1. We have recently identified a candidate gene for rat genetic hypert
ension, termed S-A, by identifying an mRNA species that shows markedly
higher expression in the kidneys of spontaneously hypertensive rats (
SHR) than in those of Wistar-Kyoto rats (WKY). 2. Subsequent genetic c
o-segregation analyses by ourselves and others indicated that the S-A
gene locus did indeed influence blood pressure. Moreover, in a prelimi
nary association study, we found an association of a polymorphism of t
he human S-A gene with essential hypertension. 3. Further studies to i
dentify functions of the S-A gene products are required before reachin
g a definite conclusion.