Key result
Inactivation of the Ace gene in mouse kidney blunted the hypertensive response to infused angiotensin II, suggesting that locally produced angiotensin II mediates salt retention and hypertension.
Highlights evidence from mouse models that the intrarenal renin-angiotensin system is a critical mediator of hypertension, challenging the primary role of the circulating RAS.
Essential hypertension, which accounts for 90%-95% of all cases of hypertension seen in the clinic, is also referred to as idiopathic hypertension, because we simply don't understand the cause(s). Although many theories have been advanced, in the current issue of the JCI, Gonzalez-Villalobos et al. present further evidence implicating the intrarenal renin-angiotensin system and take us one step further by proposing a mechanism underlying this pathology.
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Timothy L. Reudelhuber (2013) conducted an editorial in Hypertension. Intrarenal ACE inactivation vs. Wild-type or control mice was evaluated. Inactivation of the Ace gene in mouse kidney blunted the hypertensive response to infused angiotensin II, suggesting that locally produced angiotensin II mediates salt retention and hypertension.
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