Browsing Pathways

Tinzaparin is a low molecular weight heparin (LMWH), it is an anticoagulant that halts the formation of thrombi. It binds to antithrombin III forming a complex that speeds up the inhibition of factor Xa. This stops the generation of thrombin and the coagulation cascade, it is administered via subcutaneous injection. Through the liver, it is metabolized through sulfation and polymerization and is eliminated through the kidneys. There is some risk of osteoporosis with increasing duration of use, bleeding, alopecia, and heparin-induced thrombocytopenia (HIT). It can interact with herbs and supplements, so avoid those with anticoagulants and antiplatelet activity such as garlic, ginger, bilberry, danshen, piracetam and ginkgo bilba.

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

Timolol is a non-selective beta-adrenergic blocker used in the treatment of elevated intraocular pressure in ocular hypertension or open angle glaucoma. Timolol competes with adrenergic neurotransmitters for binding to beta(1)-adrenergic receptors in the heart and the beta(2)-receptors in the vascular and bronchial smooth muscle. This leads to diminished actions of catecholamines, which normally bind to adrenergic receptors and exert sympathetic effects leading to an increase in blood pressure and heart rate. The blockade of beta(2) receptors by timolol in the blood vessels leads to a decrease in peripheral vascular resistance, reducing blood pressure. The exact mechanism by which timolol reduces ocular pressure is unknown at this time, however, it likely decreases the secretion of aqueous humor in the eye. Timolol, when administered by the ophthalmic route, rapidly reduces intraocular pressure. When administered in the tablet form, it reduces blood pressure, heart rate, and cardiac output, and decreases sympathetic activity. It can be found under the brand names Azarga, Betimol, Combigan, Cosopt, Duotrav, Istalol, Timoptic, and Xalacom. Some side effects of using Timolol may include eye pain, swollen eyelids, and dry mouth.

Timolol is a non-selective beta-adrenergic blocker used in the treatment of elevated intraocular pressure in ocular hypertension or open angle glaucoma. Timolol competes with adrenergic neurotransmitters for binding to beta(1)-adrenergic receptors in the heart and the beta(2)-receptors in the vascular and bronchial smooth muscle. This leads to diminished actions of catecholamines, which normally bind to adrenergic receptors and exert sympathetic effects leading to an increase in blood pressure and heart rate. Beta(1)-receptor blockade by timolol leads to a decrease in both heart rate and cardiac output during rest and exercise, and a decrease in both systolic and diastolic blood pressure. In addition to this, a reduction in reflex orthostatic hypotension may also occur. Timolol, when administered by the ophthalmic route, rapidly reduces intraocular pressure. When administered in the tablet form, it reduces blood pressure, heart rate, and cardiac output, and decreases sympathetic activity. It can be found under the brand names Azarga, Betimol, Combigan, Cosopt, Duotrav, Istalol, Timoptic, and Xalacom. Some side effects of using Timolol may include eye pain, swollen eyelids, and dry mouth.

Timolol is a non-selective beta-adrenergic blocker used in the treatment of elevated intraocular pressure in ocular hypertension or open angle glaucoma. Timolol competes with adrenergic neurotransmitters for binding to beta(1)-adrenergic receptors in the heart and the beta(2)-receptors in the vascular and bronchial smooth muscle. This leads to diminished actions of catecholamines, which normally bind to adrenergic receptors and exert sympathetic effects leading to an increase in blood pressure and heart rate. Beta(1)-receptor blockade by timolol leads to a decrease in both heart rate and cardiac output during rest and exercise, and a decrease in both systolic and diastolic blood pressure. In addition to this, a reduction in reflex orthostatic hypotension may also occur. The blockade of beta(2) receptors by timolol in the blood vessels leads to a decrease in peripheral vascular resistance, reducing blood pressure. The exact mechanism by which timolol reduces ocular pressure is unknown at this time, however, it likely decreases the secretion of aqueous humor in the eye.

Timolol is a beta blocker medication, making it part of the antihypertensive drug class. It relieves symptoms such as tachycardia, vascular headaches, hypertension, angina and tremors. Timolol, much like propranolol or oxprenolol, begins its journey by inhibiting the beta-1 adrenergic receptors in the heart. Entering the myocyte, this activates a G-protein signalling cascade, which activates cAMP -dependent protein kinase type 1-alpha regulatory subunit. From there, cAMP-dependent protein kinase catalytic subunit alpha activates outage-dependent L-type calcium channel subunit alpha 1C and 2 other transports which bring calcium into the myocyte from outside of the cell. cAMP-dependent protein kinase catalytic subunit alpha is activated through ryanodine receptor 2, which is also transporting calcium into the myocyte from the the sarcoplasmic reticulum. The calcium and calmodulin then activate myosin light chain kinase, which is located in the smooth vascular muscle. This, paired with the calcium activating a series of troponin enzymes that activate tropomyosin enzymes in the striated muscle, results in a muscle contraction. Then in the cell membrane we have PIP2(16:0/20:3(8Z,11Z,14Z)) catalyzing into DG(14:0/14:1(9Z)/0:0) and inositol 1,4,5-triphosphate with the help of the enzyme 1-phosphatidylinositol 4,5-biphosphate phosphodiesterase beta-1. This enzyme is activated through the G-protein signalling cascade, which stems from the type-1 angiotensin II receptor. Around the cell there are many transports happening through many different transporters, leading in and out of the cell Some of the transports into the cell include sodium and calcium, while transports are also working hard to constantly export potassium from the cell. Returning to the sarcoplasmic reticulum, cardiac phospholamban inhibits the transporter sarcoplasmic/endoplasmic reticulum calcium ATPase 2, which sees water and ATP catalyzed through it to become phosphorus and ADP, while transporting calcium into the sarcoplasmic reticulum.