High salt intake aggravates aortic dysfunction in rats with adenine‐induced chronic renal failure (1136.13)

Abstract

Rats with adenine‐induced chronic renal failure (ACRF) develop a reduced rate of relaxation, and increased stiffness of the aorta. The aim of this study was to investigate the effects of 2 weeks of high NaCl intake on vascular function in rats with ACRF.Male Sprague‐Dawley rats received either chow containing adenine (ACRF) or were pair‐fed a control diet (Controls, C). Two weeks prior to sacrifice animals were randomized to diet containing either normal salt (0.6% NaCl, NS) or high salt (4% NaCl, HS), resulting in four groups: C‐NS, C‐HS, ACRF‐NS and ACRF‐HS (n=11‐15 per group). Animals were sacrificed at 7‐10 weeks after study start and mesenteric arteries and thoracic aorta were analyzed with wire myograph.Animals with ACRF showed significant increases in serum creatinine and systolic blood pressure that was aggravated by high NaCl intake (138±14, 164±10, 152±7 and 202±14 mmHg in groups C‐NS, ACRF‐NS, C‐HS and ACRF‐HS, respectively). A decreased sensitivity to norepinephrine was found in mesenteric arteries of ACRF‐HS rats (P<0.05). In the thoracic aorta, the sensitivity to both sodium nitroprusside (SNP) and acetylcholine (ACh) were reduced only in ACRF‐HS animals (P<0.05). Furthermore, the ACRF‐HS group exhibited a marked decrease in aortic relaxation rate compared to ACRF‐NS animals (P<0.01).In rats with ACRF two weeks of high NaCl intake reduced the sensitivity to ACh and SNP in the thoracic aorta and aggravated the impairment in relaxation rate whereas vasodilator responses were unaffected in resistance arteries. These results indicate an abnormality in vascular smooth muscle function specifically in the thoracic aorta of ACRF animals that is augmented by high NaCl intake.