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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Role of mast cell chymase in angiotensin-induced vascular contraction of hamster cheek pouch microvessels.

We investigated the contribution of chymase-dependent conversion of angiotensin I to angiotensin II in hamster cheek pouch. To investigate the converting activities in intact tissues, angiotensin I or II was applied to microvessels of the intact cheek pouch, and the vascular contractile response was recorded. Angiotensin I or angiotensin II (20 nM) induced a rapid contraction of arterioles, irrespective of their diameter. In the presence of I mM captopril, there was no contraction in response to angiotensin I in arterioles < 25 microm in diameter, whereas contraction was still observed in larger arterioles. Chymostatin (100 microM) treatment also reduced the response to angiotensin I in arterioles > 40 microm in diameter. Treatment with 1 mM captopril and 100 microM chymostatin resulted in the loss of response to angiotensin I, but not to angiotensin II, in all arterioles. Treatment of microvessels with 100 microg/ml compound 48/80 enhanced angiotensin I-induced vascular contraction response, suggesting the significance of mast cells as a source of cheek pouch chymase.[1]


  1. Role of mast cell chymase in angiotensin-induced vascular contraction of hamster cheek pouch microvessels. Katada, J., Muramatsu, M., Hayashi, M., Hattori, M. Eur. J. Pharmacol. (1999) [Pubmed]
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