title: Effects of vasoconstrictive and vasodilative agents on lymphatic smooth muscles in isolated canine thoracic ducts.
abstract: A study was made of the isometric responses of isolated canine thoracic ducts to several physiological vasoactive substances. Contractions of the lymphatic smooth muscles were induced by epinephrine, norepinephrine, 5-hydroxytryptamine, histamine (HIS) and prostaglandin F2 alpha in a dose-dependent manner. The decreasing order of potency in the contractile responses was as follows: epinephrine greater than norepinephrine greater than 5-hydroxytryptamine much greater than HIS not equal to prostaglandin F2 alpha. There were no significant regional differences in the responses to vasoconstrictive agents. Phenylephrine, xylazine and clonidine caused a dose-dependent contraction in the lymphatic preparations. Prazosin (10(-8) to 10(-7) M) inhibited the phenylephrine-induced vasoconstriction in a competitive manner. Xylazine-induced responses were inhibited competitively by yohimbine (10(-8) to 10(-7) M). These results suggest that both alpha-1 and alpha-2 adrenoceptors are located on the lymphatic smooth muscles of canine thoracic ducts. On the other hand, acetylcholine, isoproterenol, HIS, adenosine and ATP caused dose-dependent relaxations in canine thoracic ducts precontracted by 10(-5) M norepinephrine. The decreasing order of potency in the relaxant responses was as follows: acetylcholine much greater than isoproterenol much greater than adenosine not equal to HIS not equal to ATP. There were no significant regional differences in the relaxant responses to the agents. Procaterol, salbutamol, dobutamine and denopamine caused a dose-dependent relaxation of isolated canine thoracic ducts. Propranolol (10(-9) to 10(-8) M) inhibited procaterol- and dobutamine-induced vasorelaxations in a competitive manner. Metoprolol (10(-8) to 10(-7) M) inhibited only the dobutamine-induced vasorelaxation, but did not significantly influence the procaterol-induced response.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: 1st Department of Physiology, Shinshu University School of Medicine, Matsumoto, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Takahashi
authors.forename: Y
authors.initials: Y
authors.lastname: Kawai
authors.forename: T
authors.initials: T
authors.lastname: Ohhashi
mesh_terms: D000818:Animals; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects* / Q000502:physiology; D011942:Receptors, Adrenergic, alpha / Q000032:analysis; D011943:Receptors, Adrenergic, beta / Q000032:analysis; D013897:Thoracic Duct / Q000187:drug effects* / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents