**1. Introduction**

In many countries, the prevalence of obesity is increasing, and one-third of the worldwide population is described as obese or overweight [1]. Obesity is currently considered a pandemic and is frequently associated with metabolic syndromes such as hypertension, insulin resistance, and abnormal blood lipid levels [2,3]. A high-fat diet (HFD) increases excessive body fat storage and is a major factor in obesity [4]. This diet represents a risk factor for the development and/or worsening of several chronic diseases, including cardiovascular diseases [5].

Perivascular adipose tissue (PVAT) is the adipose tissue that surrounds the blood vessels. PVAT differs based on the species and anatomic location and is generally classified as brown (thermoactive adipocytes), beige (brown-like adipocytes), or white adipose tissue (lipid-storing adipocytes) [6]. PVAT releases a wide range of adipokines, vasoactive and pro- /anti-inflammatory mediators that influence vascular function in a paracrine manner [7]. PVAT plays a beneficial role by releasing anticontractile factors such as hydrogen sulfide, adiponectin, and nitric oxide (NO) in equilibrium. A great number of contractile factors are produced in obesity, such as angiotensin II, chemerin, serotonin, dopamine, norepinephrine, calpastatin, and so on [8]. Moreover, obesity is frequently associated with structural

**Citation:** Lee, S.; Jang, S.; Kim, J.Y.; Kim, I. Dahl Salt-Resistant Rat Is Protected against Hypertension during Diet-Induced Obesity. *Nutrients* **2022**, *14*, 3843. https:// doi.org/10.3390/nu14183843

Academic Editors: Shane Phillips and Abeer M. Mahmoud

Received: 12 August 2022 Accepted: 14 September 2022 Published: 16 September 2022

**Copyright:** © 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).

and functional alterations in PVAT, leading to vascular dysfunction that involves the endothelium and smooth muscle as well as increased overall cardiovascular risk [9].

Hypertensive patients account for 25% of all patients with chronic kidney disease (CKD), and hypertensive patients with obesity are at the greatest risk for developing CKD [10,11]. The development of obesity leads to significant lipid deposits around or within non-adipose tissues and organs (ectopic fat), which impairs both tissue and organ function [12]. Obesity also affects the kidney, which has assigned roles in dyslipidemia, the production of adipokines and angiotensin II, oxidative stress, hyperfiltration, immune activation, and lipotoxicity [13,14]. The activation of the renin-angiotensin-aldosterone system (RAAS) is the main mechanism by which obesity induces the development of high blood pressure [15]. Because experimental results from animals and humans have suggested the activation of the RAAS in hypertension with obesity, the RAAS is considered important in controlling blood pressure in obesity [16].

A recent study showed that a HFD increases blood pressure in the Dahl salt-sensitive (SS) rat model [17]. The SS rat has been regarded as the most popular model of human salt-sensitive hypertension. Salt-sensitive hypertension is more likely to cause multiple organ damage and results in a higher prevalence of cardiovascular and renal diseases among hypertensive subjects [18]. Several studies have shown that the Dahl salt-resistant (SR) rat remains normotensive in resistance to diet-induced hypertension, such as with high salt or high fructose intake, as compared with the SS rat [19]. However, it is of interest whether the SR rat is protected against hypertension after diet-induced obesity. Therefore, we tested the hypothesis that SR rat is protected against hypertension during diet-induced obesity.
