Autonomic and autacoid activity in antigen‐sensitized and control ovine pulmonary vein and artery
- 1 June 1982
- journal article
- Published by Wiley in Journal of Veterinary Pharmacology and Therapeutics
- Vol. 5 (2) , 137-144
- https://doi.org/10.1111/j.1365-2885.1982.tb00509.x
Abstract
Spirally cut strips of ovine pulmonary vein and artery were studied in isolated organ baths and their responses to selected autacoid and autonomic agents were compared. In addition blood vessels taken from horse plasma‐sensitized sheep were compared with their respective controls. Pulmonary vein and artery exhibited qualitative and quantitative differences in their autacoid and autonomic reactivity. Veins were more sensitive in responding with contractions to histamine (HIST) and carbachol (CARB) when compared with arteries. Responses of these vessels differed qualitatively to 5‐Hydroxytryptamine (5HT); phenylephrine (PE) and adrenaline (ADR): arteries responded with strong contraction and veins with relaxations. Isoproterenol (ISOP) effectively relaxed veins but was either without effect or produced 10%–15% relaxations of precontracted arterial strips. Phentolamine competitively antagonized ADR and PE‐induced contractile responses of arteries while on veins, ISOP and PE dose—response curves (DRCs) were shifted to the right in the presence of propranolol. Mepyramine inhibited venous and arterial responses to HIST.Comparisons between sensitized and non‐sensitized sheep vasculature revealed a significant (P < 0.05) decrease in the activity of spasmolytic agonists on veins, i.e. relaxant actions of 5HT, PE and ISOP were significantly impaired. In addition the activity of 5HT to contract pulmonary artery was significantly (P < 0.05) increased when compared with controls. Present investigation suggests: (i) the predominance of H1‐histaminergic receptors in ovine pulmonary vasculature; (ii) the preponderance of α and β‐adrenergic receptors in pulmonary artery and vein, respectively; (iii) that antigenic sensitization exaggerates the pathological state by causing a decrease in spasmolytic activity with a parallel increase in spasmogenic activity.Keywords
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