Ke. Berge et K. Berg, NO EFFECT OF TAQI POLYMORPHISM AT THE HUMAN RENAL KALLIKREIN (KLK1) LOCUS ON NORMAL BLOOD-PRESSURE LEVEL OR VARIABILITY, Clinical genetics, 44(4), 1993, pp. 196-202
Renal kallikrein is a component of the kallikrein-kinin-system (KKS).
Kallikrein has been shown to cleave the precursor kininogen to release
small kinins, which cause vasodilatation, increased diuresis and natr
iuresis. We have studied a normal restriction fragment length polymorp
hism (RFLP) at the renal kallikrein locus (KLK1), detectable with the
restriction enzyme TaqI. In one series of 167 unrelated individuals we
found a trend towards an association between genotypes in this polymo
rphism and level of diastolic blood pressure (DBP), but in two other s
eries comprising 123 and 213 unrelated individuals, respectively, we f
ound no suggestion of an association. Since the three series did not e
xhibit a consistent pattern of association between DBP levels and geno
types in this RFLP, we conclude that the association that appeared in
one of the series was probably a chance event. There was no difference
between genotypes in any of the three series, with respect to systoli
c blood pressure (SBP). In two series of, respectively, 157 and 120 co
mplete monozygotic (MZ) twin pairs, there was no difference between ge
notypes with respect to within-pair variation in SBP or DBP. This indi
cates that normal KLK1 genes, expressed as variants in this RFLP, do n
ot participate in the determination of the limits within which life-st
yle factors may cause blood pressure (BP) changes. We conclude that ne
ither ''level gene'' effects nor ''variability gene'' effects at the K
LK1 locus are detectable with the polymorphism analyzed, in the Norweg
ian population.