Article date: October 1993
By: A. Robichaud, C. Saunier, M.C. Michoud, P. Souich, in Volume 110, Issue 2, pages 804-808
The aim of the present work was to investigate under which circumstances atrial natriuretic peptide (ANP) modulates airway resistance.
Of the six groups of rabbits (n = 5) studied, three received an infusion of ANP (80 ng min−1 kg−1 i.v.) for a period of 100 min, while the other three were infused with the vehicle. Before receiving the infusion of ANP or the vehicle, the animals were pretreated with atropine (0.5 mg kg−1 i.v.), propranolol (2 mg kg−1 i.v.) or not pretreated. After 75 min of infusion of ANP, bronchoconstriction was induced by inhalation of histamine. Respiratory resistance (Rrs) was measured before and 3, 5, 10, 15 and 20 min post‐histamine challenge.
Following 75 min of ANP infusion, plasma ANP concentration increased from 153 ± 52 (mean ± s.e.mean) to 1441 ± 203 pg ml−1 (P < 0.05) without affecting baseline Rrs. Control Rrs values (12.5–20.4 cmH2O l−1 s) were significantly increased following the inhalation of histamine (P < 0.001). By themselves, atropine, propranolol or ANP did not modify the histamine‐induced increase in Rrs. However, when the animals were pretreated with atropine, ANP infusion significantly reduced the increase in Rrs induced by histamine (30 ± 2 vs 51 ± 6 cmH2O l−1 s; P < 0.05).
These data suggest that ANP has an indirect modulating effect on the airway smooth muscle and will decrease Rrs when muscarinic receptors are blocked.
The aim of the present work was to investigate under which circumstances atrial natriuretic peptide (ANP) modulates airway resistance.
Of the six groups of rabbits (n = 5) studied, three received an infusion of ANP (80 ng min−1 kg−1 i.v.) for a period of 100 min, while the other three were infused with the vehicle. Before receiving the infusion of ANP or the vehicle, the animals were pretreated with atropine (0.5 mg kg−1 i.v.), propranolol (2 mg kg−1 i.v.) or not pretreated. After 75 min of infusion of ANP, bronchoconstriction was induced by inhalation of histamine. Respiratory resistance (Rrs) was measured before and 3, 5, 10, 15 and 20 min post‐histamine challenge.
Following 75 min of ANP infusion, plasma ANP concentration increased from 153 ± 52 (mean ± s.e.mean) to 1441 ± 203 pg ml−1 (P < 0.05) without affecting baseline Rrs. Control Rrs values (12.5–20.4 cmH2O l−1 s) were significantly increased following the inhalation of histamine (P < 0.001). By themselves, atropine, propranolol or ANP did not modify the histamine‐induced increase in Rrs. However, when the animals were pretreated with atropine, ANP infusion significantly reduced the increase in Rrs induced by histamine (30 ± 2 vs 51 ± 6 cmH2O l−1 s; P < 0.05).
These data suggest that ANP has an indirect modulating effect on the airway smooth muscle and will decrease Rrs when muscarinic receptors are blocked.
DOI: 10.1111/j.1476-5381.1993.tb13883.x
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