A high-fat diet (HFD) frequently causes obesity-induced hypertension. Because Dahl salt-resistant rats are protected against hypertension after high-salt or high-fructose intake, it is of interest whether this model also protects against hypertension after diet-induced obesity. We tested the hypothesis that Dahl salt-resistant rat protects against hypertension during diet-induced obesity. Dahl salt-sensitive (SS) and Dahl salt-resistant (SR) rats were fed a HFD (60% fat) or a chow diet (CD; 8% fat) for 12 weeks. We measured blood pressure using the tail-cuff method. The paraffin sections of thoracic perivascular adipose tissue (tPVAT) were stained with hematoxylin/eosin and trichrome. The expression of genes in the tPVAT and kidneys were measured by reverse transcription-quantitative polymerase chain reaction. The HFD induced hypertension in SS (p < 0.01) but not SR rats, although it increased body weight gain (p < 0.05) and tPVAT weight (p < 0.01) in both rats. The HFD did not affect the expression of genes related to any of the adipocyte markers in both rats, although SR rats had reduced beige adipocyte marker Tmem26 levels (p < 0.01) and increased anti-inflammatory cytokine adiponectin (p < 0.05) as compared with SS rat. The HFD did not affect the mRNA expression of contractile factors in the tPVAT of SS and SR rats. SR rats are protected against hypertension during diet-induced obesity. This result implies that the genetic trait determining salt sensitivity may also determine fructose and fat sensitivity and that it is associated with the prevention of hypertension.
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http://dx.doi.org/10.3390/nu14183843 | DOI Listing |
Life Sci
January 2025
Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea; Cardiovascular Research Institute, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea; BK21 Plus KNU Biomedical Convergence Program, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea; Department of Biomedical Science, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea. Electronic address:
Aims: Although the immune system participates in the development of hypertension, the proportional contributions of distinct immune cells remain poorly understood. With the development of transcriptomics, we can profile the transcriptomes of individual immune cells and assess the relative contribution of each immune cell to the development of hypertension. So, we tested the hypothesis that increased lamina propria B cells play roles in fructose-induced hypertension of Dahl salt-sensitive (SS) rats.
View Article and Find Full Text PDFHypertension
December 2024
Department of Physiology, Medical College of Wisconsin, Milwaukee (A.W.C., M.M.S., T.K., S.S.).
Clin Exp Hypertens
December 2024
Department of Nephrology, Chongqing Fuling Hospital, School of Medicine, Chongqing University, Chongqing, China.
Am J Physiol Renal Physiol
August 2024
Department of Pharmacology and Experimental Therapeutics, Whitaker Cardiovascular Institute, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts, United States.
Hypertension affects approximately one in two United States adults and sex plays an important role in the pathogenesis of hypertension. The Na-Cl cotransporter (NCC), regulated by a kinase network including with-no-lysine kinase (WNK)1 and WNK4, STE20/SPS1-related proline alanine-rich kinase (SPAK), and oxidative stress response 1 (OxSR1), is critical to Na reabsorption and blood pressure regulation. Dietary salt differentially modulates NCC in salt-sensitive and salt-resistant rats, in part by modulation of WNK/SPAK/OxSR1 signaling.
View Article and Find Full Text PDFJ Cardiovasc Dev Dis
October 2023
Department of Pharmacology, School of Medicine, Daegu, 41944, Republic of Korea.
This study aimed to delineate the effect of sodium chloride on the induction of inflammatory responses and the development of hypertension in Dahl salt-sensitive (SS) and salt-resistant (SR) rats. Splenocytes were isolated from the spleens of SS and SR rats, and cultured on anti-CD3-coated plates for 5 days. The cultured splenic T-cells were challenged with a hypertonic salt solution (0, 20, or 40 mM) in the absence or presence of IL-6 (0, 20, or 60 ng/mL), TGF-β (0, 5, or 15 ng/mL), or IL-23 (0, 10, or 30 ng/mL), and analyzed via ELISA, flow cytometry, and immunofluorescence.
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