Effect of tobacco smoke on hydrogen sulfide-induced rat thoracic aorta relaxation

Abstract

Levels of hydrogen sulfide (H2S), a gaseous signaling molecule, are reduced in the serum of individuals who smoke. We hypothesized that tobacco smoke influenced smooth muscle relaxation by decreasing H2S levels and this effect could also influence expression of cystathionine γ-lyase (CSE) and sulfonylurea receptor-2 (SUR-2). The aim of this study was to explore the effect of tobacco smoke on H2S-mediated rat thoracic aorta relaxation and its possible mechanism. Thirty-two Sprague-Dawley rats were divided into four groups: control (C) group, short-term smoker (SS) group, mid-term smoker (MS) group, and long-term smoker (LS) group. H2S concentrations in serum, action of H2S on rat aortic vascular relaxation, and expression of CSE and SUR-2 in thoracic aortic smooth muscle were measured. Although there was no significant difference in H2S between the C and the SS groups, concentration of H2S was significantly reduced in both the LS and MS groups compared to control (P<0.01). Furthermore, H2S was significantly lower in the LS than in the MS group (P<0.05). Rat aortic vascular relaxation was lower in all three treatment groups compared to the control, with the most significant decrease observed in the LS group (P<0.05 compared to the MS group). Expression of CSE and SUR-2 was reduced in the LS and MS groups compared to control (P<0.05), with the lowest levels observed in the LS group (P<0.05). Therefore, tobacco smoke reduced expression of CSE and SUR-2 in rat thoracic aorta, which may inhibit H2S production and vascular dilation.

Perivascular adipose tissue remodeling impairs vasoreactivity in thermoneutral-housed rats

“…We interpret this as the visualization of PVAT regulation of the vessel as compared with the vessels' maximal vasodilation. This observation agrees with multiple prior reports with PVAT removed (52)(53)(54). We acknowledge that we are testing these phenomena ex situ, and the actual changes in aorta diameter, as controlled by PVAT, are a model and may differ from in vivo regulation.…”

Mechanisms by which hydrogen sulfide attenuates muscle function following ischemia–reperfusion injury: effects on Akt signaling, mitochondrial function, and apoptosis

“…Colonic smooth muscle cells treated with 1 mM NaHS displayed increased K ATP activity and SUR2 but not Kir6.1 sulfhydration [79], suggesting that H 2 S can increase expression or at least activity of K ATP pore subunits. One report showed that rats exposed to inhaled tobacco smoke displayed lower levels of serum H 2 S, and reduced gene expression of CSE and SUR2 in aortic smooth muscle, inhibiting both endogenous H 2 S levels and action [80]. However another study observed that NaHS protected against neuronal damage in both wild type and Kir6.2 knockout mice, and that uncoupling protein (UCP) 2 knockout mice were not affected by NaHS administration, leading to the suggestion that H 2 S activity was dependent on the presence of UCP-2, not K ATP pore subunits [75].…”

Effects of aminooxyacetic acid on hippocampal mitochondria in rats with chronic alcoholism: the analysis of learning and memory-related genes

“…H2S plays an important role in signal transduction and the regulation in various tissues of the whole body, including the mammalian central nervous system, digestive system, and urogenital system (Du et al, 2004;Huang et al, 2016;Yuan et al, 2015). H2S is synthesized from L-cysteine in the body by the action of CBS (Zhang et al, 2017). CBS, which is highly expressed in the nervous system (Chen et al, 2005), is a major enzyme in the brain that is responsible for the production of H2S.…”