Pathways

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.

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.

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.

Metabolites of sildenafil are predicted with biotransformer.

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.

alpha-Linolenic acid is a poly-unsaturated fatty acid with an 18-carbon chain and three cis double bonds. Its primary role in Arabidopsis thaliana is in being a precursor of the phytohormone jasmonic acid. Being a precursor for jasmonic acid, it plays a role in gene responses to feeding from insects. It is also a precursor to other molecules involved in defense signalling such as cis-3-hexenyl acetate. alpha-Linolenic acid itself modulates gene transcription in response to hyperosmotic salinity, heat acclimation, and oxidative stress. alpha-Linolenic acid is released from the hydrolysis of a phosphatidylcholine membrane lipid. It then has a hydroperoxy group added by a dioxygenase in either the 2, 9, or 13 position to form 2(R)-HPOT, 9(S)-HPOT, or 13(S)-HPOT respectively. The oxidation of alpha-linolenic acid to 13(S)-HPOT is the first step in the jasmonic acid synthesis and leads to that separate pathway. 2(R)-HPOT is formed in an oil body and undergoes a spontaneous decarboxylation to form a heptadecatrienal. 9(S)-HPOT, or 13(S)-HPOT are both formed in a chloroplast and cleaved by probable inactive linolenate hydroperoxide lyase to form an aldehyde and an oxo-carboxylic acid. The hexenal from 13(S)-HPOT is reduced by alcohol dehydrogenase class-P to form a hexenol, which undergoes an esterification with acetyl-CoA to form 3-hexenyl acetate.