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05-23-0500

Sigma-Aldrich

Bradykinin

Induces the release of nitric oxide.

Synonym(s):

Bradykinin, Kallidin, RPPGFSPFR, callidin

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About This Item

Empirical Formula (Hill Notation):
C50H73N15O11
CAS Number:
58-82-2
Molecular Weight:
1060.21
UNSPSC Code:
12352202
NACRES:
NA.77

Quality Level

100

Assay

≥97% (HPLC)

form

lyophilized solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
desiccated (hygroscopic)

color

white to off-white

solubility

5% acetic acid: 1 mg/mL

shipped in

ambient

storage temp.

−20°C

InChI

1S/C50H73N15O11/c51-32(16-7-21-56-49(52)53)45(72)65-25-11-20-39(65)47(74)64-24-9-18-37(64)43(70)58-28-40(67)59-34(26-30-12-3-1-4-13-30)41(68)62-36(29-66)46(73)63-23-10-19-38(63)44(71)61-35(27-31-14-5-2-6-15-31)42(69)60-33(48(75)76)17-8-22-57-50(54)55/h1-6,12-15,32-39,66H,7-11,16-29,51H2,(H,58,70)(H,59,67)(H,60,69)(H,61,71)(H,62,68)(H,75,76)(H4,52,53,56)(H4,54,55,57)/t32-,33-,34-,35-,36-,37-,38-,39-/m0/s1

InChI key

QXZGBUJJYSLZLT-FDISYFBBSA-N

General description

Bradykinin, a nonapeptide, is produced in plasma under inflammatory conditions by cleavage of kininogen by kallikrein. Bradykinin is involved in a number of physiological functions, including the release of nitric oxide, stimulation of pain receptors, induction of antimitogenic effects, inhibition of cAMP accumulation, induction of smooth muscle contraction, and vasodilation, as well as in inflammation processes. Also involved in edema resulting from trauma or injury. Improves post-ischemic recovery of the heart via a nitric oxide-dependent mechanism.

Application

Bradykininhas been used in studying the changes in colonic afferent response tobradykinin.

Biochem/physiol Actions

Cell permeable: no
Primary Target
Induces the release of nitric oxide
Product does not compete with ATP.
Reversible: no

Packaging

Yes

Sequence

H-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg-OH

Physical form

Supplied as an acetate salt.

Reconstitution

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Other Notes

Mombouli, J.V., and Vanhoutte, P.M. 1995. Am. J. Hypertens.8, 195.
Zhu, P., et al. 1995. Cardiovasc. Res.29, 658.
Bedarida, G.V., et al. 1994. Horm. Metab. Res. 26, 109.
Altiok, N., and Fredholm, B.B. 1993. Cell Signal. 5, 279.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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KV7 but not dual small and intermediate KCa channel openers inhibit the activation of colonic afferents by noxious stimuli
Charity N. Bhebhe, et al.
American Journal of Physiology: Gastrointestinal and Liver Physiology, 325(5), G436-G445 (2023)
Immune System, Pain and Analgesia
H.L. Rittner, et al.
Journal of Separation Science, 5, 407-427 (2008)
Ch Golias et al.
Hippokratia, 11(3), 124-128 (2007-07-01)
The present review article regarding the kinin system-bradykinin is dealing with the biological effects of the abovementioned entity mediated by specific B1 and B2 receptors as well as with its clinical implications known nowadays. The activation of the kinin system-bradykinin
Charity N Bhebhe et al.
American journal of physiology. Gastrointestinal and liver physiology, 325(5), G436-G445 (2023-09-05)
In numerous subtypes of central and peripheral neurons, small and intermediate conductance Ca2+-activated K+ (SK and IK, respectively) channels are important regulators of neuronal excitability. Transcripts encoding SK channel subunits, as well as the closely related IK subunit, are coexpressed
Kwun Nok Mimi Man et al.
eLife, 12 (2023-06-20)
The cellular mechanisms mediating norepinephrine (NE) functions in brain to result in behaviors are unknown. We identified the L-type Ca2+ channel (LTCC) CaV1.2 as a principal target for Gq-coupled α1-adrenergic receptors (ARs). α1AR signaling increased LTCC activity in hippocampal neurons.

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