Does Excess Tissue Sodium Storage Regulate Blood Pressure?

Abstract

Purpose of review: The regulation of blood pressure is conventionally conceptualised into the product of "circulating blood volume" and "vasoconstriction components". Over the last few years, however, demonstration of tissue sodium storage challenged this dichotomous view.

Recent findings: We review the available evidence pertaining to this phenomenon and the early association made with blood pressure; we discuss open questions regarding its originally proposed hypertonic nature, recently challenged by the suggestion of a systemic, isotonic, water paralleled accumulation that mirrors absolute or relative extracellular volume expansion; we present the established and speculate on the putative implications of this extravascular sodium excess, in either volume-associated or -independent form, on blood pressure regulation; finally, we highlight the prevalence of high tissue sodium in cardiovascular, metabolic and inflammatory conditions other than hypertension. We conclude on approaches to reduce sodium excess and on the potential of emerging imaging technologies in hypertension and other conditions.

Keywords: Blood pressure; Blood vessels; Hypertension; Tissue sodium; Volume.

Fig. 1

Sodium and regulation of blood pressure: classic and novel perspectives. A The vasoconstriction–volume spectrum of clinical hypertension (ref 4); Na⁺ (salt shaker) is considered the main determinant of the “intravascular volume” extreme of the spectrum, which variably combines with the independent “vasoconstriction” extreme to sustain different forms of high blood pressure (BP). B The current understanding of tissue Na⁺ accumulation expands beyond the vascular bed. Water-paralleled (osmotic) interstitial Na⁺, in equilibrium with the intravascular compartment, determines a whole-body volume excess; non-osmotic storage capacity could provide a buffering system which prevents a rise in BP, but lacks confirmation. Interstitial Na⁺ could simultaneously impact vascular function and increase peripheral resistance by inducing a local inflammatory state, endothelial damage, water-paralleled expansion of the extracellular volume (ECV) and changes in intracellular Na⁺ in the vascular wall