{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,18]],"date-time":"2026-03-18T01:35:36Z","timestamp":1773797736588,"version":"3.50.1"},"reference-count":34,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2016,10,1]]},"abstract":"<jats:p> Patients with hypertension and hyperaldosteronism show an increased risk of stroke compared with patients with essential hypertension. Aim of the study was to assess the effects of aldosterone on left atrial function in rats as a potential contributor to thromboembolism. Osmotic mini-pumps delivering 1.5 \u03bcg aldosterone\/h were implanted in rats subcutaneously (Aldo, n = 39; controls, n = 38). After 8 wk, left ventricular pressure-volume analysis of isolated working hearts was performed, and left atrial systolic and diastolic function was also assessed by atrial pressure-diameter loops. Moreover, left atrial myocytes were isolated to investigate their global and local Ca<jats:sup>2+<\/jats:sup> handling and contractility. At similar heart rates, pressure-volume analysis of isolated hearts and in vivo hemodynamic measurements revealed neither systolic nor diastolic left ventricular dysfunction in Aldo. In particular, atrial filling pressures and atrial size were not increased in Aldo. Aldo rats showed a significant reduction of atrial late diastolic A wave, atrial active work index, and increased V waves. Consistently, in Aldo rats, sarcomere shortening and the amplitude of electrically evoked global Ca<jats:sup>2+<\/jats:sup> transients were substantially reduced. Sarcoplasmic reticulum-Ca<jats:sup>2+<\/jats:sup> content and fractional Ca<jats:sup>2+<\/jats:sup> release were decreased, substantiated by a reduced sarcoplasmic reticulum calcium ATPase activity, resulting from a reduced CAMKII-evoked phosphorylation of phospholamban. Hyperaldosteronism induced atrial systolic and diastolic dysfunction, while atrial size and left ventricular hemodynamics, including filling pressures, were unaffected in rats. The described model suggests a direct causal link between hyperaldosteronism and decreased atrial contractility and diastolic compliance. <\/jats:p>","DOI":"10.1152\/ajpheart.00261.2016","type":"journal-article","created":{"date-parts":[[2016,9,11]],"date-time":"2016-09-11T00:07:48Z","timestamp":1473552468000},"page":"H1014-H1023","source":"Crossref","is-referenced-by-count":18,"title":["Hyperaldosteronism induces left atrial systolic and diastolic dysfunction"],"prefix":"10.1152","volume":"311","author":[{"given":"Jan-Christian","family":"Reil","sequence":"first","affiliation":[{"name":"Klinik f\u00fcr Innere Medizin III (Kardiologie, Angiologie, Internistische Intensivmedizin), Universit\u00e4tsklinikum des Saarlandes, Homburg\/Saar, Germany;"},{"name":"Klinik f\u00fcr Innere Medizin II, Kardiologie, Angiologie und Internistische Intensivmedizin, Universit\u00e4res Herzzentrum L\u00fcbeck, Universit\u00e4tsklinikum Schleswig-Holstein, L\u00fcbeck, 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