Abstract

Redistribution of Ca++ in response to K+-induced depolarization and/or nitrendipine (10(-6) M) was studied in isolated rabbit renal arteries using 1) isometric tension measurements, 2) 45Ca uptake measurements and 3) 45Ca electron microscopic autoradiography. Renal artery rings developed a mean tension of 1.67 +/- 0.30 g in response to high K+. Preincubation with 10(-6) M nitrendipine for 1 hr inhibited 80% of the initial portion and 100% of the sustained portion of the K+-induced contraction, without affecting rest tension. Using the modified lanthanum technique, cellular uptake of 45Ca increased 25% in muscles exposed to K+-substituted solution compared to control muscles (P less than .001). Preincubation with nitrendipine for 1 hr inhibited the K+-induced increase, whereas exposure to nitrendipine alone decreased 45Ca uptake compared to control muscles (P less than .001). Electron microscopic autoradiography of control renal arteries showed that relative 45Ca activities for the plasma membrane (PM), sarcoplasmic reticulum (SR) and mitochondria were higher than the cytoplasmic 45Ca activity, whereas activities for the nucleus were similar to that for the cytoplasm. Exposure to high K+ solution substantially decreased 45Ca activities of both the PM and SR (P less than .001), but changes in relative activities of other sites were insignificant. Muscles exposed to nitrendipine alone or nitrendipine plus high K+ had SR and PM activities intermediate with values from control and high K+ groups. Thus, Ca++ is released from both the SR and PM during exposure to high K+ and this Ca++ may contribute to the Ca++ pool involved in a depolarization-induced contraction.