NO EFFECT OF TAQI POLYMORPHISM AT THE HUMAN RENAL KALLIKREIN (KLK1) LOCUS ON NORMAL BLOOD-PRESSURE LEVEL OR VARIABILITY

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.