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Ca 2+ mobilization in saphenous vein smooth muscle cells derived from patients with primary varicosity
Author(s) -
SchullerPetrovic S.,
Stessel H.,
Brunner F.
Publication year - 2002
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.2002.01023.x
Subject(s) - varicose veins , medicine , great saphenous vein , vein , anatomy , long saphenous vein , vascular smooth muscle , smooth muscle , endocrinology , cardiology , surgery
Background Human primary varicosity is associated with ‘weakness’ of the vein wall. We investigated whether the reduced responsiveness of varicose veins to physiological vasoconstrictors might result from impaired Ca 2+ mobilization in venous smooth muscle. Materials and methods 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 2+ levels ([Ca 2+ ] i ) were determined with the fura‐2 method in cultured medial smooth muscle cells of third to sixth passage (21–23 measurements per tissue derived from five controls and seven patients). Results Angiotensin II (10 nmol L −1 to 10 µmol L −1 ) induced a significantly ( P < 0·05) smaller rise in [Ca 2+ l i response in cells derived from incompetent or varicose segments (∼70 nmol L −1 ) than in cells derived from clinically healthy vein (∼130 nmol L −1 ) or controls (∼170 nmol L −1 ). Likewise, the effect of endothelin‐1 (100 nmol L −1 ) on [Ca 2+ ] i was considerably less in cells derived from segments with incompetent valves or from varicose vessel segments than in cells derived from control patients ( P < 0·05). In organ baths, endothelium‐denuded strips of varicose vessels contracted significantly less in response to these agonists than clinically healthy segments from the same patient. Conclusions The reduced contractility of diseased human varicose veins in response to angiotensin II and endothelin‐1 involves impaired Ca 2+ mobilization.