Pathways

Carprofen (also named Rimadyl or Imadyl) is a nonsteroidal anti-inflammatory drug that can treat various joint pain or post-operative pain. Carprofen can block prostaglandin synthesis by the action of inhibition of prostaglandin G/H synthase 1 and 2. Prostaglandin G/H synthase 1 and 2 catalyze the arachidonic acid to prostaglandin G2, and also catalyze prostaglandin G2 to prostaglandin H2 in the metabolism pathway. Decreased prostaglandin synthesis in many animal model's cell is caused by presence of Carprofen.

Carprofen is a non-steroidal anti-inflammatory drug (NSAID) used as a pain reliever in the treatment of joint pain and post-surgical pain. It is no longer used in the clinical setting, but is approved for use in dogs. It targets the prostaglandin G/H synthase-1 (COX-1) and prostaglandin G/H synthase-2 (COX-2) in the cyclooxygenase pathway. The cyclooxygenase pathway begins in the cytosol with phospholipids being converted into arachidonic acid by the action of phospholipase A2. The rest of the pathway occurs on the endoplasmic reticulum membrane, where prostaglandin G/H synthase 1 & 2 converts arachidonic acid into prostaglandin H2. Prostaglandin H2 can either be converted into thromboxane A2 via thromboxane A synthase, prostacyclin/prostaglandin I2 via prostacyclin synthase or prostaglandin E2 via prostaglandin E synthase. COX-2 is an inducible enzyme, and during inflammation, it is responsible for prostaglandin synthesis. It leads to the formation of prostaglandin E2 which is responsible for contributing to the inflammatory response by activating immune cells and for increasing pain sensation by acting on pain fibers. Carprofen inhibits the action of COX-1 and COX-2 on the endoplasmic reticulum membrane. This reduces the formation of prostaglandin H2 and therefore, prostaglandin E2 (PGE2). The low concentration of prostaglandin E2 attenuates the effect it has on stimulating immune cells and pain fibers, consequently reducing inflammation and pain.

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Carteolol (also known as Cartrol or Ocupress) is a selective β1 adrenergic receptor antagonist (beta blocker), which can be used for treatment of high blood pressure (hypertension) and irregular heartbeats (arrhythmias). Carteolol also has the ability to mild intrinsic sympathomimetic activity (ISA) with effective range of dosage. Adrenaline (also known as epinephrine) can activate β1 adrenergic receptor so that the heart rate and output will be increased. Renin is a hormone that generated from kidney, which could lead to constriction of blood vessels. Beta blockers could efficiently prohibit renin release.

Carteolol is a cardio non-selective beta blocker. It can be administered orally, where it passes through hepatic portal circulation, and enters the bloodstream and travels to act on cardiomyocytes. In bronchial and vascular smooth muscle, carteolol can compete with epinephrine for beta-2 adrenergic receptors. By competing with catecholamines for adrenergic receptors, it inhibits sympathetic stimulation of the heart. The reduction of neurotransmitters binding to beta receptor proteins in the heart inhibits adenylate cyclase type 1. Because adenylate cyclase type 1 typically activates cAMP synthesis, which in turn activates PKA production, which then activates SRC and nitric oxide synthase, its inhibition causes the inhibition of cAMP, PKA, SRC and nitric oxide synthase signaling. Following this chain of reactions, we see that the inhibition of nitric oxide synthase reduces nitric oxide production outside the cell which results in vasoconstriction. On a different end of this reaction chain, the inhibition of SRC in essence causes the activation of Caspase 3 and Caspase 9. This Caspase cascade leads to cell apoptosis. The net result of all these reactions is a decreased sympathetic effect on cardiac cells, causing the heart rate to slow and arterial blood pressure to lower; thus, carteolol administration and binding reduces resting heart rate, cardiac output, afterload, blood pressure and orthostatic hypotension. By prolonging diastolic time, it can prevent re-infarction. One potentially less than desirable effect of non-selective beta blockers like carteolol is the bronchoconstrictive effect exerted by antagonizing beta-2 adrenergic receptors in the lungs. Clinically, it is used to increase atrioventricular block to treat supraventricular dysrhythmias. Carteolol also reduce sympathetic activity and is used to treat hypertension, angina, migraine headaches, and hypertrophic subaortic stenosis.

Carteolol is a beta adrenergic antagonist used to treat arrhythmia, angina, hypertension, and glaucoma. For the treatment of intraocular hypertension and chronic open-angle glaucoma. Carteolol is a beta1 and beta2 (non-selective) adrenergic receptor-blocking agent that does not have significant intrinsic sympathomimetic, direct myocardial depressant, or local anesthetic (membrane-stabilizing) activity. Carteolol, when applied topically to the eye, has the action of reducing elevated, as well as normal, intraocular pressure, whether or not accompanied by glaucoma. Elevated intraocular pressure is a major risk factor in the pathogenesis of glaucomatous visual field loss and optic nerve damage. Carteolol reduces intraocular pressure with little or no effect on pupil size or accommodation in contrast to the miosis which cholinergic agents are known to produce. The primary mechanism of the ocular hypotensive action of carteolol in reducing intraocular pressure is most likely a decrease in aqueous humor production. This process is initiated by the non-selective beta1 and beta2 adrenergic receptor blockade. It can be found under the brand name Ocupress and by blocking the beta-2 and beta-1 adrenergic receptor, it is able to decrease the rate at which the aqueous humour flows into the eye, therefore reducing the intraocular pressure. By antagonizing the beta-1 adrenergic receptor and blocking G(s) signalling, smooth muscle constriction of the ciliary muscles of the eye make it more difficult for the aqueous humour to reach the eye. Some side effects of using carteolol may include chest pain, fatigue, and shortness of breath.

Carteolol is a beta adrenergic antagonist used to treat arrhythmia, angina, hypertension, and glaucoma. For the treatment of intraocular hypertension and chronic open-angle glaucoma. Carteolol is a beta1 and beta2 (non-selective) adrenergic receptor-blocking agent that does not have significant intrinsic sympathomimetic, direct myocardial depressant, or local anesthetic (membrane-stabilizing) activity. Carteolol, when applied topically to the eye, has the action of reducing elevated, as well as normal, intraocular pressure, whether or not accompanied by glaucoma. Elevated intraocular pressure is a major risk factor in the pathogenesis of glaucomatous visual field loss and optic nerve damage. Carteolol reduces intraocular pressure with little or no effect on pupil size or accommodation in contrast to the miosis which cholinergic agents are known to produce. The primary mechanism of the ocular hypotensive action of carteolol in reducing intraocular pressure is most likely a decrease in aqueous humor production. This process is initiated by the non-selective beta1 and beta2 adrenergic receptor blockade. It can be found under the brand name Ocupress and by blocking the beta-2 adrenergic receptor, it is able to decrease the rate at which the aqueous humour flows into the eye, therefore reducing the intraocular pressure. By antagonizing the beta-2 adrenergic receptor, smooth muscle constriction of the ciliary muscles of the eye make it more difficult for the aqueous humour to reach the eye. Some side effects of using carteolol may include chest pain, fatigue, and shortness of breath.

Carteolol is metabolized in the liver by Cytochrome P450 2D6. The product of this reaction is 8-Hydroxycarteolol which is transported into the blood by a member of the Organo anion transporter family. (DrugBank)