S‐nitroso‐L‐cysteine increases intracellular calcium in prenatal rat carotid body glomus cells

Abstract

Carotid body (CB) glomus (Type I) cells detect decreases in arterial oxygen (O2) tension (hypoxia) by depolarizing, opening voltage‐gated calcium channels (VGCCs) and releasing neurotransmitters. These neurotransmitters activate chemoafferent terminals within the carotid sinus nerve (CSN), which signal respiratory regions of the brainstem to increase ventilation and restore blood O2 levels. Low‐molecular mass S‐nitrosothiols (SNOs), such as S‐nitroso‐Lcysteine (LSNC), are recently being used as chemical agents for studying the biochemistry underlying the ventilatory response to hypoxia. Unpublished work from our lab shows that LSNC alters macroscopic outward potassium currents in carotid body glomus cells under both normoxic and hypoxic conditions. However, the effect of LSNC on intracellular calcium concentration ([Ca2+]i) is unknown. Our objective was to determine whether LSNC elicits changes in [Ca2+]i in CB glomus cells. We hypothesized that LSNC increases [Ca2+]i via influx through VGCCs. To test this we isolated CB glomus cells from postnatal (P) P11–P15 Sprague Dawley male rat pups, and used Ca2+ imaging to investigate for the first time the effect of LSNC on CB glomus cell [Ca2+]i. Our preliminary data reveals that 50μM LSNC causes a rise in [Ca2+]i under normoxic conditions (n=2). This data suggests that LSNC increases CB glomus cell [Ca2+]i, and this rise may trigger Ca2+‐dependent release of neurotransmitters and activation of chemoafferent fibers within the CSN.Support or Funding InformationNIH SPARC 1OT2OD023860‐02 SJLewisThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.