Key result
Midkine deficiency prevented the induction of hypertension and reduced renal damage severity in mice after 5/6 nephrectomy, indicating midkine regulates the renin-angiotensin system.
Midkine is a novel regulator of the renin-angiotensin system that mediates hypertension and renal damage via kidney-lung interactions.
Hypothesis-generating for midkine inhibition in hypertension; leaves open translation to human CKD trials.
The renin-angiotensin system plays a pivotal role in regulating blood pressure and is involved in the pathogenesis of kidney disorders and other diseases. Here, we report that the growth factor midkine is what we believe to be a novel regulator of the renin-angiotensin system. The hypertension induced in mice by 5/6 nephrectomy was accompanied by renal damage and elevated plasma angiotensin II levels and was ameliorated by an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin receptor blocker. Notably, ACE activity in the lung, midkine expression in the lung, and midkine levels in the plasma were all increased after 5/6 nephrectomy. Exposure to midkine protein enhanced ACE expression in primary cultured human lung microvascular endothelial cells. Furthermore, hypertension was not induced and renal damage was less severe in midkine-deficient mice. Supplemental administration of midkine protein to midkine-deficient mice restored ACE expression in the lung and hypertension after 5/6 nephrectomy. Oxidative stress might be involved in midkine expression, since expression of NADH/NADPH oxidase-1, -2, and -4 was induced in the lung after 5/6 nephrectomy. Indeed, the antioxidative reagent tempol reduced midkine expression and plasma angiotensin II levels and consequently ameliorated hypertension. These results suggest that midkine regulates the renin-angiotensin system and mediates the kidney-lung interaction after 5/6 nephrectomy.
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Hobo et al. (2009) studied Hypertension and renal damage. Midkine deficiency or midkine protein administration vs. Wild-type mice or vehicle was evaluated on Hypertension, renal damage, ACE expression, and plasma angiotensin II levels. Midkine deficiency prevented the induction of hypertension and reduced renal damage severity in mice after 5/6 nephrectomy, indicating midkine regulates the renin-angiotensin system.
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