preincubation with 100 muM ol/l captopril for 40 min significantly reduced the angiotensin II ind uced [Ca2+]i increase in VSMC from 90 +/- 10 nmol/l to 51 +/- 16 nmol/ l (n = 53, mean +/- SEM, p <0.05). In the absence of external calcium captopril did not significantly change the angiotensin II induced [Ca2 +]i increase (42 +/- 11 nmol/l vs 48 +/- 12 nmol/l) indicating that ca ptopril mainly affected the transplasmamembrane calcium influx. Preinc ubation with 100 muMol/l captopril for 40 min also significantly reduc ed the bradykinin induced [Ca2]i increase in VSMC from 114 +/- 27 nmol /l to 11 +/- 7 nmol/l (n = 20, p <0.01). In contrast, captopril had no significant effect on the norepinephrine (NE) or BayK8644 (BayK) indu ced [Ca 2]i increase in VSMC (NE: 67 +/- 14 nmol/l vs 71 +/- 17 nmol/l ; BayK: 86 +/- 8 nmol/l vs 84 +/- 14 nmol/l). The results indicate tha t captopril had a direct effect on the agonist-induced transplasmamemb rane calcium influx. That effect may be responsible for some of the an tihypertensive properties of captopril.