Abstract
Cigarette smoke, including secondhand smoke (SHS), has significant detrimental vascular effects, but its effects on myogenic tone of small resistance arteries and the underlying mechanisms are understudied. Although it is apparent that SHS contributes to endothelial dysfunction, much less is known about how this toxicant alters arterial myocyte contraction, leading to alterations in myogenic tone. The study's goal is to determine the effects of SHS on mesenteric arterial myocyte contractility and excitability. C57BL/6J male mice were randomly assigned to either filtered air (FA) or SHS (6 h/d, 5 d/wk) exposed groups for a 4, 8, or 12-weeks period. Third and fourth-order mesenteric arteries and arterial myocytes were acutely isolated and evaluated with pressure myography and patch clamp electrophysiology, respectively. Myogenic tone was found to be elevated in mesenteric arteries from mice exposed to SHS for 12 wk but not for 4 or 8 wk. These results were correlated with an increase in L-type Ca2+ channel activity in mesenteric arterial myocytes after 12 wk of SHS exposure. Moreover, 12 wk SHS exposed arterial myocytes have reduced total potassium channel current density, which correlates with a depolarized membrane potential (Vm). These results suggest that SHS exposure induces alterations in key ionic conductances that modulate arterial myocyte contractility and myogenic tone. Thus, chronic exposure to an environmentally relevant concentration of SHS impairs mesenteric arterial myocyte electrophysiology and myogenic tone, which may contribute to increased blood pressure and risks of developing vascular complications due to passive exposure to cigarette smoke.
Highlights
Exposure to cigarette smoke (CS) is a major cause of cardiovascular complications, including stroke and coronary and peripheral artery diseases.[1,2] Importantly, even passive exposure to CS aerosols significantly elevates lifelong cardiovascular risk.[3]
Small resistance arteries and arterial myocytes from mice exposed to filtered air (FA) and secondhand smoke (SHS) were used to assess the effects of SHS on arterial contractility and smooth muscle electrophysiology
We found that resistance mesenteric arteries from mice exposed to SHS for 12 wk have higher levels of myogenic tone than arteries from control FA exposed mice
Summary
Exposure to cigarette smoke (CS) is a major cause of cardiovascular complications, including stroke and coronary and peripheral artery diseases.[1,2] Importantly, even passive exposure to CS aerosols (ie secondhand smoke, SHS) significantly elevates lifelong cardiovascular risk.[3] Despite widespread national and local media campaigns, SHS continues to be a prevalent indoor pollutant,[4,5,6,7] with deleterious vascular effect.[2,8] Whereas the multifactorial nature of changes in the vasculature is well-established (eg endothelial dysfunction and aberrant central control regulation),[2,9,10] the mechanisms contributing to this, including impairment of arterial myocytes function, remains poorly studied. How SHS alters arterial myocyte function and whether this contributes to altered myogenic tone is unclear
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