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J Physiol. 2019 Sep;597(17):4451-4464. doi: 10.1113/JP276844. Epub 2019 Jul 29.

K+ and the renin-angiotensin-aldosterone system: new insights into their role in blood pressure control and hypertension treatment.

Author information

1
Department of Biomedicine, Aarhus University, Aarhus, DK-8000, Denmark.

Abstract

Approximately 25% of the adult population is diagnosed with hypertension and it is therefore one of the biggest challenges for the health sector. The renin-angiotensin-aldosterone system (RAAS) adjusts effective circulating volume and ultimately blood pressure (BP). Accordingly, antihypertensive drugs targeting the RAAS have been a major focus in modern medical treatment. Low and high dietary K+ intakes are associated with increased or decreased BP and risk of cardiac failure, respectively, suggesting that dietary K+ augmentation has the potential to supplement or replace conventional anti-hypertensive drugs. Animal studies have indicated that the beneficial effects of high dietary K+ may be linked to a dominant regulatory role of plasma K+ on key renal transport proteins controlled by the RAAS. However, only a limited number of studies have investigated whether the reported mechanisms in animal models apply to humans. Furthermore, hypertension is often treated with so-called 'K+ sparing' drugs, thus complicating co-treatment with K+ supplementation. In this review, we revisit old concepts of RAAS effects in the kidney, relate them to effects of dietary K+ manipulation, and finally consider the clinical potential of treating hypertension with K+ supplementation alone or in combination with RAAS inhibitors. Collectively, a wealth of data suggest that increased dietary K+ intake may have beneficial effects on BP in the general population, but underlying medical conditions or current treatment regimens need to be carefully considered before implementing K+ supplementation in patients.

KEYWORDS:

blood pressure; hyperkalemia; hypertension; hypokalemia; potassium; sodium

PMID:
31294465
DOI:
10.1113/JP276844

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