ArticleBritish journal of pharmacology2000
Cardiovascular and autonomic effects of omega-conotoxins MVIIA and CVID in conscious rabbits and isolated tissue assays.
Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 53 citations in OpenAlex.
- In-depth characterization of the CaScientific reports · 2026Article
- Current Drug Development Overview: Targeting Voltage-Gated Calcium Channels for the Treatment of Pain.International journal of molecular sciences · 2023Review
- N-type calcium channel and renal injury.International urology and nephrology · 2022Review
- Non-Opioid Peptides Targeting Opioid Effects.International journal of molecular sciences · 2021Review
- Subcutaneous ω-Conotoxins Alleviate Mechanical Pain in Rodent Models of Acute Peripheral Neuropathy.Marine drugs · 2021Article
- Analgesic effects of Phα1β toxin: a review of mechanisms of action involving pain pathways.The journal of venomous animals and toxins including tropical diseases · 2021Review
- Analgesic and side effects of intravenous recombinant Phα1β.The journal of venomous animals and toxins including tropical diseases · 2020Article
- Review
- µ-Opioid receptors inhibit the exercise pressor reflex by closing N-type calcium channels but not by opening GIRK channels in rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Effects of opioid and nonopioid analgesics on canine wheal formation and cultured human mast cell degranulation.Toxicology and applied pharmacology · 2018Article
- Review
- Spinal actions of ω-conotoxins, CVID, MVIIA and related peptides in a rat neuropathic pain model.British journal of pharmacology · 2013Article
- Targeting voltage-gated calcium channels: developments in peptide and small-molecule inhibitors for the treatment of neuropathic pain.British journal of pharmacology · 2012Review
- Analgesic conotoxins: block and G protein-coupled receptor modulation of N-type (Ca(V) 2.2) calcium channels.British journal of pharmacology · 2012Review
- Analgesic effect of highly reversible ω-conotoxin FVIA on N type Ca2+ channels.Molecular pain · 2010Article
- Ziconotide: a review of its pharmacology and use in the treatment of pain.Neuropsychiatric disease and treatment · 2007Article
- Differential involvement of N-type calcium channels in transmitter release from vasoconstrictor and vasodilator neurons.British journal of pharmacology · 2004Article
- Development of small molecules that mimic the binding of omega-conotoxins at the N-type voltage-gated calcium channel.Molecular diversity · 2004Article
- Central endogenous histamine modulates sympathetic outflow through H3 receptors in the conscious rabbit.British journal of pharmacology · 2003Article
- Pharmacokinetic analysis of ziconotide (SNX-111), an intrathecal N-type calcium channel blocking analgesic, delivered by bolus and infusion in the dog.Neuromodulation : journal of the International Neuromodulation SocietyArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effects of a novel N-type voltage-operated calcium channel antagonist, omega-conotoxin CVID, were compared with omega-conotoxin MVIIA on sympathetic-evoked activation of right atria (RA), small mesenteric arteries (MA) and vasa deferentia (VD) isolated from the rat. Their effects were also compared on blood pressure and cardiovascular reflexes in conscious rabbits. 2. The pIC(50) values for MVIIA and CVID, respectively, for inhibiting sympathetic-evoked responses were equivalent in RA (8.7 and 8.7) and VD (9.0 and 8.7); however, in MA the values were 8.4 and 7.7. The cardiac to vascular (RA/MA) potency ratios, antilog (plog RA - plog MA), for MVIIA and CVID were 2 and 10. The offset rates for CVID and MVIIA were rapid, and peptide reapplication caused rapid onset of blockade, suggesting limited desensitization. 3. In the conscious rabbit, CVID and MVIIA (100 microg kg(-1) i.v.) caused a similar fall in blood pressure and a tachycardia that rapidly reached maximum. Both peptides decreased the vagal- and sympathetic-mediated components of the baroreflex, but had no effect on the vagal nasopharyngeal reflex. The orthostatic reflex to 90 degrees tilt was blocked by MVIIA with sustained postural hypotension for > or = 90 min after administration. In contrast, CVID caused postural hypotension at 30 min which recovered rapidly. 4. Neither CVID nor MVIIA (3 microg kg(-1) i.t.) significantly altered cardiovascular variables or autonomic reflexes. 5. In conclusion, CVID appears to be relatively weak at inhibiting the reflex response to tilt consistent with its weaker inhibition of rat mesenteric artery constriction to perivascular nerve stimulation. This may point to subtype N-type calcium channel selectivity.
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