Inhibition by morphine and morphine-like drugs of nicotine-induced emesis in cats

Beleslin, D.B.; Krstić, S.K.; Stefanović-Denić, Ksenija; Štrbac, Matija; Micić, D

doi:10.1016/s0361-9230(81)80017-2

Cited by 20 publications

(3 citation statements)

References 4 publications

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“…The reasons for studying opioid-nicotine interactions include the addiction to nicotine from smoking and the use of narcotics for pain relief in lung cancer patients. In addition, several reports suggest an antagonism between opioid-and nicotine-stimulated pathways on behavioral and physiological processes in humans and whole animals (11)(12)(13). The data presented here show that lung cancer cell lines of diverse histologies express multiple opioid receptors as well as receptors for nicotine and a-bungarotoxin.…”

supporting

confidence: 59%

Opioid and nicotine receptors affect growth regulation of human lung cancer cell lines.

Maneckjee

Minna

1990

Proc. Natl. Acad. Sci. U.S.A.

262

206

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Using specific ligands, we find that lung cancer cell lines of diverse histologic types express multiple, highaffinity (Kd = 10-9-10-1o M) membrane receptors for Iz, 8, and K opioid agonists and for nicotine and a-bungarotoxin. These receptors are biologically active because cAMP levels decreased in lung cancer cells after opioid and nicotine application. Nicotine at concentrations (=100 nM) found in the blood of smokers had no effect on in vitro lung cancer cell growth, whereas IA, 8, and Kopioid agonists at low concentrations (1-100 nM) inhibited lung cancer growth in vitro. We also found that lung cancer cells expressed various combinations of immunoreactive opioid pep-

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supporting

confidence: 59%

Opioid and nicotine receptors affect growth regulation of human lung cancer cell lines.

Maneckjee

Minna

1990

Proc. Natl. Acad. Sci. U.S.A.

262

206

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“…Cat Cytotoxic drugs: Cisplatin , Cyclophosphamide (Fetting et al, 1982) Intragastric irritants: Copper sulfate (Kayashima and Hyama, 1976) Motion (Crampton and Daunton, 1983) Apomorphine (Costello and Borison, 1977) Morphine (Villablanca et al, 1984) Radiation (Rabin et al, 1986b) (Rabin et al, 1986b) Nicotine (Beleslin et al, 1981) Hormones and neurotransmitters: Angiotensin II (Rabin et al, 1986a) Other: Amphetamine (Rabin and Hunt, 1992) Dog Cytotoxic drugs: Cisplatin (Gylys et al, 1979), Cyclophosphamide (Amber et al, 1990) Intragastric irritants: Ipecac (Gardner et al, 1996), Copper sulfate (Kayashima and Hayama, 1975) LiCl (Vavilova and Kassil, 1984) Apomorphine (Harrison et al, 1972) Morphine (Lefebvre et al, 1981) Radiation (Cooper and Mattsson, 1979) Nicotine (Vig, 1990) Hormones and neurotransmitters: CCK (Levine et al, 1984), Vasopressin (Wu et al, 1985), Peptide YY (Smith et al, 1989) Ferret Cytotoxic drugs: Cisplatin, cyclophosphamide (Andrews et al, 1990) Intragastric irritants: Copper sulfate, ipecac, NaCl, KCl (Andrews et al, 1990) LiCl (Rabin and Hunt, 1992) Apomorphine (Andrews et al, 1990) Morphine (Barnes et al, 1991) Radiation (Andrews et al, 1990) Guinea pig Intragastric irritants: LiCl (Braveman, 1974) …”

Section: Emesismentioning

confidence: 99%

Signals for nausea and emesis: Implications for models of upper gastrointestinal diseases

