Hypertension, one of the most common and severe comorbidities of obesity and overweight, is a worldwide epidemic affecting over 30% of the population. We induced overweight in young male rats (aged 58 days) by exposure to a hypercaloric high lipid (HL) diet in which 70% of the calories originated from fat. The HL diet also contained 33 or 57% higher Na⁺ than the control (CTR) diet. Over the following weeks the HL rats gradually became overweight (490 ± 12 g vs 427 ± 7 g in the CTR group after 15 weeks) with high visceral fat. They developed elevated systolic blood pressure (SBP) (141 ± 1.9 mmHg), which was fully restored to CTR values (128 ± 1.1 mmHg) by oral administration of Ang-(3–4) (Val-Tyr), the shortest renin-angiotensin-derived peptide. The overweight rats had lower plasma Na⁺ concentration that augmented to CTR values by Ang-(3–4) treatment. Na⁺ ingestion was depressed by 40% as result of the Ang-(3–4) treatment, whereas the urinary excretion of Na⁺ (U_NaV) remained unmodified. The preservation of U_NaV after Ang-(3–4) treatment – despite the sharp decrease in the dietary Na⁺ intake – can be ascribed to the normalization of renal type 1 angiotensin II receptors and Na⁺-transporting ATPases, both up-regulated in overweight rats. These renal effects complete a counterregulatory action on elevated renin-angiotensin activity that allows the high SBP to be normalized and body Na⁺ homeostasis to be restored concomitantly in overweight rats.

高血压是肥胖和超重最常见，最严重的合并症之一，是一种全球性流行病，影响了30％以上的人口。我们通过暴露于高热量高脂（HL）饮食中诱导了年轻雄性大鼠（58岁）的超重，其中70％的卡路里来自脂肪。HL饮食还比对照（CTR）饮食含33 ⁺ 57％高的Na ⁺。在接下来的几周中，HL大鼠逐渐变得超重（15周后CTR组为490±12 g，而CTR组为427±7 g），并伴有高内脏脂肪。他们的收缩压（SBP）升高（141±1.9 mmHg），通过口服Ang-（3–4）（Val-Tyr）（肾素最短）可完全恢复至CTR值（128±1.1 mmHg）。血管紧张素衍生的肽。超重的大鼠血浆Na ⁺较低通过Ang-（3-4）处理增加到CTR值的浓度。Ang-（3-4）治疗使Na ^+的摄入降低了40％，而Na ⁺（U _Na V）的尿排泄仍然未改变。Ang-（3-4）治疗后U _Na V的保存-尽管饮食中Na ⁺摄入量急剧减少-可归因于肾脏1型血管紧张素II受体和Na ⁺转运ATP酶的正常化，两者均升高。调节超重大鼠。这些肾功能对肾素-血管紧张素活性的升高完成了反调节作用，使高SBP得以正常化，体内Na ⁺ 超重大鼠同时恢复体内稳态。