Biochem/physiol Actions
Analgesic dipeptide; promotes the release of methionine-enkephalin
signalword
Danger
hcodes
Hazard Classifications
Carc. 1B - Eye Dam. 1 - Muta. 2 - Skin Sens. 1
Storage Class
6.1D - Non-combustible acute toxic Cat.3 / toxic hazardous materials or hazardous materials causing chronic effects
wgk_germany
WGK 2
flash_point_f
Not applicable
flash_point_c
Not applicable
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J Y Summy-Long et al.
Brain research bulletin, 45(4), 395-403 (1998-04-04)
Intracerebroventricular (I.C.V.) administration of an inhibitor of nitric oxide synthase (NOS) increases oxytocin but not vasopressin secretion, in dehydrated rats [38]. Surprisingly, central injection of L-arginine, the substrate for NOS, caused a similar effect. Kyotorphin (L-tyrosyl-L-arginine), a dipeptide formed from
T Fujita et al.
Neuroscience letters, 271(2), 117-120 (1999-09-07)
High-affinity type H+/peptide cotransporter PEPT2 is preferentially expressed in the kidney, and is responsible for reabsorption of di- and tripeptides in epithelial tubules. Interestingly, PEPT2 has been recently cloned from rat brain. However, there is very little information available on
H Takagi et al.
Nature, 282(5737), 410-412 (1979-11-22)
It is generally accepted that morphine exerts its analgesic effect by binding to specific opiate receptors in the brain and spinal cord. Since Hughes et al. isolated and identified two endogenous pentapeptides, Met- and Leu-enkephalin, from the brain and found
H Ueda
Japanese journal of pharmacology, 79(3), 263-268 (1999-05-07)
Although we have obtained a number of pharmacological tools and mutant mice lacking specific genes related to the pain, the distinct molecular basis of the pain-producing mechanism has remained to be fully clarified since we have been using conventional paradigms
M Inoue et al.
Brain research. Molecular brain research, 69(2), 302-305 (1999-06-15)
The intraplantar injection of kyotorphin (Kyo) elicited nociceptive flexor responses in mice in a dose-dependent manner between 0.1 and 100 fmol. These actions were completely blocked by substance P (NK1) receptor antagonists, such as CP-96345 and CP-99994, but not by
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