Abstract
BackgroundDifferent from current cognition, our study demonstrated that adrenergic receptors agonist phenylephrine significantly relaxed isolated pulmonary artery but constricted pulmonary veins. Through comparing differences in the effects of commonly used vasoactive drugs on pulmonary artery and veins, the study aimed to improve efficiency and accuracy of isolated pulmonary vascular experiments, and to provide experimental basis for clinical drug use.MethodsThe contractile responses of pulmonary arteries and veins from twelve-week-old Male Sprague-Dawley rats to phenylephrine, arginine vasopressin (AVP), U46619, endothelin-1, and potassium chloride (KCl) were recorded, as well as the relaxation in response to phenylephrine, AVP, acetylcholine. To further explore the mechanism, some vessels was also pre-incubated with adrenergic receptors antagonists propranolol, prazosin and nitric oxide synthesis inhibitor N[gamma]-nitro-L-arginine methyl ester (L-NAME) before addition of the experimental drugs.ResultsPhenylephrine constricted pulmonary veins directly, but constricted pulmonary artery only after incubation with propranolol or/and L-NAME. The pulmonary artery exhibited significant relaxation to AVP with or without L-NAME incubation. AVP more clearly constricted the veins after incubation with L-NAME. Changes in vascular tension also varied from pulmonary artery to veins for KCl stimulation. Different from phenomena presented in veins, acetylcholine did not relax pulmonary artery preconstricted by KCl, U46619, and endothelin-1.ConclusionsAccording to the results, phenylephrine, KCl, AVP, and acetylcholine could be used to distinguish pulmonary arteries and pulmonary veins in vitro. This also suggested that the pulmonary arteries and pulmonary veins have great differences in physiology and drug reactivity.
Highlights
Different from current cognition, our study demonstrated that adrenergic receptors agonist phenyle‐ phrine significantly relaxed isolated pulmonary artery but constricted pulmonary veins
Does phenylephrine inhibit pulmonary artery contraction and even produce a relaxation effect by activating β-receptors? what role does nitric oxide (NO), the active component of endothelium-derived relaxing factor (EDRF), play? At the same time, our experiments revealed that phenylephrine clearly resulted in contraction of the pulmonary veins, suggesting that there is a significant difference in vascular reactivity to phenylephrine between the pulmonary arteries and veins
Our study demonstrated that pulmonary artery and pulmonary veins could be distinguished by different responses to common drugs (i.e., Potassium chloride (KCl), phenylephrine, and acetylcholine), which improves the efficiency and accuracy of relevant in vitro experiments
Summary
Different from current cognition, our study demonstrated that adrenergic receptors agonist phenyle‐ phrine significantly relaxed isolated pulmonary artery but constricted pulmonary veins. Through comparing differ‐ ences in the effects of commonly used vasoactive drugs on pulmonary artery and veins, the study aimed to improve efficiency and accuracy of isolated pulmonary vascular experiments, and to provide experimental basis for clinical drug use. The pulmonary artery is the resistance vessel of the right ventricular outflow tract. It is commonly used in vascular tension experiments investigating the pathogenesis and treatment of pulmonary hypertension. Stimulation of an isolated rat pulmonary artery using phenylephrine did not produce a contractile response, but significantly increased the vascular tone of the pulmonary vein. Based on inconsistent results reported in the literature, we questioned the differences in the contractile effects of phenylephrine on the pulmonary artery and veins, and the potential effector mechanisms
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