Why the study?
Does the activity of renin-like enzymes in the arterial wall differ between spontaneously hypertensive rats and normotensive rats?
Does the activity of renin-like enzymes in the arterial wall differ between spontaneously hypertensive rats and normotensive rats?
Increased interconversion of inactive to active renin-like enzymes in the arterial wall of SHR rats may contribute to systemic hypertension through local angiotensin II generation.
Renin-like enzyme(s) in the arterial wall of the spontaneously hypertensive rat (SHR) were activated markedly by either acidic pH or treatment of proteolytic enzymes (trypsin and glandular kallikrein). The highest concentration of renin-like enzyme (active form) was localized in the renal artery (2.51 +/- 0.59 ng angiotensin I generated/mg of protein per h, mean +/- S.D.), followed by the mesenteric (1.58 +/- 0.31), the carotid (1.44 +/- 0.27) and the major aortic trunk (0.20 +/- 0.10), while the highest concentration of the inactive renin-like enzyme was localized in the major aortic trunk (0.97 +/- 0.18), followed by the carotid (0.72 +/- 0.41), the renal (0.71 +/- 0.31) and the mesenteric (0.60 +/- 0.29) arteries. In addition, the active renin-like activity from the mesenteric and the carotid arteries of SHR rats was higher significantly than that of age-matched normotensive Wistar-Kyoto (WKY) rats, despite a similar concentration of total renin-like enzyme of the corresponding arteries of both groups. These results suggest that increased interconversion of the inactive to the active renin-like enzymes in the arterial wall of SHR rats may result in local vasospasm through generation of angiotensin II, which may contribute in part at least to systemic hypertension of SHR rats.
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Mizuno et al. (1985) studied this question.
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