MEBEVERINE HCL & CHLORDIAZEPOXIDE TABLETS MANUFACTURERS SUPPLIERS - THIRD PARTY CONTRACT MANUFACTURING
COMPOSITION:MEBEVERINE HCL 135mg & CHLORDIAZEPOXIDE 5mg TABLETS
Mebeverine HCl is a musculotropic antispasmodic drug without atropic side-effects whose major therapeutic role is in the treatment of irritable bowel syndrome. It is also indicated for treatment of gastrointestinal spasm secondary to organic disorder.
Chlordiazepoxide is a sedative/hypnotic drug and benzodiazepine derivative. Chlordiazepoxide has a medium to long half life but its active metabolite has a very long half life. The drug has amnestic, anxiolytic, hypnotic and skeletal muscle relaxant properties.
Mebeverine is a musulotrophic antispasmodic with a direct effect on the smooth muscle of the gastro-intestinal tract, relieving spasm without affecting normal gut motility. Since this effect is not mediated by the autonomic nervous system, the typical anti-cholinergic side-effects are absent.
Like other thiazides, chlorothiazide promotes water loss from the body (diuretics). It inhibits Na+/Cl- reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue. Chlorothiazide affects the distal renal tubular mechanism of electrolyte reabsorption. At maximal therapeutic dosages, all thiazides are approximately equal in their diuretic efficacy. Chlorothiazide increases excretion of sodium and chloride in approximately equivalent amounts.
MECHANISM OF ACTION: –
As a diuretic, chlorothiazide inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like chlorothiazide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of chlorothiazide is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle.