Endocrine Abstracts (2012) 28 P181

Endothelial function, the renin-angiotensin-aldosterone axis (RAAS) and hypertension: the therapeutic role of potassium supplementation

Una Graham1, David McCance1, Ian Young2 & Karen Mullan1

1Regional Centre for Endocrinology and Diabetes, Royal Victoria Hospital, Belfast, United Kingdom; 2Centre for Public Health, Queen's University, Belfast, United Kingdom.

There is limited evidence on the effect of potassium (K+) supplementation on endothelial function. Three studies suggest a beneficial effect in healthy volunteers and mild hypertensives. However potassium increases aldosterone due to a direct effect on the adrenal gland and there is evidence that aldosterone excess is detrimental to cardiovascular health. We therefore aimed to determine the effect of potassium supplementation on endothelial function in patients with >10% cardiovascular disease risk. We also aimed to determine the effect of potassium supplementation on brachial and central blood pressure, the RAAS and vascular inflammation. Forty patients with >10% ten year cardiovascular disease risk were included in a randomised placebo controlled crossover study. Drugs which interfere with the RAAS were stopped and blood pressure controlled with doxazosin. Patients were assigned to either 64 mmol potassium chloride or placebo for 6 weeks with a 6 week washout period. Endothelial function was assessed using global pulse wave analysis (PWA) involving the detection of a change in augmentation index to salbutamol (endothelial dependent) and GTN (endothelial independent) induced vasodilation. Vascular inflammation was assessed using high sensitivity C-reactive protein (hsCRP). K+ supplementation improved brachial and central systolic blood pressure (P=0.013 and 0.011 respectively) but did not affect endothelial function or hsCRP. Plasma renin activity (P=0.048) and serum aldosterone (P=0.001) both increased significantly with K+ supplementation compared to placebo. Serum K+ increased with supplemental K+ vs placebo (4.1 vs 3.9 mmol/l; P=0.012) but hyperkalaemia did not develop. These data show that K+ supplementation lowered systolic blood pressure. Interestingly K+ supplementation was associated with an increase in both plasma renin activity and serum aldosterone suggesting that K+ may also stimulate the RAAS via the juxtaglomerular apparatus. Despite this rise in aldosterone K+ supplementation did not affect global PWA or hsCRP.

Declaration of interest: There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Funding: No specific grant from any funding agency in the public, commercial or not-for-profit sector.

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