The emerging role of TRPV1 in myogenic tone

Skaik, Khaled; Shahzad, Muhammad H

doi:10.1113/jp282882

Cited by 1 publication

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“…Various mechanisms have been proposed to regulate myogenic tone ( Figure 2 ). It is widely believed that pressure-induced membrane depolarization in vascular smooth muscle cells is instigated by mechanosensitive or stretch-activated cation channels including transient receptor potential (TRP) channels and epithelial Na + channels (ENaCs) [ 101 , 102 , 103 , 104 , 105 , 106 , 107 ]. The membrane depolarization leads to increased [Ca 2+ ] i and vasoconstriction [ 99 , 108 ].…”

Section: Ca V 12 In Vascular Smooth Musclementioning

confidence: 99%

Oxidative Regulation of Vascular Cav1.2 Channels Triggers Vascular Dysfunction in Hypertension-Related Disorders

Zhang

2022

Antioxidants

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Blood pressure is determined by cardiac output and peripheral vascular resistance. The L-type voltage-gated Ca2+ (Cav1.2) channel in small arteries and arterioles plays an essential role in regulating Ca2+ influx, vascular resistance, and blood pressure. Hypertension and preeclampsia are characterized by high blood pressure. In addition, diabetes has a high prevalence of hypertension. The etiology of these disorders remains elusive, involving the complex interplay of environmental and genetic factors. Common to these disorders are oxidative stress and vascular dysfunction. Reactive oxygen species (ROS) derived from NADPH oxidases (NOXs) and mitochondria are primary sources of vascular oxidative stress, whereas dysfunction of the Cav1.2 channel confers increased vascular resistance in hypertension. This review will discuss the importance of ROS derived from NOXs and mitochondria in regulating vascular Cav1.2 and potential roles of ROS-mediated Cav1.2 dysfunction in aberrant vascular function in hypertension, diabetes, and preeclampsia.

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