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Several members of the EPH kinase family and their ligands are involved in blood pressure regulation, and such regulation is often sex- or sex hormone-dependent, based on animal and human genetic studies.  EPHB6  gene knockout (KO) in mice leads to hypertension in castrated males but not in un-manipulated KO males or females. To assess whether this finding in mice is relevant to human hypertension, we conducted a human genetic study for the association of  EPHB6  and its two ligands,  EFNB1  and  EFNB3 , with hypertension in hypogonadic patients. Seven hundred and fifty hypertensive and 750 normotensive Han Chinese patients, all of whom were hypogonadic, were genotyped for single nucleotide polymorphisms (SNPs) within the regions of the genes, plus an additional 50 kb 5′ of the genes for  EPHB6 ,  EFNB1  and  EFNB3 . An imputed insertion/deletion polymorphism,  rs35530071 , was found to be associated with hypertension at  p -values below the  Bonferroni -corrected significance level of 0.0024. This marker is located 5′ upstream of the  EFNB3  gene start site. Previous animal studies showed that while male  EFNB3  gene knockout mice were normotensive, castration of these mice resulted in hypertension, corroborating the results of the human genetic study. Considering the significant associations of  EFNB3  SNPs with hypertension in hypogonadic males and supporting evidence from castrated  EFNB3  KO mice, we conclude that loss-of-function variants of molecules in the  EPHB6  signaling pathway in the presence of testosterone are protective against hypertension in humans.

Analysis of the association of EPHB6, EFNB1 and EFNB3 variants with hypertension risks in males with hypogonadism