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Vasoactive intestinal polypeptide-sensitive cyclic adenosine monophosphate generating system in the rat portal vein
D Amenta1, L Iacopino, F Amenta
1Dipartimento di Scienze Neurologiche, Università La Sapienza, Roma, Italy.
Abstract:
The effect of vasoactive intestinal polypeptide (VIP) on the 3'-5'-cyclic adenosine monophosphate (cAMP) generating system in membrane particles of rat portal vein was studied. In the presence of 10 microM GTP, VIP increased the concentration of cAMP in a dose-dependent manner. The removal of endothelium had no effect on cAMP production elicited by VIP. alpha- and beta-adrenergic as well as muscarinic receptor blocking agents did not inhibit VIP-dependent cAMP increase. Also various peptides, structurally analogous to VIP or active on portal vein smooth muscle, had no effect on cAMP production elicited by VIP. The present data, combined with those reported in the literature of an active relaxation of portal vein smooth muscle by VIP, suggest the existence of functionally active VIP receptors coupled to the adenylate cyclase system in the rat portal vein.
Insights
Vasoactive intestinal polypeptide (VIP) increases cyclic adenosine monophosphate (cAMP) in rat portal vein smooth muscle. This suggests VIP receptors are linked to the cAMP system, contributing to muscle relaxation.
Area of Science:
- Pharmacology
- Molecular Biology
- Physiology
Background:
- Vasoactive intestinal polypeptide (VIP) is known to relax vascular smooth muscle.
- The intracellular mechanisms mediating VIP-induced relaxation, particularly in the rat portal vein, require further elucidation.
Purpose of the Study:
- To investigate the effect of VIP on the cyclic adenosine monophosphate (cAMP) generating system in rat portal vein membrane particles.
- To determine if VIP-induced cAMP production is modulated by the endothelium or other receptor systems.
Main Methods:
- Incubation of rat portal vein membrane particles with varying concentrations of VIP in the presence of GTP.
- Measurement of intracellular cAMP levels using established biochemical assays.
- Assessment of the influence of endothelial removal and receptor antagonists (alpha- and beta-adrenergic, muscarinic) on VIP-stimulated cAMP production.
Main Results:
- VIP significantly increased cAMP concentration in a dose-dependent manner in rat portal vein membrane particles.
- Endothelial removal did not affect VIP-induced cAMP production.
- VIP-dependent cAMP increase was not inhibited by alpha- and beta-adrenergic or muscarinic receptor blocking agents.
- Structurally similar peptides or those active on portal vein smooth muscle did not influence VIP-mediated cAMP production.
Conclusions:
- The findings strongly suggest the presence of functionally active VIP receptors coupled to the adenylate cyclase system in the rat portal vein.
- VIP-mediated cAMP generation in the portal vein is independent of the endothelium and classical adrenergic or muscarinic receptors.
- This mechanism likely contributes to the previously observed VIP-induced relaxation of rat portal vein smooth muscle.