{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T16:19:44Z","timestamp":1783441184005,"version":"3.54.6"},"reference-count":51,"publisher":"Institute of Physiology of the Czech Academy of Sciences","issue":"Suppl 1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Physiol Res"],"published-print":{"date-parts":[[2024,8,31]]},"abstract":"<jats:p>Few studies have investigated the hemodynamic mechanism whereby primary hyperaldosteronism causes hypertension. The traditional view holds that hyperaldosteronism initiates hypertension by amplifying salt-dependent increases in cardiac output (CO) by promoting increases in sodium retention and blood volume. Systemic vascular resistance (SVR) is said to increase only as a secondary consequence of the increased CO and blood pressure. Recently, we investigated the primary hemodynamic mechanism whereby hyperaldosteronism promotes salt sensitivity and initiation of salt-dependent hypertension. In unilaterally nephrectomized male Sprague-Dawley rats given infusions of aldosterone or vehicle, we found that aldosterone promoted salt sensitivity and initiation of salt-dependent hypertension by amplifying salt-induced increases in SVR while decreasing CO. In addition, we validated mathematical models of human integrative physiology, derived from Guyton\u2019s classic 1972 model - Quantitative Cardiovascular Physiology-2005 and HumMod-3.0.4. Neither model accurately predicted the usual changes in sodium balance, CO, and SVR that normally occur in response to clinically realistic increases in salt intake. These results demonstrate significant limitations with the hypotheses inherent in the Guyton models. Together these findings challenge the traditional view of the hemodynamic mechanisms that cause salt-sensitive hypertension in primary aldosteronism.\n\nKey words: Aldosterone \u2022 Blood pressure \u2022 Salt \u2022 Sodium \u2022 Rat<\/jats:p>","DOI":"10.33549\/physiolres.935260","type":"journal-article","created":{"date-parts":[[2024,8,22]],"date-time":"2024-08-22T10:57:29Z","timestamp":1724324249000},"page":"S365-S376","source":"Crossref","is-referenced-by-count":1,"title":["Hemodynamic Mechanisms Initiating Salt-Sensitive Hypertension in Rat Model of Primary Aldosteronism"],"prefix":"10.33549","author":[{"given":"M","family":"Pravenec","sequence":"first","affiliation":[{"name":"Institute of Physiology, Czech Academy of Sciences, V\u00edde\u0148sk\u00e1 1083, 14200 Prague, Czech Republic. michal.pravenec@fgu.cas.cz"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P","family":"Mlejnek","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"\u0160im\u00e1kov\u00e1","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J","family":"\u0160ilhav\u00fd","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"19169","reference":[{"key":"ref0","doi-asserted-by":"publisher","unstructured":"1.\tEzzati M, Riboli E: Behavioral and dietary risk factors for noncommunicable diseases. 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