Hypertension is commonly observed in alcoholics. Both the renin-angiotensin system and the non-renin-angiotensin system (NRAS) have been implicated in the dynamics for the maintenance of blood pressure. Acetaldehyde has earlier been reported to enhance the generation of the rate-limiting angiotensin I (Ang I) in bilaterally nephrectomized rat plasma and to inhibit the activity of several angiotensinases (A, B, and M) in human serum, thereby promoting a hypertensive set of reactions. In the current study, the effect of acetaldehyde upon cathepsin G and mast cell chymase has been investigated. Acetaldehyde at 223.5 down to 11.2 mM concentrations enhanced cathepsin G activity at all levels employed in a statistically significant manner. Since cathepsin G is one of several enzymes transforming Ang I into Ang II and is also capable of cleaving Ang II directly from angiotensinogen, it is suggested that alcoholism, which will generate exogenous acetaldehyde from ingested alcohol, may be a contributory factor for an elevated cathepsin G activity and, consequently, hypertension via the NRAS. Mast cell chymase activity also is elevated upon exposure to 440 mM acetaldehyde and is diminished with 27 mM acetaldehyde. Since both enzymes also degrade Ang II, degradative effects may be partially neutralized.
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