Abstract
The aim of the present study is to investigate whether a disruption of the dipping pattern of blood pressure (BP) is associated with the progression of renal injury in Dahl salt-sensitive (DSS) hypertensive rats. Seven-week-old DSS rats were fed a high salt diet (HSD; 8% NaCl) for 10 weeks, followed by a transition to a normal salt diet (NSD; 0.3% NaCl) for 4 weeks. At baseline, NSD-fed DSS rats showed a dipper-type circadian rhythm of BP. By contrast, HSD for 5 days caused a significant increase in the difference between the active and inactive periods of BP with an extreme dipper type of BP, while proteinuria and renal tissue injury were not observed. Interestingly, HSD feeding for 10 weeks developed hypertension with a non-dipper pattern of BP, which was associated with obvious proteinuria and renal tissue injury. Four weeks after switching to an NSD, BP and proteinuria were significantly decreased, and the BP circadian rhythm returned to the normal dipper pattern. These data suggest that the non-dipper pattern of BP is associated with the progression of renal injury during the development of salt-dependent hypertension.
Highlights
In healthy subjects, blood pressure (BP) follows a diurnal variation, with a physiological dipping (>10%) during the nighttime compared with the daytime [1]
We recently reported that normal salt diet (NSD; 0.3% NaCl)-fed Dahl salt-sensitive (DSS) rats did not develop hypertension and exhibited a normal dipping pattern of BP [14]
high salt diet (HSD) feeding for 10 weeks increased the mean arterial pressure (MAP; 185 ± 6 mmHg at 17 weeks of age) in a time-dependent manner, while continuous NSD feeding did not alter MAP (107 ± 2 mmHg at 17 weeks of age) in DSS rats (Figure 1A)
Summary
Blood pressure (BP) follows a diurnal variation, with a physiological dipping (>10%) during the nighttime (inactive) compared with the daytime (active) [1]. The night/day ratio of sodium excretion was lower in dippers, while the ratio was greater in non-dippers [12]. In this regard, Bankir et al [1] reported that the capacity to excrete sodium during the daytime is a significant determinant of nocturnal BP and dipping. Bankir et al [1] reported that the capacity to excrete sodium during the daytime is a significant determinant of nocturnal BP and dipping These data suggest that alterations in the normal nocturnal or inactive-period dip in BP are associated with salt sensitivity of BP, as well as high sodium intake
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