Cholinergic submandibular effects and muscarinic receptor expression in blood vessels of the rat

Ryberg, Anders T.; Selberg, Hanna; Soukup, Ondřej; Gradin, K.; Tobin, Gunnar

doi:10.1016/j.archoralbio.2008.01.016

Cited by 14 publications

(12 citation statements)

References 38 publications

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“…Jolkkonen et al [44] opined that MTα and MTβ, two muscarinic toxins from Dendroaspis polylepis venom, are probably mAChR agonists, based on their capacity to contract guinea pig ileum; thus, these toxins would be expected to induce vasodilation and hypotension. Ryberg et al [45] have shown that through its actions on muscarinic receptors, acetylcholine causes vasodilation of rat carotid and submandibular arteries and vasoconstriction of jugular and submandibular veins. Acetylcholine, can cause vasodilation or vasoconstriction, depending upon the mAChR class to which it binds.…”

Section: Resultsmentioning

confidence: 99%

Coralsnake Venomics: Analyses of Venom Gland Transcriptomes and Proteomes of Six Brazilian Taxa

Aird

Silva

Qiu

et al. 2017

Toxins

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Venom gland transcriptomes and proteomes of six Micrurus taxa (M. corallinus, M. lemniscatus carvalhoi, M. lemniscatus lemniscatus, M. paraensis, M. spixii spixii, and M. surinamensis) were investigated, providing the most comprehensive, quantitative data on Micrurus venom composition to date, and more than tripling the number of Micrurus venom protein sequences previously available. The six venomes differ dramatically. All are dominated by 2–6 toxin classes that account for 91–99% of the toxin transcripts. The M. s. spixii venome is compositionally the simplest. In it, three-finger toxins (3FTxs) and phospholipases A2 (PLA2s) comprise >99% of the toxin transcripts, which include only four additional toxin families at levels ≥0.1%. Micrurus l. lemniscatus venom is the most complex, with at least 17 toxin families. However, in each venome, multiple structural subclasses of 3FTXs and PLA2s are present. These almost certainly differ in pharmacology as well. All venoms also contain phospholipase B and vascular endothelial growth factors. Minor components (0.1–2.0%) are found in all venoms except that of M. s. spixii. Other toxin families are present in all six venoms at trace levels (<0.005%). Minor and trace venom components differ in each venom. Numerous novel toxin chemistries include 3FTxs with previously unknown 8- and 10-cysteine arrangements, resulting in new 3D structures and target specificities. 9-cysteine toxins raise the possibility of covalent, homodimeric 3FTxs or heterodimeric toxins with unknown pharmacologies. Probable muscarinic sequences may be reptile-specific homologs that promote hypotension via vascular mAChRs. The first complete sequences are presented for 3FTxs putatively responsible for liberating glutamate from rat brain synaptosomes. Micrurus C-type lectin-like proteins may have 6–9 cysteine residues and may be monomers, or homo- or heterodimers of unknown pharmacology. Novel KSPIs, 3× longer than any seen previously, appear to have arisen in three species by gene duplication and fusion. Four species have transcripts homologous to the nociceptive toxin, (MitTx) α-subunit, but all six species had homologs to the β-subunit. The first non-neurotoxic, non-catalytic elapid phospholipase A2s are reported. All are probably myonecrotic. Phylogenetic analysis indicates that the six taxa diverged 15–35 million years ago and that they split from their last common ancestor with Old World elapines nearly 55 million years ago. Given their early diversification, many cryptic micrurine taxa are anticipated.

