Fine tuning by protein kinases of CaV1.2 channel current in rat tail artery myocytes

Fusi, Fabio; Mugnai, Paolo; Trezza, Alfonso; Spiga, Ottavia; Sgaragli, Giampietro

doi:10.1016/j.bcp.2020.114263

Cited by 3 publications

(2 citation statements)

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“…In vascular smooth muscle cells, the regulation of Ca v 1.2 by PKA is controversial. PKA is found to either inhibit or enhance Ca v 1.2 activity [ 51 , 52 , 53 , 54 , 55 , 56 , 57 ]. The stimulatory effect of PKA on Ca v 1.2 in vascular smooth muscle cells depends on anchoring adenyl cyclase 5 and PKA by A-kinase anchoring protein 150 (AKAP150) to the proximity of Ca v 1.2 [ 56 , 58 ].…”

Section: Ca V 12 In Vascular Smooth Musclementioning

confidence: 99%

“…Phosphorylation of Ser 1928 in the COOH-terminus of the Ca v 1.2 α1c subunit is required for PKA-stimulated channel activity in vascular smooth muscle cells [ 56 ]. Activation of PKG exhibits inhibitory effects on vascular Ca v 1.2 [ 52 , 57 , 59 , 60 ]. PKG mediates nitric oxide-induced inhibition of Ca v 1.2 [ 61 , 62 ].…”

Section: Ca V 12 In Vascular Smooth Musclementioning

confidence: 99%

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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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