Avaliação da sobrecarga salina na complacência arterial em animais espontaneamente hipertensos

Abstract

The interaction between BP and sodium intake is widely recognized and supported by numerous studies. More recently, clinical studies have shown a close relationship between increased arterial stiffness (as measured by the gold standard VOP choice) and salt consumption in populations. Our study aimed to infer arterial stiffness by VOP in SHR rats after treatment with salt (1%), a content corresponding to the average Brazilian consumption (9.34 g salt - PNS). Male Wistar and SHR rats were divided into: control (Wistar/C and SHR/C) and salt, receiving 1% NaCl solution for 60 days: (Wistar/S and SHR/S). During treatment, the rats were submitted (baseline, ~30 and ~60 days) to measurement of systolic blood pressure (SBP) by tail plethysmography and metabolic cage evaluations. After 60 days, the animals were catheterized in the carotid and femoral areas for PWV analysis and direct hemodynamic measurements. The aortas were collected and prepared for histological analysis to determine arterial thickening, elastic lamina fragmentation, collagen deposition and wall tension and stress. During treatment, we observed an increase in SBP only in animals SHR ~30 days (SHR/A 200 ± 5.2 vs. SHR/S 218 ± 3.2, P<0.01) and ~60 days (SHR/A 206 ± 5.8 vs. SHR/S 225 ± 3.3, P<0.05). After 60 days, chronic sodium intake significantly increased arterial stiffness in SHR rats, corresponding to 8% in the PWV measurement (SHR/C 6.2 ± 0.2 vs. SHR/S 6.7 ± 0.3 m /s), and 11% in PP (SHR/C 54 ± 1.3 vs. SHR/S 60 ± 1.7 mmHg). The increase in arterial stiffness was observed regardless of the concomitant increase in SBP, as we observed a decrease in SHR in the SHR/C (61 mmHg) and SHR/S (72 mmHg) groups after anesthesia in the surgical protocol, a reduction not detected in Wistar animals. Assessments of the aortic structure of the SHR/S group showed an increase of 9% in collagen deposition and 130% in elastic lamina fragmentation. Consequently, we observed an increase of 18.6% in tension and 6.1% in wall stress compared to the SHR/C group. These findings support our hypothesis that 1% sodium consumption can cause changes in vascular dynamics and structure, leading to the emergence of cardiovascular diseases, which reinforces the need to reduce salt consumption as an important strategy for the prevention of cardiovascular events.