Key result
Renal angiotensin-converting enzyme and locally generated angiotensin II play a dominant role in regulating sodium transport and the development of hypertension.
New experimental data highlight the renal ACE/angiotensin II pathway as a key element in local sodium transport regulation and the development of hypertension.
May support intrarenal ACE targeting in hypertension models; leaves open clinical translation pending trials.
PURPOSE OF REVIEW: This review presents novel findings regarding the renal angiotensin-converting enzyme (ACE) and its role in blood pressure (BP) control. RECENT FINDINGS: The textbook flow diagram of the renin-angiotensin system (RAS) shows the pulmonary endothelium as the main source of the ACE that converts angiotensin I to angiotensin II. However, ACE is made in large quantities by the kidneys, which raises the important question of what precisely is the function of renal ACE? Recent studies in gene-targeted mice indicates that renal ACE plays a dominant role in regulating the response of the kidney to experimental hypertension. In particular, renal ACE and locally generated angiotensin II affect the activity of several key sodium transporters and the induction of sodium and water retention resulting in the elevation of BP. SUMMARY: New experimental data link the renal ACE/angiotensin II pathway and the local regulation of sodium transport as key elements in the development of hypertension.
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Bernstein et al. (2013) conducted a review in Hypertension. Renal angiotensin-converting enzyme (ACE) was evaluated on Blood pressure control and development of hypertension. Renal angiotensin-converting enzyme and locally generated angiotensin II play a dominant role in regulating sodium transport and the development of hypertension.
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