Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.5 (cathepsin D)
 4,130 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mouse brain renin and kidney renin were purified by a 3-step procedure: acetone powder extraction. Sephadex G-100 chromatography, and blue agarose affinity chromatography. The latter efficiently separated from cathepsin D-like acid protease activity. Mouse brain renin had an optimum of enzyme activity of pH 7.0. This differed from mouse kidney renin, which had an optimum at pH 8.5. In vitro, brain renin formed angiotensin I from rat plasma angiotensinogen and had no angiotensinase activity. Mouse brain renin was inhibited by monospecific antibodies raised against pure mouse submandibular gland renin. In vivo activity of the enzyme was tested by injection of brain renin into the lateral brain ventricle of rats. This resulted in the formation of angiotensin I from endogenous brain angiotensinogen, in the stimulation of water uptake, and in a long-lasting increase of arterial blood pressure. The latter could be blocked by the competitive angiotensin II receptor antagonist, saralasin. The results showed that brain renin is active under physiological conditions.
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PMID:In vivo activity of purified mouse brain renin. 702 Aug 79

Anesthetized cats were infused with angiotensin II or its vehicle (0.05 M phosphate buffer) to detect actions of angiotensin II which can contribute to shock. Mild hemorrhage, or saralasin-induced angiotensin II receptor blockade, were also employed in an attempt to enhance or reduce the angiotensin II effects. Angiotensin II produced a prolonged reduction in superior mesenteric artery blood flow (50% of initial) and an elevation in plasma lysosomal hydrolase (cathepsin D) activity. Additionally, angiotensin II disrupted the normal functioning of the coronary endothelium resulting in macroscopically visible hemorrhagic patches on the myocardium. Saralasin blockade of the angiotensin II receptor prevented the pressor, splanchnic vasoconstrictor, and lysosomal labilizing actions of angiotensin, and also decreased the incidence of cardiac hemorrhages. Angiotensin II infusion after bleeding to 80 mm Hg, however, increased lysosomal hydrolase release, indicating an exacerbation of angiotensin II effects. These data indicate that high levels of angiotensin II are capable of inducing alterations similar to those occurring in hemorrhagic shock. These deleterious effects of angiotensin II were abolished by saralasin and potentiated by a mild hemorrhage.
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PMID:Shock potentiating actions of angiotensin II infusion in cats. 744 49