Pathways

Procaterol is a beta-2 adrenergic agonist that is used as a bronchodilator. It is a long acting and potent drug that can be taken orally or through inhalation for the treatment of asthma and COPD. The purpose of this drug is to increase the bronchial air flow via G protein signalling upon activation of the beta-2 adrenergic receptor in bronchial smooth muscle cells. Once procaterol is administered and it binds to the beta-2 adrenergic receptor, the G protein signalling cascade begins. The alpha and beta/gamma subunits of the G protein separate and GDP is replaced with GTP on the alpha subunit. This alpha subunit then activates adenylyl cyclase which converts ATP to cAMP. cAMP then activates protein kinase A (PKA) which in turn phosphorylates targets and inhibits MLCK through decreased calcium levels causing muscle relaxation. PKA can phosphorylate certain Gq-coupled receptors as well as phospholipase C (PLC) and thereby inhibit G protein-coupled receptor (GPCR) -PLC-mediated phosphoinositide (PI) generation, and thus calcium flux. PKA phosphorylates the inositol 1,4,5-trisphosphate (IP3) receptor to reduce its affinity for IP3 and further limit calcium mobilization. PKA phosphorylates myosin light chain kinase (MLCK) and decreases its affinity to calcium calmodulin, thus reducing activity and myosin light chain (MLC) phosphorylation. Inhibits the phosphorylation of myosin. PKA also phosphorylates KCa++ channels in ASM, increasing their open-state probability (and therefore K+ efflux) and promoting hyperpolarization. Since myosine light chain kinase is not activated, Serine/threonine-protein phosphatase continues to dephosphorylate myosin LC-P, and more cannot be synthesized so myosin remains unbound from actin causing muscle relaxation. This relaxation of the smooth muscles in the lungs causes the bronchial airways to relax which causes bronchodialation, making it easier to breathe. Procaterol is administered via Some side effects of using procaterol may include tinnitus, nausea, vomiting, dry mouth, and fatigue.

Procaine is a slow onset local ester anaesthetic used for local anesthesia, peripheral nerve block and spinal nerve block. Procaine acts mainly by inhibiting sodium influx through voltage gated sodium channels in neuronal membranes of peripheral nerves. It also binds or antagonized NMDA receptors, nicotinic acetylcholine receptors, and serotonin receptor-ion channel complex. Procaine is injected into the tissue and spreads to the nerves through infiltration. In the local post-synaptic neurons, it binds or antagonizes NMDA receptors. This prevents calcium from entering the postsynaptic neuron. This causes hyperpolarization and prevents depolarization, which has an anaesthetic effect on the local tissue

Procaine merethoxylline is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Procaine merethoxylline passes through the liver and is then excreted from the body mainly through the kidney.

Procaine benzylpenicillin is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Procaine benzylpenicillin passes through the liver and is then excreted from the body mainly through the kidney.

Procaine exerts its local anaesthetic effect by blocking voltage-gated sodium channels in peripheral neurons. Procaine diffuses across the neuronal plasma membrane in its uncharged base form. Once inside the cytoplasm, it is protonated and this protonated form enters and blocks the pore of the voltage-gated sodium channel from the cytoplasmic side. For this to happen, the sodium channel must first become active so that so that gating mechanism is in the open state. Therefore procaine preferentially inhibits neurons that are actively firing.

Procaine is an anesthetic used mainly for peripheral and spinal nerve block, it is an ester with slow onset and short duration of action, used mainly for oral surgery. Procaine has the additional effect of constricting blood vessels to reduce bleeding. It is metabolized in the plasma by pseudocholinesterase by the process of hydrolysis into para-aminobenzoic acid (PABA) when is excreted through the process of diuresis. It's mechanism of action in mainly by inhibiting sodium flux through voltage gated sodium channels, due to this an action potential cannot be conducted. It binds to the receptor site in the cytoplasmic portion of the sodium channel, it also antagonizes N-methyl-D-aspartate (NMDA), nicotinic acetylcholine and serotonin receptors.