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NK 2 receptors mediate plasma extravasation in guinea‐pig lower airways
Author(s) -
Tousignant Christine,
Chan ChiChung,
Guevremont Diane,
Brideau Christine,
Hale Jeffrey J.,
MacCoss Malcolm,
Rodger Ian W.
Publication year - 1993
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1993.tb12813.x
Subject(s) - extravasation , guinea pig , receptor , chemistry , medicine , biology , pathology , endocrinology
1 Neurokinin (NK) receptor‐mediated extravasation has been examined in guinea‐pig airways by use of a recently described marker for microvascular protein leakage, 125 I‐labelled human fibrinogen. 2 Neurokinin A (NKA) caused a dose‐dependent increase in plasma [ 125 I]‐fibrinogen extravasation in trachea, main bronchi, secondary bronchi and intraparenchymal airways. In contrast, the NK 2 selective agonist [β‐Ala 8 ]NKA(4–10) only caused extravasation in the secondary and intraparenchymal airways. 3 The NK 2 selective antagonist, SR 48968, caused a dose‐dependent inhibition of NKA and [β‐Ala 8 ]NKA(4–10)‐induced extravasation of fibrinogen in guinea‐pig secondary bronchi and intraparenchymal airways. SR 48968 was without effect on the NKA‐induced extravasation in trachea and main bronchi. 4 NKA‐ or [β‐Ala 8 ]NKA(4–10)‐induced plasma extravasation was not modified by pretreatment with histamine H 1 ‐ or H 2 ‐receptor antagonists. 5 It is concluded that NK 2 receptors mediate plasma [ 125 I]‐fibrinogen extravasation in guinea‐pig secondary bronchi and intraparenchymal airways. This effect is direct and does not depend upon histamine released from mast cells.