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Section: Resultsmentioning

confidence: 99%

Coralsnake Venomics: Analyses of Venom Gland Transcriptomes and Proteomes of Six Brazilian Taxa

Aird

Silva

Qiu

et al. 2017

Toxins

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“…The odd-numbered muscarinic receptor subtypes (M 1 , M 3 , and M 5 ) have been reported to mediate endothelium-dependent vasodilation. Based on pharmacological studies making use of subtypepreferring agents, the M 1 receptor was suggested to be involved in cholinergic vasorelaxation of rat carotid arteries, the perforating branch of the human internal mammary artery, and human pulmonary and canine lingual arteries (10,29,32,36). Other classical pharmacological studies as well as functional studies in gene-targeted mice lacking specific muscarinic acetylcholine receptor subtypes demonstrated that the M 3 receptor mediates cholinergic vasodilation in various conduit vessels, such as the aorta and the femoral artery, and in some resistance vessels, such as coronary and ophthalmic arteries (2-3, 16, 20, 25).…”

mentioning

confidence: 99%

Role of M₁, M₃, and M₅ muscarinic acetylcholine receptors in cholinergic dilation of small arteries studied with gene-targeted mice

Gericke

Sniatecki

Mayer

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…If this had been the case, the vasoconstriction would have had the same inhibitory effect on the acetylcholine‐induced fluid response as it had on the citric acid‐evoked fluid response. It is worth noting in this context that there is a strong correlation between the flow of plasma through the gland and the secretion of saliva (28) and that cholinergic stimulation is a relatively weak vasodilator in salivary glands (29–31). At least, the dominating xerogenic effect of amphetamine is probably exerted by the release of noradrenaline acting on α‐adrenoceptors in the brain that inhibit salivatory nuclei.…”

Section: Discussionmentioning

confidence: 99%

Effects of amphetamine on salivary secretion

Götrick

Giglio

Tobin

2009

European J Oral Sciences

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Amphetamine induces xerogenic effects, but its mechanism of action and xerogenic potency are unknown. In the current in vivo study on the rat parotid gland, the effects of amphetamine on reflex-evoked and acetylcholine-evoked salivation were examined in the absence and presence of adrenergic and dopaminergic antagonists. Under anaesthesia, amphetamine increased the secretion of salivary fluid and the amount of protein therein in response to acetylcholine. Phentolamine abolished the increase in salivary flow and had no effect on the salivary protein concentration, whereas propranolol only reduced the salivary protein concentration. Reflex activation of the secretion evoked a well-maintained level of secretion that was reduced by amphetamine [50% inhibitory dose (ID(50)) 1.9 +/- 0.1 mg kg(-1) intravenously); the salivary protein concentration was increased in the presence of amphetamine. Phentolamine and haloperidol reduced the amphetamine-inhibitory effect on the reflex-evoked fluid response, whereas propranolol had no effect on the fluid response. The xerogenic effect of amphetamine is mainly exerted by central mechanisms involving alpha-adrenoceptors, while, indirectly, amphetamine causes secretion of protein by inducing the release of noradrenaline from glandular nerve terminals.

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Cholinergic submandibular effects and muscarinic receptor expression in blood vessels of the rat

Cited by 14 publications

References 38 publications

Coralsnake Venomics: Analyses of Venom Gland Transcriptomes and Proteomes of Six Brazilian Taxa

Coralsnake Venomics: Analyses of Venom Gland Transcriptomes and Proteomes of Six Brazilian Taxa

Role of M₁, M₃, and M₅ muscarinic acetylcholine receptors in cholinergic dilation of small arteries studied with gene-targeted mice

Effects of amphetamine on salivary secretion

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Cholinergic submandibular effects and muscarinic receptor expression in blood vessels of the rat

Cited by 14 publications

References 38 publications

Coralsnake Venomics: Analyses of Venom Gland Transcriptomes and Proteomes of Six Brazilian Taxa

Coralsnake Venomics: Analyses of Venom Gland Transcriptomes and Proteomes of Six Brazilian Taxa

Role of M1, M3, and M5 muscarinic acetylcholine receptors in cholinergic dilation of small arteries studied with gene-targeted mice

Effects of amphetamine on salivary secretion

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Role of M₁, M₃, and M₅ muscarinic acetylcholine receptors in cholinergic dilation of small arteries studied with gene-targeted mice