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Angiotensin II formation by an alternative pathway during exercise in humans
1Department of Internal Medicine, School of Medicine, Fukuoka University, Japan.
Journal of Hypertension
|October 1, 1994
Summary
Exercise increases angiotensin II (Ang II) levels via a pathway independent of ACE. A serine protease inhibitor, nafamostat, significantly reduced this exercise-induced Ang II rise, suggesting its involvement in Ang II generation.
Area of Science:
- Cardiovascular Physiology
- Renal Physiology
- Enzymology
Background:
- The renin-angiotensin system (RAS) regulates blood pressure, with angiotensin II (Ang II) being a key effector.
- Angiotensin converting enzyme (ACE) is the primary enzyme in Ang II formation.
- An alternative Ang II generation pathway involving serine proteases has been postulated.
Purpose of the Study:
- To investigate the role of a potential kinin-tensin system in Ang II formation during human exercise.
- To determine if serine proteases contribute to the increase in plasma Ang II levels during physical activity.
Main Methods:
- Two double-blind crossover experiments were conducted in healthy volunteers.
- Experiment 1 assessed the effect of placebo versus ACE inhibitor captopril on Ang II levels during graded exercise.
- Experiment 2 evaluated the impact of a serine protease inhibitor, nafamostat, on exercise-induced Ang II increases.
Main Results:
- Plasma Ang II levels increased with exercise in both placebo and captopril groups in Experiment 1.
- Captopril did not significantly alter exercise-induced changes in Ang II levels.
- Nafamostat significantly blunted the exercise-induced rise in plasma Ang II levels in Experiment 2.
Conclusions:
- The findings support an alternative Ang II-forming pathway independent of ACE.
- One or more nafamostat-sensitive serine proteases are partly responsible for generating Ang II during exercise.