Renal response to angiotensin II is blunted in sodium-sensitive normotensive men
FW Visser, AH Boonstra, AT Lely… - American journal of …, 2008 - academic.oup.com
FW Visser, AH Boonstra, AT Lely, F Boomsma, G Navis
American journal of hypertension, 2008•academic.oup.comBackground In hypertension, sodium sensitivity (SS) of blood pressure is associated with
renal hemodynamic abnormalities related to increased activity of the renal renin–
angiotensin aldosterone system (RAAS). The renal mechanisms of SS in normotensives are
unknown. Therefore, we studied whether SS is related to renal hemodynamics and renal
responsiveness to angiotensin II (AngII) in young healthy adults. Methods Blood pressure
(mean arterial pressure (MAP)) and renal function were measured in 34 healthy men after 1 …
renal hemodynamic abnormalities related to increased activity of the renal renin–
angiotensin aldosterone system (RAAS). The renal mechanisms of SS in normotensives are
unknown. Therefore, we studied whether SS is related to renal hemodynamics and renal
responsiveness to angiotensin II (AngII) in young healthy adults. Methods Blood pressure
(mean arterial pressure (MAP)) and renal function were measured in 34 healthy men after 1 …
Background
In hypertension, sodium sensitivity (SS) of blood pressure is associated with renal hemodynamic abnormalities related to increased activity of the renal renin–angiotensin aldosterone system (RAAS). The renal mechanisms of SS in normotensives are unknown. Therefore, we studied whether SS is related to renal hemodynamics and renal responsiveness to angiotensin II (AngII) in young healthy adults.
Methods
Blood pressure (mean arterial pressure (MAP)) and renal function were measured in 34 healthy men after 1-week low-sodium diet (LS; 50 mmol Na+/24 h), 1-week high-sodium diet (HS; 200 mmol Na+/24h), and 1-week HS-ACEi (enalapril 20 mg/day). The responses of effective renal plasma flow (ERPF; 131I-Hippuran clearance) to graded infusion of AngII were assessed during each condition.
Results
The sodium-induced change in MAP ranged from −7 to +14 mm Hg. SS (a sodium-induced increase in MAP >3 mm Hg) was present in 13 subjects. ERPF was lower in SS subjects during LS and during HS-ACEi. The AngII-induced decrease in ERPF was blunted in SS on LS (−25 ± 6 vs. −29 ± 7% in sodium-resistant (SR) subjects, P < 0.05) and on HS (−30 ± 5 vs. −35 ± 6%, P < 0.05). The blunting was corrected by angiotensin-converting enzyme inhibitors (ACEi) (−36 ± 6 vs. −37 ± 7%).
Conclusion
SS normotensive subjects have a blunted renal response to exogenous AngII. This is ameliorated by ACEi, supporting a role for inappropriately high intrarenal RAAS activity. As these findings cannot be attributed to subclinical renal hypertensive damage, high intrarenal RAAS activity and altered renal hemodynamics may be primary phenomena underlying SS.
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