Key result
Calcium-activated chloride channels show altered pharmacologic and biochemical properties in human retinal microarterioles in long-standing hypertension.
Why the study?
Does the TMEM16A ionic mechanism contribute to vascular remodeling and increased vascular resistance in human retinal microarterioles during long-standing hypertension?
Does the TMEM16A ionic mechanism contribute to vascular remodeling and increased vascular resistance in human retinal microarterioles during long-standing hypertension?
This study provides preliminary evidence that altered TMEM16A allostery may be a key mechanism in retinal vascular remodeling and increased vascular resistance during chronic hypertension.
May inform future TMEM16A-targeted therapies in hypertensive retinopathy; leaves open whether this mechanism drives human retinal vascular remodeling.
We hypothesized that the calcium-activated chloride channel (CACC) transmembrane member 16A (TMEM16A) ionic mechanism may be a general mechanism in remodeling of vascular smooth muscles, including the retina. These vascular remodeling may have a critical impact on retinal ischemia during chronic hypertension. In this study, we examined TMEM16A protein interactions with calmodulin and CaMKIIδ likely cause efflux of chloride, thus resulting in increased vascular resistance by increasing vascular wall tone in long-standing hypertension. Control experiments were performed in static concentrations of calcium and using the specific TMEM16A inhibitor T16Ainh-A01 [2-[(5-ethyl-1,6-dihydro-4-methyl-6-oxo-2-pyrimidinyl)thio]-N-[4-(4-methoxyphenyl)-2-thia zolyl]acetamide]. The results of our study provide preliminary evidence that CACC shows altered pharmacologic and biochemical properties in retinal vessel in long-standing hypertension.
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Gui et al. (2015) studied long-standing hypertension. long-standing hypertension was evaluated on pharmacologic and biochemical properties of CACC in retinal vessels. Calcium-activated chloride channels show altered pharmacologic and biochemical properties in human retinal microarterioles in long-standing hypertension.
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