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Phasic contractions responsible for an NO‐dependent relaxation in rat thoracic duct
Author(s) -
Gasheva Olga Y.,
Gashev Anatoliy A.,
Zawieja David C.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a280-a
Subject(s) - chemistry , lymphatic system , thoracic duct , anatomy , shear stress , lymph , diastole , basal (medicine) , isometric exercise , medicine , biophysics , cardiology , materials science , blood pressure , biology , pathology , composite material , insulin
Wall shear stress may be generated in lymphatics by their active contractions as well as by the actions of the passive lymph driving forces. We tested the hypothesis that wall shear stress, generated by active contractions of lymphatics, plays an important role in the regulation of their tone. The diastolic diameters of isolated, cannulated and pressurized rat thoracic ducts (TD) were measured in spontaneously active vs. phasically non‐active segments and compared to the passive diameters. Both actively contracting and non‐contracting segments were treated with L‐NAME (10 −4 M) and Indomethacin (10 −5 M). We found that diastolic diameter in spontaneously contracting TD segments was ~94% at all tested levels of intravascular pressure (from 1 to 5 cm H 2 O). In non‐phasically contracting TD segments (without wall shear stress) lymphatic diastolic diameters were significantly lower (~88%), which corresponds to an approximate doubling in basal lymphatic tone. When L‐NAME was added, the shear‐dependent relaxation caused by phasic contractions was completely abolished ‐ diastolic diameter decreased to its level in segments without phasic contractions. Indomethacin did not influence this flow‐dependent relaxation. We concluded that wall shear stress, induced by active contractions in TD, causes a significant reduction in basal tone associated with the release of nitric oxide, but not prostaglandins. NIH HL‐070308