Characterization of presynaptic vascular muscarinic receptors inhibiting endogenous noradrenaline overflow in the portal vein of the freely moving rat

Remie, R; Coppes, Rob; Roffel, Af; Zaagsma, Johan

doi:10.1111/j.1476-5381.1990.tb14684.x

Cited by 18 publications

(10 citation statements)

References 17 publications

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“…In the freely moving unanaesthetized rat, muscarinic agonists inhibit electrically evoked noradrenaline overflow (Remie et al, 1990). The rank order of reversal of inhibition by muscarinic antagonists was 4DAMP > AF-DX 116 > pirenzepine.…”

Section: Relaxant Responses-indirectmentioning

confidence: 92%

Heterogeneity of vascular muscarinic receptors

Eglen¹,

Whiting²

1990

Journal of Autonomic Pharmacology

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Muscarinic receptors mediate diverse effects on the vasculature. Recently, a consensus has been arrived at with regard to muscarinic receptor classification (Levine & Birdsall, 1989). As a result, it may now be possible to clarify the role of each subtype in the responses of vascular tissues to muscarinic agonists. It is apparent that vascular muscarinic receptors form a heterogeneous population. M1 receptors contract canine venous tissue, whilst M3 receptors contract porcine and bovine coronary arteries. M3 receptors also mediate EDRF-dependent relaxant responses in the majority of tissues studied to date. M2 receptors elicit relaxations by a decrease in sympathetic outflow in canine femoral vein, rabbit ear artery and rat portal vein. These conclusions are primarily derived from functional estimations of equilibrium dissociation constants, since comparable radioligand binding data are both scarce and contradictory. It is concluded that all three major subtypes of receptors are present in the vasculature. However, the limited selectivity of the available antagonists, the lack of extensive use of such compounds and the unavailability of selective agonists clearly indicate the need for more definitive studies to be undertaken.

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Section: Relaxant Responses-indirectmentioning

confidence: 92%

Heterogeneity of vascular muscarinic receptors

Eglen¹,

Whiting²

1990

Journal of Autonomic Pharmacology

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“…In addition to modulating acetylcholine release, muscarinic receptors can modulate the release of noradrenaline as well. M2-receptor activation inhibits noradrenaline release in rat stomach (Yokotani & Osumi, 1993), rat portal vein (Remie et al, 1990) canine saphenous vein (O'Rourke & Vanhoutte, 1987) and rabbit aorta (Habermeir-Muth, Altes, Forsyth & Muscholl, 1990). Acetylcholine also inhibits noradrenaline release in canine mesenteric artery, although the muscarinic receptor subtype was not characterized (Toda, Okunishi & Okamura, 1990).…”

Section: Introductionmentioning

confidence: 99%

Hypotensive effect of an M₂‐selective muscarinic antagonist in anaesthetized guinea‐pigs

Howell

Kovalsky

1995

Journal of Autonomic Pharmacology

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1. In order to determine an involvement of muscarinic M2 receptors in the regulation of systemic arterial blood pressure, we investigated the cardiovascular effects of the M2-selective antagonist methoctramine and other agents in anaesthetized guinea-pigs. 2. Intravenous injection of methoctramine, atropine, pirenzepine (an M1-selective muscarinic antagonist) or 4-DAMP (an M3-selective muscarinic antagonist) each significantly increased heart rate in comparison to vehicle controls. 3. Methoctramine produced significant, dose-dependent decreases in mean arterial blood pressure, with an ED50 of 0.1 mg kg-1. Atropine decreased blood pressure only at high doses. Pirenzepine and 4-DAMP did not alter blood pressure, indicating that M1 or M3 receptor antagonism was not responsible for the cardiovascular effects of methoctramine. 4. The hypotensive effect of methoctramine was unaltered by indomethacin pretreatment, ruling out an alteration in arachidonic acid metabolism as the mechanism of action. 5. In contrast to methoctramine, mecamylamine (a nicotinic ganglionic receptor antagonist) greatly decreased heart rate and slightly decreased blood pressure, suggesting that ganglionic blockade was not the mechanism for the cardiovascular effects of methoctramine. 6. Methoctramine (0.3 mg kg-1) pretreatment did not alter the hypertensive effect of intravenous noradrenaline, demonstrating that methoctramine did not directly inhibit vascular reactivity and indicating an indirect hypotensive of action of methoctramine. 7. In summary, the results suggest that the hypotensive action of methoctramine resulted from selective M2 receptor antagonism. Therefore, muscarinic M2 receptors appear to play a role in the regulation of systemic arterial blood pressure in guinea-pigs. However, the anatomical site(s) of action of methoctramine remains to be determined.

