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Cholinergic regulation of single-vessel hydraulic conductivity (Lp) during normoxia and hypoxia was tested in single mesenteric vessels of pithed frogs (Rana pipiens). Capillaries were cannulated in situ and perfused with frog Ringer's solution containing 10 mg/ml albumin and human erythrocytes while the mesentery was continuously superfused with frog Ringer's solution (15 degrees C). Lp was first measured under normoxic (room air equilibrated) conditions by the modified Landis microocclusion method. Repeated measurements of filtration coefficient under control conditions, for periods up to 80 minutes, demonstrated that Lp did not change with time in normoxic vessels (n = 18). After initial control measurement (Lpo), perfusion with 1 microM acetylcholine increased Lp by 4.6 +/- 1.0-fold (mean +/- SEM, n = 6). The response to acetylcholine was antagonized by the addition of 10 microns atropine to the perfusate (Lp/Lpo = 1.8 +/- 0.4). Perfusion with atropine alone reduced Lp in three of six capillaries Lp/Lpo = 0.56 +/- 0.04); Lp in the remaining three vessels was unaffected. Tissue hypoxia was simulated by exposing the mesentery to deoxygenated superfusate Po2 less than or equal to 10 mm Hg) for 10-15 minutes. Tissue hypoxia had no effect on Lp in atropine-treated vessels (n = 8). Without atropine, tissue hypoxia increased Lp by 2.3 +/- 0.7-fold, whereas the addition of atropine completely antagonized this response (n = 5). In contrast to the inhibitory action of atropine during tissue hypoxia, Lp rose 5.2 +/- 1.6-fold (n = 4) in vessels simultaneously exposed to deoxygenated perfusate.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence for cholinergic regulation of microvessel hydraulic conductance during tissue hypoxia.