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

Autor: Frank C. Howarth, Gunnar Norstedt, Oleksiy I. Boldyriev, Muhammad A. Qureshi, Ozaz Mohamed, Khatija Parekh, Balaji Venkataraman, Sandeep Subramanya, Anatoliy Shmygol, Lina T. Al Kury
Jazyk: angličtina
Rok vydání: 2020
Předmět:
Zdroj: Heliyon, Vol 6, Iss 4, Pp e03797- (2020)
Druh dokumentu: article
ISSN: 2405-8440
DOI: 10.1016/j.heliyon.2020.e03797
Popis: 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 Ca2+ transport in the streptozotocin (STZ) – induced diabetic and in age-matched control rats were investigated. PRL receptor protein, myocyte shortening, intracellular [Ca2+], L-type Ca2+ 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 Ca2+ 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 Ca2+ transients however, PRL significantly increased the fractional release of Ca2+ in myocytes from control (21 %) and diabetic (14 %) and heart. The rate of Ca2+ transient recovery following PRL treatment was significantly increased in myocytes from diabetic and control heart. Amplitude of L-type Ca2+ current was not significantly altered by diabetes or by PRL. PRL increased the amplitude of shortening and Ca2+ transients in myocytes from control and diabetic heart. Increased fractional release of sarcoplasmic reticulum Ca2+ may partly underlie the positive inotropic effects of PRL in ventricular myocytes from control and STZ-induced diabetic rat.
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