Objectives The small conductance calcium-activated potassium (SKCa) channel is a key factor in the regulation of vessel tone and blood pressure. It has been proposed that activation of endothelial SK3 channel plays an important role in the arteriolar dilation through EDHF signal pathway. Nowdays, the expression of SK3 channel has been researched in a variety of hypertensive rat models. However, the results are not completely identical and the expression of SK3 channel in human with hypertension is undefined. To clarify the alteration of SK3 channel in human with hypertension, we quantified the expression of SK3 mRNA and protein in mesenteric artery of hypertension patients.
Methods Mesenteric arterial tissues were collected from the removed tissues by abdominal operations in Han Chinese normotensive and primary hypertensive patients. The human tissue collection protocol was approved by the Ethics Committee of Luzhou medical College. Informed consent was obtained from the patients for the use of vascular tissue (which is usually discarded). The expression of mRNA was detected using quantitative Real-time PCR and analyzed with 2-ΔΔCT method. The artery protein extractions were detected using western blot with SK3 antibody (alomone labs, APC-025). The statistical analysis was done using independent-samples T test by SPSS 19.0.
Results Average age of hypertension group (HP) used in this research was 55.0000 ± 10.2425 (n = 12), while the age of normotensive group (NP) was 58.5000 ± 12.2808 (n = 12). The value of ΔCt in HP was 10.6808 ± 1.4035 (n = 12), while it was 12.1015 ± 1.3541 (n = 12) in NP. The expression of SK3 mRNA in HP was 2.36 times higher than in NP. The relative expression of SK3 protein in HP was 1.0748 ± 0.4089 (n = 12), while it was 0.7671 ± 0.1643 (n = 12) in NP, P<0.05. Expression levels of SK3 mRNA and protein were significant up-regulation in hypertension patients.
Conclusions The alteration of SK3 channel in human with hypertension is obvious enhancement but not decrease. This is contrary to results which were reported in spontaneously hypertensive rats. The nosogenesis of hypertension is quite complex, it is a result of synergism involving a series of factors and pathways. The up-regulation of SK3 channel maybe compensate deficient activity of other factors in the vasculature of hypertensive patients.