Matsuura, H., Ichiki, T., Ikeda, J., Takeda, K., Miyazaki, R., Hashimoto, T., Narabayashi, E., Kitamoto, S., Tokunou, T. and Sunagawa, K. (2011) Inhibition of prolyl hydroxylase domain-containing protein downregulates vascular angiotensin II type 1 receptor. Hypertension, 58, 386-393. doi10.1161/HYPERTENSIONAHA.110.167106 - References

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Matsuura, H., Ichiki, T., Ikeda, J., Takeda, K., Miyazaki, R., Hashimoto, T., Narabayashi, E., Kitamoto, S., Tokunou, T. and Sunagawa, K. (2011) Inhibition of prolyl hydroxylase domain-containing protein downregulates vascular angiotensin II type 1 receptor. Hypertension, 58, 386-393. doi:10.1161/HYPERTENSIONAHA.110.167106

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AUTHORS: Nickolaj F. Starodub, Ljubov M. Samokhina

KEYWORDS: Endothelial Elastase; Cathepsin G; Cobalt Chloride; Mercury Chloride; Rats

JOURNAL NAME: Advances in Biological Chemistry, Vol.3 No.2, April 30, 2013

ABSTRACT: CoCl2 introduction increased cathepsin G activity in the heart and liver as well as endothelial elastase (EEl) in kidney that indicated the development of destructive processes. CoCl2 introduction decreased EEl and cathepsin G activities in blood serum and cathepsin G in lungs. HgCl2 injection decreased EEl in blood serum, heart, liver, kidney and cathepsin G in blood serum. These decreasing of proteinases activities may be caused by cytotoxic effects of heavy metals and/or the inclusion of these proteases in the destructive processes and absence of their synthesis and/or release.

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