Abstract 18520: Endogenous Cardiotonic Steroids in Salt- sensitive Hypertension

• Published in: Circulation (New York, N.Y.) N.Y.), 2015-11, Vol.132 (Suppl_3 Suppl 3), p.A18520-A18520
• Main Authors: Estape, Estela S, Torres-Negron, Ivette, Fedorova, Olga V, Gonzalez-Rodriguez, Claribel, Gonzalez-Sepulveda, Lorena, Bagrov, Alexei Y, Wei, Wen, Franqui, Sandra, Rodriguez-Rivera, Ingrid, Garcia-Rivera, Enid, Santiago, Fernando, Lopez-Candales, Angel, Martinez-Maldonado, Manuel
• Format: Article
• Language: English
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/circ.132.suppl_3.18520

IntroductionAn endogenous inhibitor of Na,K-ATPase (CTS) is increased in Dahl salt-sensitive (DS) rats and in human cardiovascular pathologies.HypothesisChronic hypertension is a major cause of CTS release which will not be corrected by treatment, and that effectively treated hypertensive patients (HT) will have increased plasma CTS, compared to ischemic stroke patients (STR) after thrombolytic treatment and controls ( CTL).MethodsForty (40) subjects (age and sex matched) were recruited and grouped into three groupsSTR (n = 13), HT (n = 13), and CTL (n = 14). Plasma was collected 1-2 days after diagnosis of ischemic stroke and thrombolytic treatment. CTS levels was determined in all groups by measuring the bufadienolide CTS marinobufagenin (MBG) using a fluoroimmunoassay. Fisher Exact test, Kruskal-Wallis test, and Mann-Whitney test with Bonferroni correction were used, when appropriate, to analyze all data.ResultsParticipants mean age was 61 ± 12 years; 56% were male. CTS levels within the normal range (200-400 pmoles/L) were found in 62% of the whole cohort. Median plasma CTS was significantly higher in HT as compared to CTL (437.6 vs. 326.8 pmoles/L, p= 0.018) and STR (437.6 vs. 286.9 pmoles/L, p=0.005). Blood pressure did not differ between HT and CTL groups (p>0.05). Extreme CTS values (> 1,000 pmoles/L) were observed in four HT and one CTL, despite normal BP.ConclusionAs predicted, HT patients had high CTS levels compared to CTL suggesting a strong relationship between hypertension and CTS. Plasma CTS may be lowered by thrombolytic but not anti-hypertension therapy. Further studies are required to define the role of CTS in human pathological states.