{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,30]],"date-time":"2026-01-30T06:54:59Z","timestamp":1769756099785,"version":"3.49.0"},"reference-count":37,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2002,9,23]],"date-time":"2002-09-23T00:00:00Z","timestamp":1032739200000},"content-version":"vor","delay-in-days":22,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Clin Investigation"],"published-print":{"date-parts":[[2002,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:bold>Background\u2002<\/jats:bold> Human primary varicosity is associated with \u2018weakness\u2019 of the vein wall. We investigated whether the reduced responsiveness of varicose veins to physiological vasoconstrictors might result from impaired Ca<jats:sup>2+<\/jats:sup> mobilization in venous smooth muscle.<\/jats:p><jats:p><jats:bold>Materials and methods\u2002<\/jats:bold> The hypothesis was tested in cells derived from phenotypically different vein segments that were obtained from the inguinal saphenous vein (tissue with incompetent valves), the distal portion of the long saphenous vein just above the medial ankle (clinically healthy tissue), and from a tributary to the long saphenous vein just below the knee (incompetent and overtly varicose tissue). Saphenous vein from patients undergoing cardiac surgery served as control. Cytosolic free Ca<jats:sup>2+<\/jats:sup> levels ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>) were determined with the fura\u20102 method in cultured medial smooth muscle cells of third to sixth passage (21\u201323 measurements per tissue derived from five controls and seven patients).<\/jats:p><jats:p><jats:bold>Results\u2002<\/jats:bold> Angiotensin II (10\u00a0nmol\u00a0L<jats:sup>\u22121<\/jats:sup> to 10\u00a0\u00b5mol\u00a0L<jats:sup>\u22121<\/jats:sup>) induced a significantly (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b705) smaller rise in [Ca<jats:sup>2+<\/jats:sup>l<jats:sub>i<\/jats:sub> response in cells derived from incompetent or varicose segments (\u223c70\u00a0nmol\u00a0L<jats:sup>\u22121<\/jats:sup>) than in cells derived from clinically healthy vein (\u223c130\u00a0nmol\u00a0L<jats:sup>\u22121<\/jats:sup>) or controls (\u223c170\u00a0nmol\u00a0L<jats:sup>\u22121<\/jats:sup>). Likewise, the effect of endothelin\u20101 (100\u00a0nmol\u00a0L<jats:sup>\u22121<\/jats:sup>) on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> was considerably less in cells derived from segments with incompetent valves or from varicose vessel segments than in cells derived from control patients (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b705). In organ baths, endothelium\u2010denuded strips of varicose vessels contracted significantly less in response to these agonists than clinically healthy segments from the same patient.<\/jats:p><jats:p><jats:bold>Conclusions\u2002<\/jats:bold> The reduced contractility of diseased human varicose veins in response to angiotensin II and endothelin\u20101 involves impaired Ca<jats:sup>2+<\/jats:sup> mobilization.<\/jats:p>","DOI":"10.1046\/j.1365-2362.2002.01023.x","type":"journal-article","created":{"date-parts":[[2003,3,11]],"date-time":"2003-03-11T15:55:32Z","timestamp":1047398132000},"page":"649-656","source":"Crossref","is-referenced-by-count":9,"title":["Ca<sup>2+<\/sup> mobilization in saphenous vein smooth muscle cells derived from patients with primary 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