Artificial light at night suppresses the expression of sarco/endoplasmic reticulum Ca2+ -ATPase in the left ventricle of the heart in normotensive and hypertensive rats.
Hana Mauer SutovskaMatus MiklovicLubos MolcanPublished in: Experimental physiology (2021)
Artificial light at night (ALAN) affects the circadian rhythm of the heart rate in normotensive Wistar rats (WT) and spontaneously hypertensive rats (SHR) through the autonomic nervous system, which regulates the heart's activity through calcium handling, an important regulator in heart contractility. We analysed the expression of the sarco/endoplasmic reticulum Ca2+ -ATPase (SERCA2) and other selected regulatory proteins involved in the regulation of heart contractility, angiotensin II receptor type 1 (AT1 R), endothelin-1 (ET-1) and tyrosine hydroxylase (TH), in the left ventricle of the heart in WT and SHR after 2 and 5 weeks of ALAN with intensity 1-2 lx. Expression of SERCA2 was decreased in WT (control: 0.53 ± 0.07; ALAN: 0.46 ± 0.10) and SHR (control: 0.72 ± 0.18; ALAN: 0.56 ± 0.21) after 5 weeks of ALAN (P = 0.067). Expression of AT1 R was significantly decreased in WT (control: 0.51 ± 0.27; ALAN: 0.34 ± 0.20) and SHR (control: 0.38 ± 0.07; ALAN: 0.23 ± 0.09) after 2 weeks of ALAN (P = 0.028) and in SHR after 5 weeks of ALAN. Expression of ET-1 was decreased in WT (control: 0.51 ± 0.27; ALAN: 0.28 ± 0.12) and SHR (control: 0.54 ± 0.10; ALAN: 0.35 ± 0.23) after 5 weeks of ALAN (P = 0.015). ALAN did not affect the expression of TH in WT or SHR. In conclusion, ALAN suppressed the expression of SERCA2, AT1 R and ET-1, which are important for the regulation of heart contractility, in a strain-dependent pattern in both WT and SHR.