CHOLINESTERASE ACTIVITY IN HUMAN PULMONARY-ARTERIES AND VEINS

1 Human isolated pulmonary vessels were treated with cholinesterase (C hE) inhibitors to determine the role of these enzymes in regulating va scular muscle tone. In addition, kinetic parameters were determined fo r acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) in huma n pulmonary vessel homogenates. 2 Carbachol (CCh) and acetylcholine (A Ch) were equipotent contractile agonists in human pulmonary arteries ( pD(2) values, 5.28+/-0.05 and 5.65+/-0.16; E-max, 0.91+/-0.26 and 0.98 +/-0.30 g wt. for CCh and ACh, respectively; n = 7). In venous prepara tions, ACh was ineffective and CCh induced small contractions (E-max, 0.08+/-0.04 g wt.; n = 13). 3 In human pulmonary arteries following pr etreatment with tetraisopropylpyrophosphoramide (iso-OMPA, 100 mu M), an increased sensitivity to the contractile agonist ACh was observed ( pD(2) values, 5.80+/-0.13 and 6.37+/-0.19 for control and treated prep arations, respectively; n = 5). This pretreatment had no effect on the CCh concentration response curve. In contrast, human pulmonary veins pretreated with iso-OMPA failed to elicit a contractile response to AC h. 4 Neither Iso-OMPA nor neostigmine elicited concentration-dt penden t contractions in human isolated pulmonary arteries or veins. These re sults suggest the absence of sufficient spontaneous release of ACh to modulate human pulmonary vessel basal tone. 5 CCh was less potent than ACh in relaxing precontracted human isolated pulmonary arteries (pD(2 ) value, CCh: 6.55+/-0.15 and ACh: 7.16+/-0.13, n = 4) and veins (pD(2 ) value, CCh: 4.95+/-0.13; n = 5 and ACh: 5.56+/-0.17; n = 6). Pretrea tment of vessels with either iso-OMPA or neostigmine did not modify AC h relaxant responses in either type of preparation. 6 In human pulmona ry veins, the ChE activity was two fold greater than in arteries (n = 6). V-max for AChE was 1.73+/-0.24 and 3.36+/-0.26 min mg(-1) protein in arteries and veins, respectively, whereas V-m for BChE was 1.83+/-0 .22 and 4.71+/-0.17 min mg(-1) protein, in these respectively. 7 In hu man pulmonary arteries, BChE activity may play a role in the smooth mu scle contraction but not on the smooth muscle endothelium-dependent re laxation induced by ACh. A role for ChE activity in the control of ven ous tone is presently difficult to observe, even though this tissue co ntains a greater amount of enzyme than the artery.