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

Cefpodoxime proxetil Uses, Side Effects, and More

Cefpodoxime proxetil Brand name:- cefoprox ,cepodem,DOXCEF 100,200mg cap. Cefpodoxime Proxetil is an antibiotic. It kills the bacteria by preventing them from forming the bacterial protective covering (cell wall) which is needed for them to survive. Pharmacodynamic:- Cefpodoxime is shown to be effective against most Gram positive and Gram negative bacteria, except Pseudomonas aeruginosa, Enterococcus, and Bacteroides fragilis. Mechanism of action:- Cefpodoxime is active against a wide spectrum of Gram-positive and Gram-negative bacteria. Cefpodoxime is stable in the presence of beta-lactamase enzymes. As a result, many organisms resistant to penicillins and cephalosporins, due to their production of beta-lactamase, may be susceptible to cefpodoxime. Cefpodoxime is inactivated by certain extended spectrum beta-lactamases. The bactericidal activity of cefpodoxime results from its inhibition of cell wall synthesis. The active metabolite of cefpodoxime binds preferentially to penicilli

Cephalexin ( ZYD ) ( Cefalexin ) Uses, Side Effects, and More

Cephalexin (ZYD) (Cefalexin) Brand name:- Cephacillin 250,500mg cap; Sporidex, Alcephin,Cephaxin cap. Cephalexin (also called Cefalexin) is the most common used orally effective first generation cephalosporin , similar in spectrum to cefazolin , but less active against penicillinase producing staphylococci and H. Influenza. Plasma protein binding is low; it attains High concentration in bile and is excreted unchanged in urine; t½ - 60min. Pharmacodynamic:- Cephalexin (also called Cefalexin) is a first generation cephalosporin antibiotic. It is one of the most widely prescribed antibiotics, often used for the treatment of superficial infections that result as complications of minor wounds or lacerations.Label It is effective against most gram-positive bacteria through its inihibition of the cross linking reaction between N-acetyl muramicacid and N-acetylglucosamine in the cell wall, leading to cell lysis. Pharmacokinetics:- Cephalexin is rapidly and almost completely absorbed from t

BASILIXIMAB Uses, Side Effects, and More

BASILIXIMAB BRAND NAME:- Simulect BASILIXIMAB is another anti CD - 25 antibody with higher affinity for the IL-2 receptor, but shorter plasma t½ (1 week) . is a monoclonal antibody used to prevent rejection in kidney transplants. It is a chimeric mouse-human monoclonal antibody to the α chain (CD25) of the IL-2 receptor of T cells. It is used in combination with other medicines used to prevent organ rejection. PHARMACODYNAMIC:- Basiliximab functions as an IL-2 receptor antagonist. Specifically it inhibits IL-2-mediated activation of lymphocytes, a critical pathway in the cellular immune response involved in allograft rejection. MECHANISM OF ACTION:- Basiliximab competes with IL-2 to bind to the alpha chain subunit of the IL2 receptor on the surface of the activated T lymphocytes and thus prevents the receptor from signaling. This prevents T cells from replicating and also from activating B cells, which are responsible for the production of antibodies, which would bind to the trans

webmedi

Search This Blog