Pathways

Alprazolam is a triazolobenzodiazepine with intermediate onset commonly used to treat panic disorders and generalized anxiety in addition to anxiety associated with depression. Alprazolam is also indicated, either as a standard or extended-release formulation, for the treatment of panic disorder with or without agoraphobia in adults. Alprazolam may also be prescribed off-label for insomnia, premenstrual syndrome, and depression. . Alprazolam allosterically binds on the benzodiazepine receptors in the post-synaptic GABA-A ligand-gated chloride channel in different sites of the central nervous system (CNS). This binding will result in an increase on the GABA inhibitory effects which is translated as an increase in the flow of chloride ions into the cell causing hyperpolarization and stabilization of the cellular plasma membrane. Benzodiazepine receptor associated GABA(a) receptors exist both peripherally and in the CNS, this activity consequently facilitates various effects like sedation, hypnosis, skeletal muscle relaxation, anticonvulsant activity, and anxiolytic action.

Metabolites of sildenafil are predicted with biotransformer.

Alprenolol (also known as alfeprol, alpheprol or alprenololum) a beta blocker (non-selective) that block beta-1 adrenergic receptor in heart. Blocking beta-1 adrenergic receptor could prevent the binding of epinephrine and norepinephrine, which could efficiently reduce blood pressure and heart rate. In the juxtaglomerular apparatus, alprenolol can also bind to beta-2 receptors to prevent the production and release of renin (also known as angiotensinogenase). Without renin, angiotensin II and aldosterone could not be produced, which ultimately prevent water retention and vasoconstriction.

Alprenolol is a non-selective beta blocker for the treatment of hypertension, edema, ventricular tachycardias, and atrial fibrillation. It can be administered intravenously or orally, where it passes through hepatic portal circulation, and enters the bloodstream and travels to act on cardiomyocytes. In bronchial and vascular smooth muscle, alprenolol 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, alprenolol 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 alprenolol 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. Alprenolol also reduce sympathetic activity and is used to treat hypertension, angina, migraine headaches, and hypertrophic subaortic stenosis.

Alprostadil is a medication used for two distinct purposes. First, it is employed in the treatment of erectile dysfunction in men for whom oral treatment is either contraindicated or ineffective. It can be administered either through an intracavernosal injection or an intraurethral suppository. Alprostadil, a synthetic form of prostaglandin E1 (PGE1), acts as a potent vasodilator, promoting smooth muscle relaxation within the corpus cavernosum of the penis. This relaxation allows for increased blood flow into the penis, resulting in penile swelling, elongation, and rigidity, thus facilitating erections. Second, alprostadil is used in neonatal patients with congenital heart defects that depend on a patent ductus arteriosus (DA) for survival until corrective or palliative surgery can be performed. In this context, alprostadil acts as a smooth muscle relaxant, preventing or reversing the functional closure of the DA that naturally occurs shortly after birth. By relaxing the DA smooth muscle, alprostadil ensures continued pulmonary or systemic blood flow in neonates with congenital heart defects. It's important to note that the use of alprostadil for these purposes should be under the supervision of healthcare professionals, as it involves specific dosages and administration methods tailored to the patient's condition.

Alteplase is the generic version of the drugs Activase and Actilyse. It is a thrombolytic drug prescribed to treat acute myocardial infarctions and other blood clotting conditions. Alteplase if often used to treat ischaemic stroke within hours of onset. The drug acts by breaking up blood clots. Alteplase binds fibrin in the blood clot to converts plasminogen to plasmin. Plasmin is a proteolytic enzyme that causing the degradation of fibrin. A side effect of the drug is bleeding, angioedema, allergic reactions and fever.

Alteplase is a recombinant plasminogen activator present in human tissue, also known as Activase, Cathflo and Cathflo Activase used to treat emergencies such as myocardial infarction, ischemic stroke and pulmonary emboli. It is administered intravenously and goes to act on plasminogen which acts on fibrin clots to degrade them into fibrin degradation products known as fibrinolysis. Alteplase binds to fibrin and cleaves an arginine-valine bond of plasminogen converting it into its active form and acting on the fibrin matrix. It is metabolized by the liver through receptor-mediated endocytosis. Due to its nature of anticoagulant and antiplatelet activity herbs and supplements with similar activity should be avoided such as garlic, ginger, bilberry, danshen, piracetam and ginkgo biloba.

Alteplase is fibrinolytic drug that functions as a recombinant tissue plasminogen activator. It is administered intravenously and used to treat conditions caused by arterial blood clots such as acute ischemic stroke, acute myocardial infarction, acute massive pulmonary embolism and blocked central venous access devices. It targets plasminogen in blood vessels where these clots occur. The clotting process consists of two pathways, intrinsic and extrinsic, which converge to create stable fibrin which traps platelets and forms a hemostatic plug. The intrinsic pathway is activated by trauma inside the vasculature system, when there is exposed endothelial collagen. Endothelial collagen only becomes exposed when there is damage. The pathway starts with plasma kallikrein activating factor XII. The activated factor XIIa activates factor XI. Factor IX is then activated by factor XIa. Thrombin activates factor VIII and a Calicum-phospholipid-XIIa-VIIIa complex forms. This complex then activates factor X, the merging point of the two pathways. The extrinsic pathway is activated when external trauma causes blood to escape the vasculature system. Activation occurs through tissue factor released by endothelial cells after external damage. The tissue factor is a cellular receptor for factor VII. In the presence of calcium, the active site transitions and a TF-VIIa complex is formed. This complex aids in activation of factors IX and X. Factor V is activated by thrombin in the presence of calcium, then the activated factor Xa, in the presence of phospholipid, calcium and factor Va can convert prothrombin to thrombin. The extrinsic pathway occurs first, producing a small amount of thrombin, which then acts as a positive feedback on several components to increase the thrombin production. Thrombin converts fibrinogen to a loose, unstable fibrin and also activates factor XIII. Factors XIIIa strengthens the fibrin-fibrin and forms a stable, mesh fibrin which is essential for clot formation. The blood clot can be broken down by the enzyme plasmin. Plasmin is formed from plasminogen by tissue plasminogen activator. Alteplase acts as a tissue plasminogen activator. It binds to clots with fibrin where it causes hydrolysis of the arginine-valine bond in plasminogen, aiding its conversion to plasmin. The plasmin degrades the stable fibrin and causes lysis of the clot. The activity of alteplase depends on the presence of fibrin. Only small amounts of plasmin is formed from plasminogen when there is no fibrin. Alteplase in the presence of fibrin obtains a higher affinity for plasminogen, thus leading to its increased activity. Alteplase undergoes hepatic metabolism and is excreted in urine. Adverse effects such as bleeding, nausea, vomiting, anaphylaxis, fever and angioedema can occur from the use of alteplase.