Fig. 2: GPR39 knockout ameliorates hypertension and endothelium-dependent vascular dysfunction.
From: Targeting GPR39 in structure-based drug discovery reduces Ang II-induced hypertension
a–c Graphs displaying systolic pressure, diastolic pressure, and mean arterial pressure (tail artery measurements, n = 6) across saline, Ang II, GPR39 KO, and Ang II + GPR39 KO mouse groups. d, e Blood flow speckle analyses in the mesenteric artery of live mice, with statistical interpretation of mean blood flow (intensity of red indicates blood flow density, n = 6). f, g Examination of p-eNOS and eNOS protein levels in the aorta across the four groups (n = 6). h–k Analysis of isolated aortic vessel contraction and relaxation in the four mouse groups (n = 3). Pgf-2α and Ach assessed endothelium-dependent vascular responses, while Norepinephrine (NA) and sodium nitroprusside (SNP) were used for endothelium-independent systolic and diastolic function evaluation Data are expressed as the mean ± SEM. Statistical significance is indicated as ns (not significant), *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001; #P < 0.05, ##P < 0.01, ###P < 0.001, ####P < 0.0001.
