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 (AT 1 R) antagonist, were also measured. The expressions of renal AT 1 R 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 AT 1 R 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.

Wrangle with hypertension: lowered salt intake may not compromise iodine status among tribes of Central India

“…We observed that higher Urinary sodium and UIC were proportionately related to high blood pressure. We also observed in another study that salt uptake was directly associated with high blood pressure (14) . Our findings were supported by Surya Bali et al (18) .…”

“…But, reduction of salt intake to control hypertension has been opposed by experts involved in Iodine Deficiency Disorder (IDD) (12) . Further, a few studies have demonstrated a positive correlation between low salt intake and higher risk of hypertension or cardiovascular events (14,14) . Moreover, prolonged practice of low salt increases blood pressure through activation of the renin-angiotensin and sympathetic nervous systems (13) .…”

Sodium Intake and Incidence of Diabetes Complications in Elderly Patients with Type 2 Diabetes—Analysis of Data from the Japanese Elderly Diabetes Intervention Study (J-EDIT)

“…A previous prospective study in 17 countries reported that mortality and cardiovascular events are greater on both a high sodium excretion, as well as on a low sodium excretion [ 25 ], and some populations demonstrate an increase in blood pressure on a low sodium diet and are considered to be inverse salt sensitive [ 26 ]. Therefore, some patients with diabetes who are inverse salt-sensitive and follow national federal guidelines for lower sodium consumption may have elevated blood pressure by activation of renin-aldosterone and sympathetic nerve systems [ 27 ], leading to the development of vascular complications. Second, elderly type 2 diabetes patients with low sodium intake have lower intakes of food groups and nutrition that were reported to be associated with reduced risk of diabetic complications and mortality.…”

Paternal long-term PM2.5 exposure causes hypertension via increased renal AT1R expression and function in male offspring

“…To ensure the reliability of the measurements, rats were trained for one week to acclimatize them to the process of measurement. Blood pressure was measured using a computerized noninvasive tail-cuff manometry system (MODEL MK-2000; Muromachi Kikai Co. Ltd, Tokyo, Japan) in conscious rats between 2 and 5 PM every day, as reported in our previous studies [17,18].…”

“…The protein expressions of angiotensin II type 1 receptor (AT 1 R), G-protein-coupled receptor kinase type 4 (GRK4), GAPDH and tubulin were determined by immunoblotting, as reported in our previous studies [14,[16][17][18]. In brief, equal amounts of total extracted proteins (100 μg) were separated on SDS-PAGE and were transferred onto nitrocellulose membranes (Amersham Life Science, Arlington, TX).…”