Author + information
- Liu Fuqiang1,2,
- Yang Wang2,
- Junjian Mu2,
- Yong Zhang1,
- Junkui Wang1,
- Gongchang Guan1 and
- Fuqiang Liu1,2
Renal dysfunctional metabolism of sodium play a key role in the formation of salt sensitivity. The renal Mcoln3 genes of Dahl salt sensitive rat were screened using Genechip method in our previous study, which was over-expressed in kidney. We hypothesized that Mcoln3 may be the trigger point of renal dysfunctional sodium metabolism. The present study detemined whether the impairment of the renal Mcoln3 pathway was responsible for salt sensitive hypertension in Dahl S rats.
Male Dahl sensitive rats and 13 BN -SS rats were randomly divided into nornal salt group, high salt group and high salt plus Mcoln3 inhibition Gadolinium group respectively; After 6-week diet intervention, Mcoln3, SGK1 - ENaC, renin, angiotensinogen mRNA and protein expression level were determined.
The renal expression of Mcoln3 was higher in Dahl salt sensitive rat. Dietary high salt could increase the expression of SGK1 and alpha ENaC in Dahl salt sensitive rats. However, when given Mcoln3 inhibition Gadolinium, SGK1 - ENaC mRNA and protein expression level also significantly lowered at the same time, but the RAAS system has no obvious change.
Mcoln3 maybe play a role of regulating blood pressure by regulating kidney SGK1 - ENaC pathways. We believe that it would been of great significance to uncover the etiology of salt sensitive hypertension as well as to seek another drug targets for treatment of essential hypertension.