U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

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Showing 61 - 70 of 136 results

Status:
Other

Class (Stereo):
CHEMICAL (ACHIRAL)


Conditions:

4-(M-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium (McN-A-343) is a selective muscarinic M1 receptors agonist, which leads to its widespread use as an aid to distinguish responses mediated through M₁ receptors from those utilizing M₂ or M₃ muscarinic receptor subtypes, especially in the CNS. McN-A-343 has a number of non-muscarinic actions. These include activation of some types of nicotinic acetylcholine receptors, antagonism of serotonin 5-HT₃ and 5-HT₄ receptor subtypes, inhibition of the uptake mechanism and a local anesthetic action.
Status:
Other

Class (Stereo):
CHEMICAL (ABSOLUTE)

Status:
Other

Class (Stereo):
CHEMICAL (ACHIRAL)

Status:
Other

Class (Stereo):
CHEMICAL (ACHIRAL)

Status:
US Previously Marketed
First approved in 1961

Class (Stereo):
CHEMICAL (RACEMIC)



Polythiazide is a thiazide diuretic with actions and uses similar to those of hydrochlorothiazide. Polythiazide under brand name Rense is indicated as adjunctive therapy in edema associated with congestive heart failure, hepatic cirrhosis, and corticosteroid and estrogen therapy. Renese is indicated in the management of hypertension either as the sole therapeutic agent or to enhance the effectiveness of other antihypertensive drugs in the more severe forms of hypertension. The mechanism of action results in an interference with the renal tubular mechanism of electrolyte reabsorption. At maximal therapeutic dosage, all thiazides are approximately equal in their diuretic potency. The mechanism whereby thiazides function in the control of hypertension is unknown, but as a diuretic, polythiazide inhibits active chloride reabsorption at the early distal tubule via the thiazide-sensitive Na-Cl cotransporter (TSC), resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like polythiazide 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 polythiazide 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.