Abstract

We evaluated whether long‐term kefir treatment affects cardiac function (cardiac contractility and calcium‐handling proteins) and sympathetic control in spontaneously hypertensive rats (SHR). Male normotensive rats (WKYs) and SHRs were separated into three groups: SHRs treated with milk fermented by the grains of kefir (5%; SHR‐Kefir; oral gavage, 0.3mL/100g daily/9weeks), and WKYs and SHRs treated with milk. At the end of treatment, direct MAP and HR were measured via artery catheterization. Hemodynamic parameters (left ventricular (LV) systolic pressure (LVSP), left ventricular isovolumetric relaxation time constant (Tau), maximal and minimal pressure decay (+/−dP/dt) were acquired through left ventricular catheter implantation. LV protein expressions of phospholamban (PLB, and phosphorylated (p)‐PBL), and sarcoplasmic reticulum Ca2+‐ATPase (SERCA2a) were determined by Western blot. Tyrosine hydroxylase (TH) protein expression was evaluated via immunofluorescence within the paraventricular nucleus of the hypothalamus (PVN) and rostral ventrolateral medulla (RVLM). We found that the SHR‐Kefir group presented lower MAP (132±0.99mmHg) and HR (321±4.9bpm) compared to SHR (MAP: 167±0.74mmHg; HR: 393±7.3bpm; P<0.01). Kefir ameliorated cardiac hypertrophy (LV weight/body weight ratio: WKY, 1.006±0.04; SHR, 1.900±0.09; SHR‐Kefir; 1.488±0.09mg/g; P<0.05) and promoted reduced expression of PBL (WKY, 100%; SHR, 143.5±19.9%; SHR‐Kefir, 112.2±10.7%), p‐PBL (WKY, 100%; SHR, 127.2±8.9%; SHR‐Kefir, 101.4±10.3%), and SERCA2a (WKY, 100%; SHR, 134.3±7.8%; 69.2±16%; P<0.05) contractile proteins. Within the PVN and RVML, TH protein overexpression observed in SHRs was reduced by kefir treatment (PVN: WKY, 7.42±0.8; SHR, 14.2±0.8; SHR‐Kefir, 8.1±0.7, and RVLM: WKY, 1.39±0.05; SHR, 1.7±0.13; SHR‐Kefir, 1.2±0.09 arbitrary units). In addition, kefir treatment improved cardiac hemodynamic parameters in SHR, including: LVSP (WKY, 115.5±1.2; SHR, 172.2±1.1; SHR‐Kefir, 137.01±1.2 mmHg; P<0.01, Tau (WKY, 0.046±0.003; SHR, 0.027±0.0007; SHR‐Kefir, 0.04±0.001 s; P<0.05), +dP/dt (WKY, 3021±53.5; SHR, 4926±46.5 ; SHR‐Kefir, 3955±32.5 mmHg/sec; P<0.01), and ‐dP/dt (WKY, −3241±313.2; SHR, −4151±81.9; SHR‐Kefir, −2705±41.8 mmHg/sec; P<0.01). Altogether, our data show that long‐term kefir treatment reduced blood pressure by mechanisms involving reduction of cardiac hypertrophy, ameliorating cardiac function by improvement of cardiac contractility and calcium‐handling proteins, and a reduction in the CNS regulation of the sympathetic activity.Support or Funding InformationWork supported by CAPES; Finance Code 001, BRA, and FAPES 0279/2016.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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