Abstract: Dihydropyridine receptors (DHPR) participate in changes of the membrane potential during muscle unloading [1, 2, 3]. We used nifedipine, a dihydropyridine derivative and Ca2+ antagonist to study the role of L-type Ca2+ channels (Cav1.1, DHPR) in Ca2+ and energy metabolism of musculus soleus during unloading. Male Wistar rats were divided into 3 groups (n=8 in each): vivarium control with placebo (C), 3-day hindlimb suspension with placebo (HS) and 3-day hindlimb suspension with intraperitoneal administration of the nifedipine (N). It was found that the nifedipine administration during himdlimb suspension prevents: 1) the ATP accumulation; 2) the reduction of the maximum force of a single contraction and the time of contraction; 3) the increase in the content of intramitochondrial and myoplasmic calcium. Thus, DHPR participates in the energy and Ca2+ metabolism and affects the functional properties of m. soleus during unloading.

Cite: Zaripova K.A. , Sharlo K.A. , Sidorenko D.A. , Tyganov S.A. , Nemirovskaya T.L.
Effect of DHPR inhibition on energy and Ca2+ metabolism of rat m. soleus during unloading
Biomembranes 2024 07-11 Oct 2024