Key result
Nitric oxide deficiency may be an important mediator, but is likely not the sole missing link between malignant hypertension and thrombotic microangiopathy.
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The authors suggest that nitric oxide deficiency is a mediator but not the sole missing link between malignant hypertension and thrombotic microangiopathy.
We read with interest the comments by Thachil 1 regarding our article on the association between ADAMTS-13 and thrombotic microangiopathy (TMA) in malignant hypertension. Thachil 1 proposes a role for NO as a link between malignant hypertension and TMA. We believe that the lack of NO may be an important mediator, but believe it is not the "missing link" between malignant hypertension and TMA. Although previous experiments have shown that administration of the endothelial NO synthase inhibitor N G -nitro-L-arginine methyl ester results in more severe tissue injury and end-organ dysfunction in various animal models of TMA, For example, in the study by Sethi et al, 4 administration of N G -nitro-L-arginine methyl ester led to the development of TMA in mice that were transgenic for the human renin and angiotensinogen genes. The same degree of tissue injury was also observed when these mice were placed on a high-salt diet. Administration of N G -nitro-L-arginine methyl ester in control animals did not lead to tissue injury and fibrin thrombi associated with TMA.
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Born et al. (2008) conducted a letter in Malignant hypertension and thrombotic microangiopathy. Nitric oxide (NO) deficiency was evaluated. Nitric oxide deficiency may be an important mediator, but is likely not the sole missing link between malignant hypertension and thrombotic microangiopathy.
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