Long-term low salt diet increases blood pressure by activation of the renin-angiotensin and sympathetic nervous systems

ABSTRACT

Background The aim of this study was to investigate the effect of long-term low salt diet on blood pressure and its underlying mechanisms.

Methods Male Sprague-Dawley (SD) rats were divided into normal salt diet group (0.4%) and low salt diet group (0.04%). Blood pressure was measured with the non-invasive tail-cuff method. The contractile response of isolated mesenteric arteries was measured using a small vessel myograph. The effects on renal function of the intrarenal arterial infusion of candesartan (10 μg/kg/min), an angiotensin II receptor type 1 (AT₁R) antagonist, were also measured. The expressions of renal AT₁R and mesenteric arterial α_1A, α_1B, and α_1D adrenergic receptors were quantified by immunoblotting. Plasma levels of angiotensin II were also measured.

Results Systolic blood pressure was significantly increased after 8 weeks of low salt diet. There were no obvious differences in the renal structure between the low and normal salt diet groups. However, the plasma angiotensin II levels and renal AT₁R expression were higher in low than normal salt diet group. The intrarenal arterial infusion of candesartan increased urine flow and sodium excretion to a greater extent in the low than normal salt diet group. The expressions of α_1A and α_1D, but not α_1B, adrenergic receptors, and phenylephrine-induced contraction were increased in mesenteric arteries from the low salt, relative to the normal salt diet group.

Conclusion Activation of the renin-angiotensin and sympathetic nervous systems may be involved in the pathogenesis of long-term low salt diet-induced hypertension.

KEYWORDS:

• Hypertension
• low salt diet
• renin-angiotensin system
• sympathetic nervous system
• sodium excretion
• vascular contraction

Acknowledgments

These studies were supported in part by grants from the National Natural Science Foundation of China (31730043, 81570379), Program of Innovative Research Team by National Natural Science Foundation (81721001), and the National Institutes of Health (5R01DK039308-31, 5R01HL092196-10, and 5P01HL074940-11).

Disclosure statement

The authors declare that they have no competing interests. This manuscript is an original contribution not previously published, and not under consideration for publication elsewhere.

Additional information

Funding

This work was supported by the the National Natural Science Foundation of China [31730043, 81570379];Program of Innovative Research Team by National Natural Science Foundation [81721001];the National Institutes of Health [5R01DK039308-31, 5R01HL092196-10, and 5P01HL074940];