{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T14:22:45Z","timestamp":1781706165032,"version":"3.54.5"},"reference-count":35,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"9","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2021,5,4]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">Increased potassium intake lowers blood pressure in patients with hypertension, but increased potassium intake also elevates plasma concentrations of the blood pressure\u2010raising hormone aldosterone. Besides its well\u2010described 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\u2010independent actions are also thought to be involved.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              To gain further insight into the effect of increased potassium intake and potassium\u2010stimulated hyperaldosteronism on the human cardiovascular system, we conducted a randomized placebo\u2010controlled double\u2010blind crossover study in 25 healthy normotensive men, where 4\u00a0weeks treatment with a potassium supplement (90\u00a0mmol\/day) was compared with 4\u00a0weeks 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\u2010monitoring), and Doppler ultrasound. The study showed that higher potassium intake increased plasma potassium (mean\u00b1SD, 4.3\u00b10.2 versus 4.0\u00b10.2\u00a0mmol\/L;\n              <jats:italic>P<\/jats:italic>\n              =0.0002) and aldosterone (median [interquartile range], 440 [336\u2013521] versus 237 [173\u2013386] pmol\/L;\n              <jats:italic>P<\/jats:italic>\n              &lt;0.0001), and based on a linear mixed model for repeated measurements, increased potassium intake potentiated AngII\u2010stimulated aldosterone secretion (\n              <jats:italic>P<\/jats:italic>\n              =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.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">Increased potassium intake potentiates AngII\u2010stimulated aldosterone secretion without affecting systemic cardiovascular hemodynamics in healthy normotensive men.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Registration<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              EudraCT Number: 2013\u2010004460\u201066; URL:\n              <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/www.ClinicalTrials.gov\">https:\/\/www.ClinicalTrials.gov<\/jats:ext-link>\n              ; Unique identifier: NCT02380157.\n      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