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Inflammation: the underlying foe in renovascular hypertension?

The development of renal artery stenosis invariably results in renovascular hypertension, which has severe implications for kidney function. It initiates a cascade of events leading to an initial activation of the renin– angiotensin system and thereafter a structural remodelling, evidenced by fibrosis and vascular deterioration in the affected kidney, which then finally progresses into end-stage renal failure [1]. The initial activation of the renin–angiotensin system tends to resolve once a stable maintained blood pressure (BP) is reached, but it is evident that the initial elevation of plasma angiotensin II could precipitate macrophage infiltration, thereby initiating an inflammatory response within the kidney [2]. A key chemokine in this inflammatory process is the monocyte chemoattractant protein-1 (MCP-1), and this factor may also induce oxidative stress by activating NAD(P)H oxidase activity and stimulating transforming growth factor beta 1 (TGF-b1) with subsequent fibroblast proliferation. This inflammatory cascade may well underlie the degenerative processes within the kidney as its renal artery begins to narrow. This hypothesis was investigated by Zoja et al. [3] using a novel compound, bindarit, which selectively blocks MCP-1 production, but without affecting the generation of other cytokines, and determining its impact on the changes in renal function as renovascular hypertension developed using a swine model of renovascular hypertension.