Abstract
Our previous report suggested that increased serum angiotensin-converting enzyme (ACE) activity plays a central part in the pathogenesis of essential hypertension in man. In the present study, we investigated whether such findings can be seen in spontaneously hypertensive rats (SHR). The results suggested that serum carboxypeptidase N and kallikrein, rather than ACE, plays a central part in this experimental model. The ACE activity was decreased rather than increased in spontaneously hypertensive rat when compared with that in Wistar-Kyoto rats.
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