Low-salt diet increases NO bioavailability and COX-2 vasoconstrictor prostanoid production in spontaneously hypertensive rats

The ability of dietary sodium restriction to reduce the incidence of cardiovascular mortality and improve vascular function in hypertension still remains poorly understood. The aim of this study was to observe the effects of a long period of salt restriction on the vascular reactivity of mesenteric resistance arteries of SHRs.

Male SHRs received either standard-salt diet (0.3% NaCl) or low-salt diet (0.03% NaCl) for 28weeks. Vascular reactivity was studied in mesenteric artery segments and the influence of cyclooxygenase-2 (COX-2), reactive oxygen species (ROS) and participation of the renin-angiotensin system were analyzed. Key findings: Decreased salt intake did not affect phenylephrine-induced vasoconstriction but increased acetylcholine-induced vasodilatation and also increased the response to phenylephrine after inhibition of NO synthase by L-NAME (100μM) and iNOS protein expression was elevated. Cyclooxygenase inhibitor indomethacin (10μM) and COX-2 inhibitor NS 398 (1μM) decreased the reactivity to phenylephrine in low-salt-treated group, and COX-2 protein expression was elevated in low-salt group. The effects of apocynin (10μM); superoxide anion scavenger, tiron (1mM); hydrogen peroxide scavenger, catalase (1000UmL(-1)); and ACE and AT1 receptor blockers, enalapril (10μM) and losartan (10μM) on vascular reactivity were not different between two groups. The levels of AT1 protein expression were similar in both groups. Significance: Low-salt diet modulates mesenteric vascular responses via increased NO bioavailability suggested by increased iNOS protein expression and vasoconstrictor prostanoid production via COX-2 pathway, in SHRs. Neither ROS nor the local renin-angiotensin system is involved in these responses.

Low-salt diet modulates mesenteric vascular responses via increased NO bioavailability suggested by increased iNOS protein expression and vasoconstrictor prostanoid production via COX-2 pathway, in SHRs. Neither ROS nor the local renin-angiotensin system is involved in these responses.