Evidence for Cholinergic Regulation of Microvessel Hydraulic Conductance During Tissue Hypoxia

• Published in: Circulation research Vol. 66; no. 2; pp. 517 - 524
• Main Authors: Tucker, Vicky L, Huxley, Virginia H
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD American Heart Association, Inc 01-02-1990; Lippincott
• Subjects: Acetylcholine - pharmacology; Animals; Atropine - pharmacology; Biological and medical sciences; Body Water - metabolism; Capillaries - metabolism; Fundamental and applied biological sciences. Psychology; Hypoxia - metabolism; Hypoxia - physiopathology; Intestine. Mesentery; Parasympathetic Nervous System - physiopathology; Rana pipiens; Time Factors; Vascular Resistance; Vertebrates: digestive system; Nervous control; Digestive system; Frog; Gut; Amphibia; Salientia; Hydraulic conductivity; Mesentery; Cholinergic pathway; Microcirculation; Vertebrata; Blood vessel; Hypoxia; Circulatory system
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.RES.66.2.517

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 Ringerʼs solution containing 10 mg/ml albumin and human erythrocytes while the mesentery was continuously superfused with frog Ringerʼs solution (15° 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 (Lp), perfusion with 1,μM acetylcholine increased Lp by 4.6±1.0-fold (mean+SEM, n=6). The response to acetylcholine was antagonized by the addition of 10±m atropine to the perfusate (Lp/Lp°=1.8±0.4). Perfusion with atropine alone reduced Lp in three of six capillaries (Lp/Lp°=0.56±0.04); Lp in the remaining three vessels was unaffected. Tissue hypoxia was simulated by exposing the mesentery to deoxygenated superfusate (PO2≤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 + 07-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±16-fold (n=4) in vessels simultaneously exposed to deoxygenated perfusate. We conclude that cholinergic stimulation elevates Lp in frog mesenteric capillaries and that enhanced water conductivity during tissue but not intraluminal hypoxia involves a cholinergic-muscarinic mechanism.