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Vertebrate skeletal muscle contraction and relaxation is a complex process that depends on Ca 2+  ions to promote the interaction of actin and myosin. This process can be modulated by nitric oxide (NO), a gas molecule synthesized endogenously by (nitric oxide synthase) NOS isoforms. At nanomolar concentrations NO activates soluble guanylate cyclase (sGC), which in turn activates protein kinase G via conversion of GTP into cyclic GMP. Alternatively, NO post-translationally modifies proteins via S-nitrosylation of the thiol group of cysteine. However, the mechanisms of action of NO on Ca 2+  homeostasis during muscle contraction are not fully understood and we hypothesize that NO exerts its effects on Ca 2+  homeostasis in skeletal muscles mainly through negative modulation of Ca 2+  release and Ca 2+  uptake via the NO-sGC-PKG pathway. To address this, we used 5–7 days-post fecundation-larvae of zebrafish, a well-established animal model for physiological and pathophysiological muscle activity. We evaluated the response of muscle contraction and Ca 2+  transients in presence of SNAP, a NO-donor, or L-NAME, an unspecific NOS blocker in combination with specific blockers of key proteins of Ca 2+  homeostasis. We also evaluate the expression of NOS in combination with dihydropteridine receptor, ryanodine receptor and sarco/endoplasmic reticulum Ca 2+  ATPase. We concluded that endogenous NO reduced force production through negative modulation of Ca 2+  transients via the NO-sGC pathway. This effect could be reversed using an unspecific NOS blocker or sGC blocker.

NO-sGC Pathway Modulates Ca2+ Release and Muscle Contraction in Zebrafish Skeletal Muscle