Hypoxia vs hydrogen sulfide (H2S) acting at the carotid body (CB) and elsewhere systemically

Abstract

In vascular smooth muscle hydrogen sulfide (H2S) mimics the effects of hypoxia (HH). The purpose of this study was to determine if in the cat carotid body (CB) H2S mimicked HH. CBs were harvested from anesthetized cats, cleaned of fat and connective tissue, incubated in a salt solution at 37 C and bubbled with 30%O2/5%CO2 for 20min of recovery. Protocols and euthanizing methods were approved by the University's Animal Care and Use Committee. Set 1 of sectioned CBs (5μm) was incubated with antibody to cystathione‐β‐synthase (CBS; a H2S synthesizing enzyme); set 2, with the antibody for the Kir 6.1 subunit of the KATP channel. Set 3 was challenged with HH (6%O2/5%CO2) followed by a challenge with 100μM Na2S (precursor of H2S) while bubbled with 30%O2/5%CO2. The incubation medium was analyzed for release of two excitatory (in cat and rat) transmitters –ACh and ATP. A positive immunohistochemical signal for CBS and for the Kir 6.1 subunit were detected in the CBs’ transmitter‐containing glomus cells. And whereas HH produced a significant increase in ACh and ATP release compared to control, 100μM Na2S produced a significantly reduced release compared to control. The data suggest that Na2S may open the KATP channels producing hyperpolarization (as it does in vascular smooth muscle) reducing the release of the transmitters. Airway smooth muscle was also relaxed by Na2S in two species. Supported in part by NIH award: HL 050712