The importance of the kidneys, as well as the renal function curve, in determining the arterial pressure (BP) has been widely-accepted (long-term BP regulation). Our recent studies have suggested that kidneys may participate in the pathogenesis of a circadian BP rhythm (short-term BP regulation). We have postulated that sodium sensitivity of BP is increased by both reduced glomerular ultrafiltration coefficient and by enhancement of tubular sodium reabsorption in chronic kidney disease (CKD). Glomerular filtration rate (GFR) is reduced in the former condition and is augmented in the latter. In patients with high-sodium sensitivity, the nocturnal BP dip is diminished, resulting in non-dipper pattern of circadian BP rhythm irrespectively of the mechanisms causing sodium sensitivity. We have found that in patients with more severe renal dysfunction it took longer “dipping time” for their nocturnal mean arterial pressure to fall below 90% of their daytime mean value and showed non-dipper circadian rhythms for BP and natriuresis. These findings encourage us to postulate that reduced renal capacity to excrete sodium into urine causes nocturnal elevation of BP (i.e. non-dipper) in order to compensate for diminished daytime natriuresis by enhancing night-time pressure-natriuresis. Both high sodiumsensitivity and non-dippers are risks for cardiovascular disease. Investigation on the renal mechanisms of non-dipper and nocturnal hypertension may be the shortest way to solve cardio-renal connection.
Keywords: Circadian blood pressure rhythm, sodium sensitivity, non-dipper, natriuresis, chronic kidney disease (CKD), cardio-renal continuum, renal dysfunction, glomerular ultrafiltration coefficient, proteinuria, ventricular hypertrophy
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