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Moderately High Salt Intake does not Raise Blood Pressure but does Activate Peripheral Immune Cells with the Capacity to Raise Blood Pressure
Author(s) -
ZUBCEVIC Jasenka,
Ahmari Niousha,
Diaz Devon,
Malphurs Wendi,
Redlitz Conrad M,
Andrade Marry Ann,
Toney Glenn M
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1003.4
Subject(s) - blood pressure , immune system , medicine , endocrinology , angiotensin ii , interleukin 17 , immunology , peripheral blood mononuclear cell , chemistry , biochemistry , in vitro
Arterial hypertension (HTN) is often salt sensitive and accompanied by renin‐angiotensin (RAS) and immune system activation. For example, activated T cells contribute significantly to Angiotensin II (Ang II)‐dependent HTN. In a salt‐sensitive model, rats fed a moderately high salt diet (2% NaCl) experience neuroadaptations that increase excitability of PVN sympathetic control neurons without developing overt HTN. Dietary salt is also linked with autoimmune diseases (e.g., psoriatic arthritis, lupus, etc.) that are often co‐morbid with HTN and associated with T cell‐dependent interleukin 17 (IL17) signaling. Here, we hypothesized that elevated dietary salt will increase IL17 expression in T lymphocytes and contribute to the salt‐sensitivity of arterial HTN, possibly by priming of the pre‐sympathetic circuitry. METHODS Adult Sprague‐Dawley rats were placed on either a normal (0.4% NaCl) or high salt (2% NaCl) diet for two weeks. Blood and bone marrow (BM) were collected to determine levels of CD4+IL17+ T lymphocytes by FACS. Additionally, adult C57BL/6‐Il17a tm1Bcgen /J mice (Jax Labs), with constitutive expression of EGFP as a marker of IL17a activity, were subjected to a similar experimental protocol. Blood pressures (BP) were measured once a week by tail cuff. Whole body fluorescence imaging was performed in all mice to detect group differences in the levels of IL17a. BM was collected both from normal and high salt fed mice, and fluorescence sorting separated IL17+ from IL17‐cells. Adoptive transfer was performed by injecting the same number of harvested cells via tail vein into separate groups of naïve C57BL6/J adult mice (n=6/group). BP was measured twice a week for two weeks following the adoptive transfer. RESULTS In rats, high salt intake increased expression of IL17a in BM, but not in circulating CD4+ T cells. There was no change in the total CD4+ T cell population. In mice, whole body fluorescence revealed a ~12% increase of IL17 reporter fluorescence selectively in the head region in the high salt group. We observed a significant increase of systolic BP (113±6 to 135±3 mm Hg; P<0.05) within one week of adoptive transfer of IL17a+ BM cells from the high salt group. CONCLUSION A moderately high salt diet is not sufficient to raise BP in the whole animal. Nevertheless, it does activate a population of IL17‐expressing immune cells which alone are capable of raising BP. We speculate that suppression of endogenous RAS by high salt intake might offset or otherwise preclude the pro‐HTN effects of immune cell activation. Support or Funding Information AHA14SDG18300010&UFCVM (JZ); NIH HL102310 (GMT)