Potassium supplement upregulates the expression of renal kallikrein and bradykinin b2 receptor in spontaneously hypertensive rats. Jin, Lan, Lee Chao, and Julie Chao. Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, South Carolina 29425
APStracts 5:0206F, 1998.
High potassium intake is known to attenuate hypertension, glomerular lesion, ischemic damage and stroke-associated death. Our recent studies showed that expression of recombinant kallikrein by somatic gene delivery reduced high blood pressure, cardiac hypertrophy and renal injury in hypertensive animal models. The aim of this study is to explore the potential role of the tissue kallikrein-kinin system in blood pressure reduction and renal protection in spontaneously hypertensive rats (SHR) on a high potassium diet. Young SHR were given drinking water with or without 1% potassium chloride for 6 weeks. Systolic blood pressure was significantly reduced beginning at 1 week and the effect lasted for 6 weeks in the potassium supplemented group as compared to that in the control group. Potassium supplement induced 70% and 40% increases in urinary kallikrein levels and renal bradykinin B2 receptor density, respectively (P<0.05), but did not change serum kininogen levels. Similarly, Northern blot analysis showed that renal kallikrein mRNA levels increased 2.7 fold, whereas hepatic kininogen mRNA levels remained unchanged in rats with high potassium intake. No difference was observed in beta-actin mRNA levels in the kidney or liver of both groups. Competitive RT-PCR showed a 1.7-fold increase in renal bradykinin B2 receptor mRNA levels in rats 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. 

Received 24 July 1998; accepted in final form 17 November 1998.
APS Manuscript Number F182-8.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 9 December 1998