Cat Tracheal Muscle Research Articles

A comparative study with impromidine (SKF 92676), a potent agonist for histamine H2-receptors

Histamine, dimaprit and impromidine caused a relaxation on the isolated cat tracheal muscle contracted by acetylcholine or serotonin. Mepyramine partially inhibited the relaxing effect of histamine without altering that of impromidine and dimaprit. Both impromidine and dimaprit produced a dose-dependent fall in perfusion pressure of the isolated perfused guinea-pig lung while histamine has a pressor effect in this preparation which reversed into a depressor one in the presence of mepyramine. Both dimaprit and impromidine also produced a fall in perfusion pressure and urine flow of the isolated perfused rabbit kidney. A rapid tachyphylaxis developed to the effect of impromidine in the kidney but not to dimaprit. A cross-tachyphylaxis was also observed between impromidine and dimaprit. The agonistic potency of impromidine was found to be very much higher than histamine and dimaprit. Metiamide has a competitive inhibitory effect against impromidine and dimaprit on the isolated perfused lung, kidney and tracheal muscle. It was concluded that impromidine is a very potent pure histamine H2-receptor agonist when compared with histamine and dimaprit on the investigated tissues.

The effects of angiotensin I and angiotensin II on the isolated tracheal muscle of the cat.

The effects of Asp1-beta-amide-Val5-angiotensin II (A II) and Asp1-Ile5-angiotensin I (A I) have been studied on the isolated continuously superfused cat tracheal muscle contracted by 5-hydroxytryptamine (5-HT). Both peptides have been shown to induce dose-dependent relaxation on this muscle. Similar effects have been obtained with synthetic bradykinin, prostaglandin E2 (PGE2), noradrenaline and histamine. The effects of bradykinin, A I and A II have been shown to be inhibited by aspirin but not by propranolol, metiamide, SC 19220 or a specific, competitive antagonist of A II. The relaxing effect of A I is not due to the conversion of decapeptide to octapeptide A II. The possible mechanism of the relaxing effects of A I and A II on the cat isolated tracheal muscle is discussed.

Release of prostaglandin-like material from isolated cat tracheal muscle by electrical and mechanical stimulation.

Release of PGE-like material has been studied on the isolated continuously-superfused cat tracheal muscle using dynamic bioassay methods. The effluent of transmural electrically-stimulated cat tracheal muscle induced a contraction when superfused over the rat stomach fundus strip. This response did not alter with atropine, methysergide, phentolamine and propranolol but was inhibited by aspirin and Sc 19220. The same myotropic activity in the effluent was found when trachea was mechanically stimulated by an additional increase in tension. The effluent from mechanically- and electrically-stimulated tracheal muscle caused a definite relaxation when superfused over a second cat tracheal muscle contracted by serotonin and pretreated with propranolol. Electrically-stimulated cat trachea itself gave a relaxant response which was blocked by propranolol but potentiated by aspirin. From these results it was concluded that both electrical and mechanical stimulation can elicit a release of PGE-like material from isolated cat tracheal muscle.

THE INHIBITORY ACTIONS OF PROSTAGLANDINS ON RESPIRATORY SMOOTH MUSCLE.

Prostaglandin E(1), in concentrations as low as 1 ng/ml., relaxed isolated tracheal muscle from cat, monkey, rabbit, guinea-pig and ferret. Tracheal muscle from the cat, monkey and rabbit did not exhibit inherent tone and the effect of prostaglandin E(1) on these preparations was seen only after a sustained contraction had been produced by a previous dose of acetylcholine or of another agonist. Prostaglandins E(2), E(3) and F(1alpha) also relaxed isolated cat tracheal muscle which had been stimulated by acetylcholine: their activities relative to that of prostaglandin E(1) were, respectively, 1.0, 0.2 and 0.002. In the anaesthetized cat prostaglandin E(1) increased lung "resistance to inflation" (presumably comparable to bronchial resistance) and the heart rate. In the anaesthetized rabbit and guinea-pig, prostaglandin E(1) antagonized the rise in resistance to inflation of the lungs obtained after vagal stimulation or after the intravenous injection of histamine; it sometimes lowered the resistance to inflation in these species. The possibility that prostaglandin may have a local physiological role in the control of bronchial smooth muscle tone is discussed.