Andrews

Horn

2006

Autonomic Neuroscience

221

201

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Nausea and vomiting are amongst the most common symptoms encountered in medicine as either symptoms of diseases or side effects of treatments. In a more biological setting they are also important components of an organism's defences against ingested toxins. Identification of treatments for nausea and vomiting and reduction of emetic liability of new therapies has largely relied on the use of animal models, and although such models have proven invaluable in identification of the anti-emetic effects of both 5-hydroxytryptamine3 and neurokinin1 receptor antagonists selection of appropriate models is still a matter of debate. The present paper focuses on a number of controversial issues and gaps in our knowledge in the study of the physiology of nausea and vomiting including: The choice of species for the study of emesis and the underlying behavioural (e.g. neophobia), anatomical (e.g. elongated, narrow abdominal oesophagus with reduced ability to shorten) and physiological (e.g. brainstem circuitry) mechanisms that explain the lack of a vomiting reflex in certain species (e.g. rats); The choice of response to measure (emesis[retching and vomiting], conditioned flavour avoidance or aversion, ingestion of clay [pica], plasma hormone levels[e.g. vasopressin], gastric dysrhythmias) and the relationship of these responses to those observed in humans and especially to the sensation of nausea; The stimulus coding of nausea and emesis by abdominal visceral afferents and especially the vagus-how do the afferents encode information for normal postprandial sensations, nausea and finally vomiting?; Understanding the central processing of signals for nausea and vomiting is particularly problematic in the light of observations that vomiting is more readily amenable to pharmacological treatment than is nausea, despite the assumption that nausea represents "low" intensity activation of pathways that can evoke vomiting when stimulated more intensely.

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“…Thus, our findings not only demonstrate that HCN1 may be involved in vomiting induced by ZD7288, but also shows efficacy differences in the capacity of HCN blockers in evoking emesis. Of further interest, there are several well-known proemetic drugs with additional HCN channel-blocking activities: (1) Nicotine is a cholinergic agonist with proemetic effects in animals when given subcutaneously ( Beleslin et al, 1981 ; Ueno et al, 1987 ; Yamamoto et al, 2004 ; Parker et al, 2009 ; Horn et al, 2014 ). Moreover, neuronal excitability induced by nicotine has been shown to be mediated via binding and inhibiting the HCN channels ( Griguoli et al, 2010 ; Kodirov et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

The HCN Channel Blocker ZD7288 Induces Emesis in the Least Shrew (Cryptotis parva)

Zhong

Darmani

2021

Front. Pharmacol.

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Subtypes (1–4) of the hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are widely expressed in the central and peripheral nervous systems, as well as the cells of smooth muscles in many organs. They mainly serve to regulate cellular excitability in these tissues. The HCN channel blocker ZD7288 has been shown to reduce apomorphine-induced conditioned taste aversion on saccharin preference in rats suggesting potential antinausea/antiemetic effects. Currently, in the least shew model of emesis we find that ZD7288 induces vomiting in a dose-dependent manner, with maximal efficacies of 100% at 1 mg/kg (i.p.) and 83.3% at 10 µg (i.c.v.). HCN channel subtype (1–4) expression was assessed using immunohistochemistry in the least shrew brainstem dorsal vagal complex (DVC) containing the emetic nuclei (area postrema (AP), nucleus tractus solitarius and dorsal motor nucleus of the vagus). Highly enriched HCN1 and HCN4 subtypes are present in the AP. A 1 mg/kg (i.p.) dose of ZD7288 strongly evoked c-Fos expression and ERK1/2 phosphorylation in the shrew brainstem DVC, but not in the in the enteric nervous system in the jejunum, suggesting a central contribution to the evoked vomiting. The ZD7288-evoked c-Fos expression exclusively occurred in tryptophan hydroxylase 2-positive serotonin neurons of the dorsal vagal complex, indicating activation of serotonin neurons may contribute to ZD7288-induced vomiting. To reveal its mechanism(s) of emetic action, we evaluated the efficacy of diverse antiemetics against ZD7288-evoked vomiting including the antagonists/inhibitors of: ERK1/2 (U0126), L-type Ca2+ channel (nifedipine); store-operated Ca2+ entry (MRS 1845); T-type Ca2+ channel (Z944), IP3R (2-APB), RyR receptor (dantrolene); the serotoninergic type 3 receptor (palonosetron); neurokinin 1 receptor (netupitant), dopamine type 2 receptor (sulpride), and the transient receptor potential vanilloid 1 receptor agonist, resiniferatoxin. All tested antiemetics except sulpride attenuated ZD7288-evoked vomiting to varying degrees. In sum, ZD7288 has emetic potential mainly via central mechanisms, a process which involves Ca2+ signaling and several emetic receptors. HCN channel blockers have been reported to have emetic potential in the clinic since they are currently used/investigated as therapeutic candidates for cancer therapy related- or unrelated-heart failure, pain, and cognitive impairment.

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Inhibition by morphine and morphine-like drugs of nicotine-induced emesis in cats

Cited by 20 publications

References 4 publications

Opioid and nicotine receptors affect growth regulation of human lung cancer cell lines.

Opioid and nicotine receptors affect growth regulation of human lung cancer cell lines.

Signals for nausea and emesis: Implications for models of upper gastrointestinal diseases

The HCN Channel Blocker ZD7288 Induces Emesis in the Least Shrew (Cryptotis parva)

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