Effects of prolactin on ventricular myocyte shortening and calcium transport in the streptozotocin-induced diabetic rat

The physiological role of prolactin (PRL) in the heart, and in particular the diabetic heart, are largely unknown. The effects of PRL on ventricular myocyte shortening and Ca(2+) transport in the streptozotocin (STZ) – induced diabetic and in age-matched control rats were investigated. PRL receptor protein, myocyte shortening, intracellular [Ca(2+)], L-type Ca(2+) current were measured by Western blot, cell imaging, fluorescence photometry and whole-cell patch-clamp techniques, respectively. Compared to normal Tyrode solution (NT), PRL (50 ng/ml) significantly (p < 0.05) increased the amplitude of shortening in myocytes from control (7.43 ± 0.38 vs. 9.68 ± 0.46 %) and diabetic (6.57 ± 0.24 vs. 8.91 ± 0.44 %) heart (n = 44–49 cells). Compared to NT, PRL (50 ng/ml) significantly increased the amplitude of Ca(2+) transients in myocytes from control (0.084 ± 0.004 vs. 0.115 ± 0.007 Fura-2 ratio units) and diabetic (0.087 ± 0.007 vs. 0.112 ± 0.006 Fura-2 ratio units) heart (n = 36–50 cells). PRL did not significantly alter the amplitude of caffeine-evoked Ca(2+) transients however, PRL significantly increased the fractional release of Ca(2+) in myocytes from control (21 %) and diabetic (14 %) and heart. The rate of Ca(2+) transient recovery following PRL treatment was significantly increased in myocytes from diabetic and control heart. Amplitude of L-type Ca(2+) current was not significantly altered by diabetes or by PRL. PRL increased the amplitude of shortening and Ca(2+) transients in myocytes from control and diabetic heart. Increased fractional release of sarcoplasmic reticulum Ca(2+) may partly underlie the positive inotropic effects of PRL in ventricular myocytes from control and STZ-induced diabetic rat.