Summary. The administration of leucine aminopeptidase purified from human placenta was found to be effective in lowering the blood pressure in rats with experimental hypertension induced by the infusion of angiotensin II or renin.Systemic hypertension is one of the most common chronic diseases; its diagnosis and treatment constitutes one of our greatest medical challenges today. The renin-angiotensin system is an important regulator of blood pressure in normal and hypertensive individuals. The renal enzyme renin, reacting with a substrate present in blood, produces first an inactive decapeptide, angiotensin I; angiotensin I is then converted to the active octapeptide angiotensin II which is the most potent vasoconstrictor hormone. Since the demonstration by Brunner and Gavaras 3 that receptor antagonists of angiotensin II, such as saralasin, and inhibitors of the enzyme responsible for the conversion of angiotensin I to angiotensin II, such as teprotide 4 and captopril 5, reduce blood pressure in severely hypertensive patients, treatment of hypertension by regulating the angiotensin concentration has been the focus of interest. However, these agents have not yet received unequivocal acceptance; it has been reported that these agents cause serious side-effects, such as agranulocytosis and renal failure 6,7. We present here, using animal models, a different method for the treatment of hypertension due to overactivity of the renin-angiotensin system, using leucine aminopeptidase (arylamidase, LAP), which directly destroys angiotensin in the circulation.
ABSTRACT-The present study was designed to elucidate pathophysiological changes in the brain energy metabolism after cerebral ischemia. Cerebral ischemia was induced in rats by administering microspheres into the right carotid canal, and the time course of changes in cerebral energy metabolism was examined up to the 7th day after the operation. Approximately 50% of the operated rats revealed typical symptoms of stroke. In the right hemisphere, cerebral ATP and creatine phosphate of the rat on the 1st to 7th day were greatly reduced by the microsphere-induced cerebral embolism (maximally 52 and 61%, respectively), whereas the tissue lactate level was increased on the 1st, 3rd and 5th day after the embolism (maximally 125%), suggesting an induction of microsphere-induced cerebral ischemia. These changes in the tissue metabolites were accompanied by a decrease in the mitochondrial oxidative phosphorylation measured in the presence of succinate. A similar trend in the changes of biochemical markers was observed in the left hemisphere, but to a lesser degree or to an insignificant degree. The pathophysiological alterations in behavior and cerebral metabolism of microsphere-injected rats tended to return toward the normal levels on the 7th day after the operation. The results provided information on a useful model for therapeutic studies of anti-ischemic agents in the brain.
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