The effects of histamine and dimaprit on intestinal smooth muscle contractility were investigated on isolated cells from longitudinal muscle of the guinea pig ileum. Both histamine (10(-14)-10(-10) M) and dimaprit (10(-13)-10(-10) M) exerted a concentration-dependent contraction of intestinal cells, causing a maximum decrease in cell length of about 20%. This effect was not significantly different from that induced by cholecystokinin-octapeptide (CCK-8) 10(-9) M. The concentration-response curves to histamine and dimaprit were shifted to the left in the presence of the histamine H-2-receptor antagonist famotidine (10(-7) M) indicating the occurrence in the smooth muscle of H-2 receptors mediating relaxation. Whereas the contraction produced by histamine was competitively antagonized by the HI receptor antagonist mepyramine (10(-8) M), neither mepyramine (10(-7) M) nor temelastine (10(-7) M) did modify the contractile effect of dimaprit. In contrast, atropine (10(-8) M) significantly depressed the maximum response to dimaprit without affecting that exerted by histamine. These data indicate that histamine and dimaprit can modify intestinal contractility, by acting via different mechanisms; while the contractile action of histamine is related to H-1 receptor activation, that produced by dimaprit involves cholinergic pathways.

Different mechanisms are responsible for the contractile effects of histaminergic compounds on isolated intestinal smooth muscle cells / G., Bertaccini; Morini, Giuseppina; G., Coruzzi. - In: JOURNAL OF PHYSIOLOGY. - ISSN 0928-4257. - 91:3-5(1997), pp. 199-202. [10.1016/S0928-4257(97)89484-3]

Different mechanisms are responsible for the contractile effects of histaminergic compounds on isolated intestinal smooth muscle cells

MORINI, Giuseppina;
1997-01-01

Abstract

The effects of histamine and dimaprit on intestinal smooth muscle contractility were investigated on isolated cells from longitudinal muscle of the guinea pig ileum. Both histamine (10(-14)-10(-10) M) and dimaprit (10(-13)-10(-10) M) exerted a concentration-dependent contraction of intestinal cells, causing a maximum decrease in cell length of about 20%. This effect was not significantly different from that induced by cholecystokinin-octapeptide (CCK-8) 10(-9) M. The concentration-response curves to histamine and dimaprit were shifted to the left in the presence of the histamine H-2-receptor antagonist famotidine (10(-7) M) indicating the occurrence in the smooth muscle of H-2 receptors mediating relaxation. Whereas the contraction produced by histamine was competitively antagonized by the HI receptor antagonist mepyramine (10(-8) M), neither mepyramine (10(-7) M) nor temelastine (10(-7) M) did modify the contractile effect of dimaprit. In contrast, atropine (10(-8) M) significantly depressed the maximum response to dimaprit without affecting that exerted by histamine. These data indicate that histamine and dimaprit can modify intestinal contractility, by acting via different mechanisms; while the contractile action of histamine is related to H-1 receptor activation, that produced by dimaprit involves cholinergic pathways.
1997
Different mechanisms are responsible for the contractile effects of histaminergic compounds on isolated intestinal smooth muscle cells / G., Bertaccini; Morini, Giuseppina; G., Coruzzi. - In: JOURNAL OF PHYSIOLOGY. - ISSN 0928-4257. - 91:3-5(1997), pp. 199-202. [10.1016/S0928-4257(97)89484-3]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11381/2636059
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