Potassium supplement upregulates the expression of renal kallikrein and bradykinin B-2 receptor in SHR

High potassium intake is known to attenuate hypertension, glomerular lesion , ischemic damage, and stroke-associated death. Our recent studies showed t hat expression of recombinant kallikrein by somatic gene delivery reduced h igh blood pressure, cardiac hypertrophy, and renal injury in hypertensive a nimal models. The aim of this study is to explore the potential role of the tissue kallikrein-kinin system in blood pressure reduction and renal prote ction in spontaneously hypertensive rats (SKR) on a high-potassium diet. Yo ung SHR were given drinking water with or without 1% potassium chloride for 6 wk. Systolic blood pressure was significantly reduced beginning at 1 wk, and the effect lasted for 6 wk in the potassium-supplemented group compared with that in the control group. Potassium supplement induced 70 and 40% in creases in urinary kallikrein levels and renal bradykinin B-2 receptor dens ity, respectively (P < 0.05), but did not change serum kininogen levels. Si milarly, Northern blot analysis showed that renal kallikrein mRNA levels in creased 2.7-fold, whereas hepatic kininogen mRNA levels remained unchanged in rats with high potassium intake. No difference was observed in beta-acti n mRNA levels in the kidney or liver of either group. Competitive RT-PCR sh owed a 1.7-fold increase in renal bradykinin B-2 receptor mRNA levels in ra ts with high potassium intake. Potassium supplement significantly increased water intake, urine excretion, urinary kinin, cAMP, and cGMP levels. This study suggests that upregulation of the tissue kallikrein-kinin system may be attributed, in part, to blood pressure-lowering and diuretic effects of high potassium intake.