Muscarinic agonists and antagonists cause vasodilation in isolated rat lung
| العنوان: | Muscarinic agonists and antagonists cause vasodilation in isolated rat lung |
|---|---|
| المؤلفون: | P. S. Wilson, P. L. Khimenko, J. W. Barnard, Aubrey E. Taylor, Timothy Moore |
| المصدر: | Journal of Applied Physiology. 78:1404-1411 |
| بيانات النشر: | American Physiological Society, 1995. |
| سنة النشر: | 1995 |
| مصطلحات موضوعية: | Male, Pulmonary Circulation, medicine.medical_specialty, Vascular smooth muscle, Physiology, Bronchoconstriction, Blood Pressure, Vasodilation, Muscarinic Antagonists, In Vitro Techniques, Muscarinic Agonists, Thromboxane A2, Physiology (medical), Internal medicine, Muscarinic acetylcholine receptor, medicine, Animals, Lung, business.industry, Muscarinic acetylcholine receptor M3, Muscarinic acetylcholine receptor M2, Muscarinic acetylcholine receptor M1, Receptors, Muscarinic, Pirenzepine, Acetylcholine, Prostaglandin Endoperoxides, Synthetic, Rats, Perfusion, Endocrinology, 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid, Vascular Resistance, business, medicine.drug |
| الوصف: | The present study investigated the ability of atropine and different muscarinic receptor subtypes to affect acetylcholine (ACh)-induced bronchoconstriction and vasodilation in the isolated rat lung model. ACh (10(-7) M) given after U-46619 decreased total (RT), precapillary, and postcapillary vascular resistances and increased peak airway pressure. Atropine (20 microM) decreased RT and precapillary and postcapillary vascular resistances and blocked ACh-induced increases in peak airway pressure. The M1-selective agonist McN-A-343 (1.3 x 10(-5) M) decreased RT from 40.27 +/- 2.98 to 29.20 +/- 2.81 cmH2O.l–1.min-100 g lung wt (P = 0.01), and ACh caused no further dilation. The M1-selective antagonist pirenzepine (1.6 x 10(-6) M) blocked ACh-induced vasodilation. The M2-selective antagonist gallamine (7.5 x 10(-7) M) decreased RT from 45.50 +/- 3.19 to 34.86 +/- 1.25 cmH2O.l–1.min.100 g lung wt (P < 0.05), and after gallamine, ACh further decreased RT to 28.59 +/- 1.75 cmH2O.l–1.min.100 g lung wt (P < 0.01). Neither the selective muscarinic agonists nor antagonists affected peak airway pressures. We conclude that ACh-induced vasodilation in isolated rat lungs preconstricted with U-46619 is mediated by M1 receptors. Atropine-induced vasodilation in this model is mediated through the inhibition of the M2 receptor. We postulate that this represents either a blockade of postganglionic receptors, permitting release of vasodilator substances from local nerve terminals, or a direct vasodilatory effect on the vascular smooth muscle. |
| تدمد: | 1522-1601 8750-7587 |
| DOI: | 10.1152/jappl.1995.78.4.1404 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d490c16f408627659884f4ac2763b42a https://doi.org/10.1152/jappl.1995.78.4.1404 |
| رقم الانضمام: | edsair.doi.dedup.....d490c16f408627659884f4ac2763b42a |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15221601 87507587 |
|---|---|
| DOI: | 10.1152/jappl.1995.78.4.1404 |