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Effect of Chronic Blockade of the Kallikrein-Kinin System on the Development of Hypertension in Rats
Author(s) -
Masataka Majima,
Makoto Katori
Publication year - 2001
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/hyp.38.4.e21
Subject(s) - blockade , kinin , medicine , endocrinology , kallikrein , essential hypertension , receptor , blood pressure , biology , bradykinin , biochemistry , enzyme
To the Editor:We found some incorrect statements in an article prepared by Nour-Eddine Rhaleb et al titled “Effect of Chronic Blockade of the Kallikrein-Kinin System on the Development of Hypertension in Rats,”1 and we consider it our duty to point out the errors (and other related irregularities) and to provide the correct information for the readers of Hypertension . It should be mentioned at the outset that Dr Majima was invited to Dr Rhaleb’s laboratory by the director of that laboratory, Dr Oscar A. Carretero, to conduct the experiments in question.In the Discussion section (pp.126, right column, ll. 28 to 38), appears the following statement”: “(1) normal BN ]Brown Norway] rats were given a subcutaneous infusion of Ang II or high salt diet alone or combined with icatibant (given intraperitoneally) and (2) BNK ]Brown Norway Katholiek] rats were given a subcutaneous infusion of a nonpressor dose of Ang II or high salt diet...we were unable to reproduce any of their findings or those of Madeddu et al.”1 However, the only 2 experiments that Majima performed with Dr Rhaleb, during a stay of nearly 1.5 months, focused solely on the effects of high salt diet in normal BN rats and on those of the infusion of Ang II in kininogen-deficient BNK rats and normal BN rats. Majima’s work with Dr Rhaleb (as far as it is possible to judge) confirmed our original results. Accordingly, the statement “we were unable to reproduce any of their findings” is not correct, and we can find no justification for it.In addition, there is no explanation in the text of why the mean blood pressure during week 1 was lower (by ≈7 mm Hg) than that in the pretreatment period. According to our data gathered over a period of >10 years, …

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