INT24472

Context Info Confidence 0.28 First Reported 1988 Last Reported 2006 Negated 0 Speculated 0 Reported most in Abstract Documents 5 Total Number 5 Disease Relevance 1.00 Pain Relevance 1.73

plasma membrane (Brs3) signal transducer activity (Brs3)

Brs3 (Rattus norvegicus)

Pain Link Frequency Relevance Heat agonist 16 98.50 qutenza 160 97.74 sodium channel 10 96.96 antagonist 2 95.56 anesthesia 2 95.52 local anesthetic 3 76.04 potassium channel 3 75.00 Calcium channel 4 65.48 c fibre 32 59.76 Action potential 22 5.00

Disease Link Frequency Relevance Heat Sudden Death 4 93.40 Arrhythmias 2 Under Development 5 92.40 Heart Rate Under Development 10 89.00 Syncope 8 82.48 Nociception 4 82.16 Heart Arrhythmia 10 76.16 Disease 7 74.44 Myocardial Infarction 3 72.08 Ventricular Tachycardia 3 71.08 Bundle-branch Block 4 69.04

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

The inhibitory effect of BAY on the time-dependent increase in BRS was suppressed by a pretreatment with PN (0.6 micrograms/kg i.c.v.) and by a pretreatment with the muscarinic antagonist atropine methylnitrate (80 micrograms/kg i.c.v.).

Positive_regulation (increase) of BRS associated with antagonist

1) Confidence 0.28 Published 1988 Journal Arch Mal Coeur Vaiss Section Abstract Doc Link 2461181 Disease Relevance 0 Pain Relevance 0.20

In SHR, i.c.v. injection of BAY (3 microgram/kg) but not PN (0.6 micrograms/kg) suppressed the time dependent increase in BRS.

Positive_regulation (increase) of BRS

2) Confidence 0.28 Published 1988 Journal Arch Mal Coeur Vaiss Section Abstract Doc Link 2461181 Disease Relevance 0 Pain Relevance 0.20

Interestingly, RTX, a high affinity ligand for VR1, did alter regularly discharging BRs even at higher relative concentrations [20].

Positive_regulation (discharging) of BRs

3) Confidence 0.03 Published 2006 Journal J Negat Results Biomed Section Body Doc Link PMC1481593 Disease Relevance 0 Pain Relevance 0.73

CAP, unlike the ultrapotent TRPV1 agonist RTX, had additional non-specific actions to inhibit discharge of pressure activated A-type aortic BRS at very high concentrations.

Positive_regulation (activated) of BRS associated with qutenza and agonist

4) Confidence 0.03 Published 2006 Journal J Negat Results Biomed Section Body Doc Link PMC1481593 Disease Relevance 0.08 Pain Relevance 0.55

In approximately 20% of the cases BrS is caused by mutations in the SCN5A gene on chromosome 3p21-23, encoding the cardiac sodium channel, a protein involved in the control of myocardial excitability.

Positive_regulation (caused) of BrS associated with sodium channel

5) Confidence 0.03 Published 2006 Journal Orphanet J Rare Dis Section Abstract Doc Link PMC1592481 Disease Relevance 0.91 Pain Relevance 0.05

General Comments

This test has worked.