The role of CYP-450 dependent arachidonic acid (AA) metabolites (vasoconstrictor 20-HETE and vasodilator EETs) and NO in control of blood pressure (MABP) and kidney function remains unclear. NO affects the activity of heme-containing enzymes, like CYP-450 related monooxygenases, moreover, their activity depends on Na(+) intake. The focus of this review and underlying studies is on the role of high sodium intake (pro-hypertensive factor) in interrelation between CYP-450 and NOS. The acute vs. chronic non-selective inhibition of CYP-450 AA metabolites (ABT), and selective inhibition of 20-HETE (HET 0016) has also been tested. The renal artery flow (RBF, Transonic probe), medullary blood flow (MBF, laser-Doppler flux), renal excretion, and medullary tissue NO (selective electrode) were measured in male anaesthetized Wistar rats. We conclude that on standard Na(+) intake, opposed effects of 20-HETE and EETs are almost in equilibrium; however, in the renal circulation the vasodilator EETs influence slightly prevails. High sodium intake stimulates NOS, which limits CYP-450 impact on MABP and kidney function. However, this protection disappears after prolonged sodium intake. Long-lasting high sodium intake lowers NO bioavailability and promotes systemic and intrarenal vasoconstrictor activity of 20-HETE. Opposed effects of NO and AA metabolites of CYP-450 on water and solute excretion are also described.
Journal of Physiology and Pharmacology
Mossakowski Medical Research Institute PAS
Library of the Mossakowski Medical Research Institute PAS
Programme Innovative Economy, 2010-2014, Priority Axis 2. R&D infrastructure
Mar 24, 2022
Dec 16, 2015
25
https://rcin.org.pl./publication/77869
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