Varicose disease affects the P2 receptor-mediated responses of human greater saphenous vein.
The aim of the present study was to investigate in vitro the differences in P2 receptor mediated responses of human greater saphenous vein (GSV) taken from patients with varicose disease and obliterating atherosclerosis. Samples of the inguinal part of the GSV were taken from the patients who underwent phlebectomia operation due to varicose disease (n=9, VD group) or femoropoplitea bypass operation using auto-vein due to obliterating atherosclerosis of lower extremities (n=11, OA group). The mechanical responses of the isolated segments of GSV to P2 receptor agonists were tested using standard organ-bath technique. ATP (10(-6)-10(-4) M), ADP (10(-6)-10(-4) M) and alpha,betamethyleneATP (10(-8)-10(-5) M) caused concentration-dependent contractions of the veins of both groups, the latter agonist being approximately tenfold more active than first two. ATP at all concentrations tested, alpha,betamethyleneATP at concentrations of 10(-6) and 10(-5) M and ADP at a concentration of 10(-6) M produced significantly higher contractions of the GSV taken from OA group than from VD group. UTP (10(-6)-10(-4) M) caused concentration-dependent contractions of the veins taken from OA group, while in VD group this agonist was virtually without effect. Adenosine (10(-6)-10(-4) M) and 2-methylthio-ATP (10(-7)-10(-5) M) had no significant contractile activity in this tissue in both groups. It is concluded from this study that there are P2 receptor and adrenoceptor mediated contractions in human greater saphenous veins, which are impaired by varicose disease, in contrast to contractions produced by histamine and carbachol which are, if anything, enhanced.
Ziganshin
Airat U
AU
Department of Pharmacology, Kazan State Medical University, 49 Butlerov Street, Kazan 420012, Russia. airatziganshin@yahoo.co.uk
Khaziakhmetov
Daniyar F
DF
Ziganshina
Lilia E
LE
Khaziakhmetova
Veronika N
VN
Jourjikiya
Roen K
RK
Ziganshin
Bulat A
BA
Giniyatova
Lucia R
LR
Burnstock
Geoffrey
G
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000494:pharmacology; D000328:Adult; D000818:Animals; D001162:Arteriosclerosis Obliterans / Q000473:pathology / Q000503:physiopathology / Q000601:surgery; D002217:Carbachol / Q000494:pharmacology; D002908:Chronic Disease; D004305:Dose-Response Relationship, Drug; D005260:Female; D006632:Histamine / Q000494:pharmacology; D006801:Humans; D007866:Leg / Q000098:blood supply / Q000503:physiopathology / Q000601:surgery; D008297:Male; D008875:Middle Aged; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology; D058910:Purinergic P2 Receptor Agonists; D018048:Receptors, Purinergic P2 / Q000502:physiology*; D012501:Saphenous Vein / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D014544:Uridine Triphosphate / Q000494:pharmacology; D014648:Varicose Veins / Q000473:pathology / Q000503:physiopathology* / Q000601:surgery
D058910:Purinergic P2 Receptor Agonists; D018048:Receptors, Purinergic P2; D000244:Adenosine Diphosphate; D006632:Histamine; D000255:Adenosine Triphosphate; D002217:Carbachol; D014544:Uridine Triphosphate; D009638:Norepinephrine