High dietary sodium blunts effects of angiotensin-converting enzyme inhibition on vascular angiotensin I-to-angiotensin II conversion in ratsKocks, MJA., Buikema, H., Gschwend, S., Boomsma, F., de Zeeuw, D. & Navis, G., Nov-2003, In : Journal of Cardiovascular Pharmacology. 42, 5, p. 601 - 606 6 p.
Research output: Contribution to journal › Article › Academic › peer-review
High sodium intake blunts the efficacy of angiotensin (Ang)-converting enzyme (ACE) inhibition (ACEi), but the underlying mechanism is incompletely characterized. High sodium has been reported to increase vascular expression and vascular activity of ACE. To investigate whether high-dietary sodium-induced effects on vascular conversion of Ang I might be involved in the sodium-induced blunting of the response to ACEi, the authors studied the vasoconstrictor responses to Ang I and Ang II of isolated aortic rings from healthy rats on low dietary sodium (LS: 0.05% NaCl) and high dietary sodium (HS: 2.0% NaCl) after 3 weeks of ACEi (lisinopril 75 mg/L) or vehicle (CON). Blood pressure was similar in LS and HS in CON, but HS blunted the blood pressure response to ACEi. Functional conversion of Ang I was assessed as the difference in dose-response curves to Ang I and Ang II in parallel aortic rings. Sodium intake did not affect the dose-response curves to Ang I and Ang II in CON. In the ACEi groups, a significant difference was present between the curves for Ang I and Ang II on LS (DeltaEC(50), 6.7 nM, range, 2.2-13 nM-, P <0.01) but not on HS (DeltaEC(50): 1.3 nM, range, 0.0-4.1 nM, median [interquartile range], NS). Thus, HS blunts the ACEi-induced reduction of functional vascular Ang I conversion compared with LS. Whether the blunted functional vascular conversion is causally related to the blunted blood pressure response remains to be elucidated.
|Pages (from-to)||601 - 606|
|Number of pages||6|
|Journal||Journal of Cardiovascular Pharmacology|
|Publication status||Published - Nov-2003|
- angiotensin-converting enzyme inhibitor, aorta, dietary sodium, rat, vascular angiotensin I conversion, DIFFERENTIAL REGULATION, BLOOD-PRESSURE, SALT INTAKE, TISSUE, ACE, PLASMA, HYPERTENSION, GENERATION, ARTERIES, PATHWAYS