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“…IV Catheter Surgery-Rats examined during cocaine self-administration studies were permanently implanted with indwelling catheters (Silastic® silicon tubing, ID 0.63 mm, OD 1.17 mm) into the right jugular vein Remie et al 1990) under a combination of ketamine (100 mg/kg) and xylazine (6 mg/kg) anesthesia. The catheter was passed subcutaneously to the rat's back where it exited through a small incision and affixed to a plastic pedestal (Plastics One, Roanoke, VA) mounted inside a harness system (Instech Laboratories, Plymouth Meeting, PA).…”

Section: Surgical Proceduresmentioning

confidence: 99%

NMDA receptors in the rat VTA: a critical site for social stress to intensify cocaine taking

et al. 2007

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Rationale-Cocaine strengthens behaviors associated with its administration. The stress response by individuals that are defeated in a brief aggressive confrontation can also promote enduring behavioral consequences similar to those of stimulants.Objectives-The study intends to find whether intermittent episodes of defeat promote cocaine's reinforcing effects by triggering N-methyl-D-aspartic acid (NMDA)-receptor-mediated plasticity in the ventral tegmental area (VTA).Materials and methods-Long-Evans rats were investigated after four social defeats in three experiments. Two experiments examined systemic or intra-VTA antagonism of NMDA receptors during stress on the later expression of behavioral sensitization and cocaine self-administration during fixed and progressive ratio (PR) schedules of reinforcement (0.3 mg/kg/infusion), including a novel 24-h variable-dose continuous access binge (0.2, 0.4, and 0.8 mg/kg/infusion, delivered in an irregular sequence). Third, the expression of receptor proteins NR1 (NMDA) and GluR1 [alphaamino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)] were examined in VTA and nucleus accumbens.Results-Intermittent defeats augment locomotor responses to cocaine and increase cocaine taking. Rates of responding during binges are increased after defeat stress. These effects are prevented when NMDA or AMPA receptor antagonists are administered before defeats. VTA infusions of the NMDA antagonist AP-5 (5 nmol/side) before stress prevents locomotor sensitization to cocaine and

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Characterization of presynaptic vascular muscarinic receptors inhibiting endogenous noradrenaline overflow in the portal vein of the freely moving rat

Cited by 18 publications

References 17 publications

Heterogeneity of vascular muscarinic receptors

Heterogeneity of vascular muscarinic receptors

Hypotensive effect of an M₂‐selective muscarinic antagonist in anaesthetized guinea‐pigs

NMDA receptors in the rat VTA: a critical site for social stress to intensify cocaine taking

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Characterization of presynaptic vascular muscarinic receptors inhibiting endogenous noradrenaline overflow in the portal vein of the freely moving rat

Cited by 18 publications

References 17 publications

Heterogeneity of vascular muscarinic receptors

Heterogeneity of vascular muscarinic receptors

Hypotensive effect of an M2‐selective muscarinic antagonist in anaesthetized guinea‐pigs

NMDA receptors in the rat VTA: a critical site for social stress to intensify cocaine taking

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Hypotensive effect of an M₂‐selective muscarinic antagonist in anaesthetized guinea‐pigs