Fig. 6 | Signal Transduction and Targeted Therapy

Fig. 6

From: NAD+ exhaustion by CD38 upregulation contributes to blood pressure elevation and vascular damage in hypertension

Fig. 6

CD38 knockout and AAV-mediated endothelial CD38 knockdown reduced BP and improved vascular function in AngII-induced hypertensive mice. a, b The change of SBP and DBP were detected by a tail-cuff plethysmography system (n = 5). c, d NAD+ and NMN levels in aortas were detected by HPLC-MS (n = 5). e Representative images of aorta sections stained with HE, Masson trichrome blue and EVG staining. Scale bar (original) = 100 μm. Scale bar (magnified) = 50 μm. f The aortic ring assay was performed (n = 5) to evaluate the vasodilation (n = 5). The differences were compared to AngII group. g In vivo aortic pulse wave velocity was measured by Doppler (n = 5). h, i The change of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were detected by a tail-cuff plethysmography system (n = 5). j The aortic ring assay was performed to evaluate the vasodilation (n = 5). k In vivo aortic pulse wave velocity was measured by Doppler (n = 5). The differences were analyzed between Scramble+AngII group and EC-KD+AngII group. *p < 0.05, ***p < 0.001

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