Role of the renal kallikrein-kinin system in the development of salt-sensitive hypertension.

M Katori, M Majima, I Hayashi, T Fujita, M Yamanaka

Department of Pharmacology, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.

Biological chemistry 2001 Jan

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The role of the renal kallikrein-kinin system in the development of salt-sensitive hypertension was studied using mutant kininogen-deficient Brown-Norway Katholiek (BN-Ka) rats, which generate no kinin in their urine, and other hypertensive rat models. It was found that ingestion of a low sodium diet or infusion of NaCl in doses slightly above 0.15 M caused hypertension and sodium accumulation in erythrocytes and the cerebrospinal fluid of kininogen-deficient BN-Ka rats. Development of hypertension in the deoxycorticosterone-acetate-salt model was completely prevented by administration of a newly discovered inhibitor, ebelactone B, of carboxypeptidase Y-like exopeptidase (an urinary kininase). The urinary kallikrein excretion of spontaneously hypertensive rats was lower than that of Wistar Kyoto rats at 4 weeks of age and did not increase by administration of furosemide, a diuretic agent, although approximately 50% of the diuretic action of this agent was dependent upon the renal kallikrein-kinin system in normal rats. In conclusion, the renal kallikrein-kinin system works as a safety valve for excess sodium intake.

Citation

M Katori, M Majima, I Hayashi, T Fujita, M Yamanaka. Role of the renal kallikrein-kinin system in the development of salt-sensitive hypertension. Biological chemistry. 2001 Jan;382(1):61-4