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AJP - Endocrinology and Metabolism, Vol 244, Issue 3 262-E265, Copyright © 1983 by American Physiological Society
ARTICLES |
M. Kobayashi, S. Suzuki and K. Hashiba
Renal kallikrein was reported to activate human inactive renin and to release active renin from rat renal cortical slices. To evaluate the role of renal kallikrein in the control of renin release in vivo, Trasylol and soybean trypsin inhibitor (SBTI) were used to determine whether they can inhibit renin release stimulated by the administration of furosemide and a 2-wk low-sodium diet. Plasma renin activity (PRA) was increased by furosemide and also by the low-sodium diet. Urinary kallikrein excretion was increased by the sodium depletions. Trasylol did not affect basal PRA; however, it inhibited PRA and urinary kallikrein excretion, when stimulated by furosemide and by a low-sodium diet. These results suggest that furosemide and low-sodium diet act on the kidney to release renin via protease production. Because SBTI affected neither PRA nor urinary kallikrein excretion stimulated by these sodium depletions, it is suggested that renal kallikrein may play an important role in the control of renin release stimulated by furosemide and by low-sodium diet.
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