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BRADYKININ Uses, Side Effects, and More

 BRADYKININ


BRAND NAME:- UNKNOWN.

BRADYKININ  is a peptide that promotes inflammation. It causes arterioles to dilate (enlarge) via the release of prostacyclin, nitric oxide, and endothelium-derived hyperpolarizing factor and makes veins constrict, via prostaglandin F2, thereby leading to leakage into capillary beds, due to the increased pressure in the capillaries. Bradykinin is a physiologically and pharmacologically active peptide of the kinin group of proteins, consisting of nine amino acids. 

MECHANISM OF ACTION:-


1.The mode of action of bradykinin -induced release/biosynthesis of prostaglandin E (PGE) was investigated using the method of the isolated perfused rabbit ear.

2.Phentolamine (1 μg /ml) hardly reduced the total amount of PGE released by bradykinin. Only in the first fraction (3 min) following bradykinin injection was PGE release significantly inhibited.

3.Papaverine (5–10 μg/ml) did not affect the bradykinin- induced PGE release but totally abolished the vasoconstriction evoked by the peptide.

4.Mepacrine (10 μg/ml) greatly inhibited the bradykinin- stimulated PGE release but did not reduce the conversion of arachidonic acid by cyclo-oxygenase into PGs when used in this concentration.

5.Phospholipase A2 — injected intra -arterially into the perfused rabbit ear — strongly stimulated the release of PGE. As with bradykinin, the phospholipase A2-induced PGE release was also significantly inhibited by meparcrine (10 μg/ml).

6.Bradykinin or arachidonic acid, even in high doses (20 or 100 μg respectively), were unable to promote the release of rabbit aorta contracting substance (RCS) from the rabbit ear.

7.PGs were not metabolized when injected intraarterially through the rabbit ear.

8.The results suggest that PGE release induced by bradykinin is hardly mediated via liberating catecholamines or the constricting vessel wall. It is concluded that bradykinin stimulates PGE release by selectively activating a phospholipase A2 without affecting cyclo-oxygenase and subsequent enzymes. The phosholipase A2 catalyzes the splitting of PG precursors from membrane phospholipids, before they are converted by the active PG synthetase system into PGs. 



PHARMACODYNAMIC:-

Not available.


#METABOLISM 


The kinin–kallikrein system makes bradykinin by proteolytic cleavage of its kininogen precursor, high-molecular-weight kininogen (HMWK or HK), by the enzyme kallikrein. Moreover, there is compelling evidence that plasmin, a fibrinolytic enzyme, is able to generate bradykinin after HMWK cleavage.[2]

In humans, bradykinin is broken down by many different kininases: angiotensin-converting enzyme (ACE, kininase II), neprilysin,[3] NEP2, aminopeptidase P (APP), carboxypeptidase N (CPN, kininase I), Carboxypeptidase M, Neutral endopeptidase 24.15, Endothelin converting enzyme-1, Endothelin converting enzyme-2. 



USED:- 


The activation of the kinin system-bradykinin is particularly important in blood pressure regulation and in inflammatory reactions, through bradykinin ability to elevate vascular permeability and to cause vasodilatation in some arteries and veins. 
& Also use in smooth muscle, neurones & kidney symptoms 


SIDE EFFECTS:-


Unknown 


DOSE:- DIRECTION BY PHYSICIAN & PHARMACIST 



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