Kallikrein, Kininogen and Kinins in Control of Blood Pressure
作者:
Ivor H. Mills,
期刊:
Nephron
(Karger Available online 1979)
卷期:
Volume 23,
issue 2-3
页码: 61-71
ISSN:1660-8151
年代: 1979
DOI:10.1159/000181611
出版商: S. Karger AG
关键词: Bradykinin;Kallikrein;Blood pressure;Hypertension
数据来源: Karger
摘要:
Plasma kallikrein releases bradykinin when activated by gram-negative septicemia or irreversible hemorrhagic shock. Pancreatitis releases glandular kallikrein causing hypotension and increased vascular permeability. Bradykinin in the brain produces hypertension. Renal kallikrein is released by high arterial pressure, vasodilators, low doses of noradrenaline, angiotensin II, mineralocorticoids and rapid volume expansion. It has a biphasic relation to sodium excretion. In essential hypertension, kallikrein release into the blood and urine is low and facilitates hypertension. High renin in Bartter’s syndrome is balanced by high PGE and kallikrein without hypertensio
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