title: Deregulation of Soluble Adhesion Molecules in Resistant Hypertension and Its Role in Cardiovascular Remodeling.
abstract: BACKGROUND
  Resistant hypertension (RHTN) and target organ damage are linked to increased inflammatory biomarkers, which may regulate adhesion molecules, such as intracellular adhesion molecule-1 (ICAM-1); vascular cell adhesion molecule-1 (VCAM-1); and the platelet (P-selectin) and endothelial (E-selectin) selectins. We investigated a previously unknown relationship between soluble P-selectin (sP-selectin), E-selectin (sE-selectin), ICAM-1 (sICAM-1) and VCAM-1 (sVCAM-1) with RHTN and target organ damage.
  
  
  RESULTS
  We included 110 subjects diagnosed for true RHTN and 112 mild-moderate hypertensive (HTN) patients. Blood pressure parameters, pulse wave velocity and left ventricular mass index (LVMI) were measured. Adhesion molecules were measured on ELISA. Both sP-selectin and sE-selectin were increased; in contrast, sICAM-1 was reduced in RHTN compared with HTN patients, while similar sVCAM-1 was noted in the groups. sP-selectin and sVCAM-1 were elevated in the presence of arterial stiffness (sP-selectin: 104±47 vs. 89±45 ng/ml, P<0.05; sVCAM-1: 1,189±411 vs. 1,060±412 ng/ml, P<0.05) and cardiac hypertrophy (sP-selectin: 105±51 vs. 88±43 ng/ml, P<0.05; sVCAM-1: 1,170±433 vs. 1,040±383 ng/ml, P<0.05) in all HTN patients. sP-selectin was associated with target organ damage after adjustment for age and BP. Apart from potential confounders, sE-selectin was a significant indicator of RHTN.
  
  
  CONCLUSIONS
  The adhesion molecule sP-selectin plays a role in cardiovascular damage, and sE-selectin in resistance to antihypertensive therapy. (Circ J 2016; 80: 1196-1201).
authors.affiliation: Laboratory of Cardiovascular Pharmacology, Faculty of Medical Sciences, University of Campinas.
authors.forename: Ana Paula
authors.initials: AP
authors.lastname: de Faria
authors.forename: Alessandra Mileni Versuti
authors.initials: AM
authors.lastname: Ritter
authors.forename: Andréa Rodrigues
authors.initials: AR
authors.lastname: Sabbatini
authors.forename: Nathália Batista
authors.initials: NB
authors.lastname: Corrêa
authors.forename: Veridiana
authors.initials: V
authors.lastname: Brunelli
authors.forename: Rodrigo
authors.initials: R
authors.lastname: Modolo
authors.forename: Heitor
authors.initials: H
authors.lastname: Moreno
mesh_terms: D015415:Biomarkers; D006332:Cardiomegaly; D002319:Cardiovascular System / Q000473:pathology; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000502:physiology*; D015331:Cohort Studies; D019040:E-Selectin / Q000032:analysis / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D019007:P-Selectin / Q000032:analysis / Q000502:physiology; D012995:Solubility; D066253:Vascular Remodeling; D059289:Vascular Stiffness
chemical_list: D015415:Biomarkers; D015815:Cell Adhesion Molecules; D019040:E-Selectin; D019007:P-Selectin