Blood volume, blood pressure and total body sodium: internal signalling and output control

• Published in: Acta Physiologica 2009, Vol.195 (1), p.187-196
• Main Author: Bie, P
• Format: Article
• Language: English
• Subjects: Animals; baroreceptors; Biological and medical sciences; Blood Pressure - physiology; Blood Volume - physiology; Fundamental and applied biological sciences. Psychology; Homeostasis; Humans; natriuresis; renal nerve activity; renin; Signal Transduction - physiology; Sodium - metabolism; Sodium, Dietary; Vertebrates: anatomy and physiology, studies on body, several organs or systems; volume homeostasis; volume receptors
• ISSN: 1748-1708; 1748-1716
• DOI: 10.1111/j.1748-1716.2008.01932.x

Total body sodium and arterial blood pressure (ABP) are mutually dependent variables regulated by complex control systems. This review addresses the role of ABP in the normal control of sodium excretion (NaEx), and the physiological control of renin secretion. NaEx is a pivotal determinant of ABP, and under experimental conditions, ABP is a powerful, independent controller of NaEx. Blood volume is a function of dietary salt intake; however, ABP is not, at least not in steady states. A transient increase in ABP after a step-up in sodium intake could provide a causal relationship between ABP and the regulation of NaEx via a hypothetical integrative control system. However, recent data show that subtle sodium loading (simulating salty meals) causes robust natriuresis without changes in ABP. Changes in ABP are not necessary for natriuresis. Normal sodium excretion is not regulated by pressure. Plasma renin is log-linearly related to salt intake, and normally, decreases in renin secretion are a precondition of natriuresis after increases in total body sodium. Renin secretion is controlled by renal ABP, renal nerve activity and the tubular chloride concentrations at the macula densa (MD). Renal nerve activity is related to blood volume, also at constant ABP, and elevates renin secretion by means of β₁-adrenoceptors. Recent results indicate that renal denervation reduces ABP and renin activity, and that sodium loading may decrease renin without changes in ABP, glomerular filtration rate or β₁-mediated nerve activity. The latter indicates an essential role of the MD mechanism and/or a fourth mediator of the physiological control of renin secretion.