vasoactive-intestinal-peptide has been researched along with 3-7-dimethyl-1-propargylxanthine* in 2 studies
2 other study(ies) available for vasoactive-intestinal-peptide and 3-7-dimethyl-1-propargylxanthine
| Article | Year |
|---|---|
Synergism between A(2A)-adenosine receptor activation and vasoactive intestinal peptide to facilitate [3H]-acetylcholine release from the rat motor nerve terminals.
The effect of vasoactive intestinal peptide (VIP) on evoked [(3)H]-acetylcholine ([(3)H]-ACh) release from motor nerve terminals, and its interaction with presynaptic facilitatory A(2A)-adenosine receptors was investigated in the rat phrenic nerve-hemidiaphragms. Facilitation of [(3)H]-ACh release by VIP (100 nM) only becomes apparent when high frequency (50 Hz) or long lasting pulses (1 ms) were delivered to the phrenic nerve; VIP excitation was prevented by removal of endogenous adenosine tonus, with adenosine deaminase (2.5 units/ml) or with the A(2A)-receptor antagonist, 3,7-dimethyl-1-propargyl xanthine, (10 microM). Pretreatment with the selective A(2A)-receptor agonist, CGS 21680C (2 nM), potentiated the neurofacilitatory action of VIP (100 nM). The results suggest that tonic A(2A)-receptors activation by endogenous adenosine is required to trigger the facilitatory action of VIP on evoked [(3)H]-ACh release from motor nerve endings. Topics: Acetylcholine; Adenosine; Adenosine Deaminase; Animals; Antihypertensive Agents; Diaphragm; Drug Synergism; Female; Male; Motor Neurons; Phenethylamines; Phrenic Nerve; Presynaptic Terminals; Purinergic P1 Receptor Antagonists; Rats; Rats, Wistar; Receptor, Adenosine A2A; Receptors, Purinergic P1; Synaptic Transmission; Theobromine; Tritium; Vasoactive Intestinal Peptide | 2001 |
Synergism between low-dose nicorandil and neuropeptides on adenosine-induced vasodepression in rats.
We hypothesized that the effect of nicorandil may be enhanced by interaction with naturally occurring vasodilators. To clarify this hypothesis, the effects of low-dose nicorandil alone and in combination with low doses of vasoactive intestinal polypeptide (VIP) or calcitonin gene-related peptide (CGRP) on adenosine-induced vasodepression were studied in rats. Intravenous (i.v.) bolus injections of adenosine (3-100 microg kg(-1)) elicited dose-dependent decreases in blood pressure, accompanied by slight decreases (except for 100 microg kg(-1)) in heart rate. Simultaneous i.v. infusion of either nicorandil (1 microg kg(-1) min(-1)) and VIP (0.003 microg kg(-1) min(-1)) or CGRP (0.1 ng kg(-1) min(-1)) significantly enhanced the adenosine-induced vasodepression, although each agent alone in the dose used had no effects on vasodepressor responses to adenosine. The potentiation of the effect of adenosine was not observed in the presence of 3,7-dimethyl-1-propargylxanthine (DMPX) (1 mg kg(-1), i.v.) or glibenclamide (20 mg kg(-1), i.v.). The present results suggest that low-dose nicorandil modifies the response to adenosine in interaction with low levels of endogenous neuropeptides such as VIP and CGRP, and that the reciprocal interaction is mediated partly through K(ATP) channel activation in vascular smooth muscle. Topics: Adenosine; Animals; Dose-Response Relationship, Drug; Drug Synergism; Glyburide; Male; Neuropeptides; Nicorandil; Rats; Rats, Sprague-Dawley; Theobromine; Vasoactive Intestinal Peptide; Vasodilator Agents | 1998 |