Effect of Increased Potassium Intake on Adrenal Cortical and Cardiovascular Responses to Angiotensin II: A Randomized Crossover Study

Abstract

Background Increased potassium intake lowers blood pressure in patients with hypertension, but increased potassium intake also elevates plasma concentrations of the blood pressure‐raising hormone aldosterone. Besides its well‐described renal effects, aldosterone is also believed to have vascular effects, acting through mineralocorticoid receptors present in endothelial and vascular smooth muscle cells, although mineralocorticoid receptors‐independent actions are also thought to be involved. Methods and Results To gain further insight into the effect of increased potassium intake and potassium‐stimulated hyperaldosteronism on the human cardiovascular system, we conducted a randomized placebo‐controlled double‐blind crossover study in 25 healthy normotensive men, where 4 weeks treatment with a potassium supplement (90 mmol/day) was compared with 4 weeks on placebo. At the end of each treatment period, we measured potassium and aldosterone in plasma and performed an angiotensin II (AngII) infusion experiment, during which we assessed the aldosterone response in plasma. Hemodynamics were also monitored during the AngII infusion using ECG, impedance cardiography, finger plethysmography (blood pressure‐monitoring), and Doppler ultrasound. The study showed that higher potassium intake increased plasma potassium (mean±SD, 4.3±0.2 versus 4.0±0.2 mmol/L; P =0.0002) and aldosterone (median [interquartile range], 440 [336–521] versus 237 [173–386] pmol/L; P <0.0001), and based on a linear mixed model for repeated measurements, increased potassium intake potentiated AngII‐stimulated aldosterone secretion ( P =0.0020). In contrast, the hemodynamic responses (blood pressure, total peripheral resistance, cardiac output, and renal artery blood flow) to AngII were similar after potassium and placebo. Conclusions Increased potassium intake potentiates AngII‐stimulated aldosterone secretion without affecting systemic cardiovascular hemodynamics in healthy normotensive men. Registration EudraCT Number: 2013‐004460‐66; URL: https://www.ClinicalTrials.gov ; Unique identifier: NCT02380157.

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“…In a previous analysis, a four-week increase in potassium consumption potentiates AngII-stimulated aldosterone secretion without affecting systemic cardiovascular hemodynamics in healthy normotensive men. This indicates that the antihypertensive effect of potassium is mediated by its diuretic effect [ 230 ]. In addition to maintaining normal plasma potassium levels, these natriuretic effects contribute to the blood pressure-lowering effect of high potassium intake.…”

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“…This, however, is difficult to reconcile with evidence showing that plasma aldosterone correlates better with plasma cortisol than with plasma renin activity ( 16 ). It is becoming increasingly clear that there are multiple factors involved in the regulation of aldosterone, including not only renin activity and ACTH ( 7 , 15 ) but also sleep structure ( 16 , 17 , 38 ) and potassium intake ( 19 ). Our participants were all on unrestricted diets, without any specific control of salt intake.…”

“…The generally held belief is that aldosterone secretion is primarily determined by the renin-angiotensin system, at least in normotensive states ( 15 ), although plasma aldosterone correlates better with plasma cortisol than with plasma renin activity ( 16 ). Studies of aldosterone support a much more complex picture, where aldosterone may also be influenced by sleep ( 17 , 18 ) in addition to modulation by ACTH ( 6 ), potassium intake ( 19 ), and renin ( 20 ).…”

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“…A growing body of evidence suggests that vascular endothelial dysfunction plays a crucial role in the pathogenesis of hypertensive renal damage [20][21][22] .…”