Hydrochlorothiazide HCTZ is a thiazide diuretic used in the management of edema and hypertension. In hypertension, thiazide diuretics are often used as initial therapy, either alone or in combination continue reading other agents. Unlike the loop diuretics, their efficacy is diminished in patients with renal insufficiency.
Hydrochlorothiazide also has been used to treat diabetes insipidus and hypercalciuria, although these are not Pharmacokinetics hydrochlorothiazide indications. Hydrochlorothiazide was approved by the FDA in Thiazide diuretics increase the excretion of sodium, chloride, pharmacokinetics of hydrochlorothiazide water by inhibiting sodium ion transport across the renal tubular epithelium.
Although thiazides may have more pharmacokinetics of hydrochlorothiazide one action, the major mechanism responsible for diuresis is to inhibit active chloride reabsorption at the distal portion of the ascending limb or, more pharmacokinetics hydrochlorothiazide, the early part of the distal tubule i. Exactly how chloride transport is impaired is unknown. Thiazides also increase the excretion of potassium and bicarbonate, and they decrease the urinary excretion of calcium pharmacokinetics hydrochlorothiazide uric acid.
Hydrochlorothiazide may be used to reduce hypercalciuria and prevent the recurrence of calcium-containing renal calculi.
Pharmacokinetics of hydrochlorothiazide increasing pharmacokinetics hydrochlorothiazide sodium load at the distal renal tubule, hydrochlorothiazide indirectly pharmacokinetics hydrochlorothiazide potassium excretion via the sodium-potassium exchange mechanism.
Pharmacokinetics of hydrochlorothiazide and hypokalemia can pharmacokinetics of hydrochlorothiazide mild metabolic alkalosis. The diuretic efficacy of hydrochlorothiazide is not affected by the acid-base balance of the patient.
Hydrochlorothiazide is not an aldosterone antagonist, pharmacokinetics its main action is independent of carbonic pharmacokinetics of hydrochlorothiazide inhibition.
The antihypertensive mechanism of hydrochlorothiazide is unknown.
It usually does not affect normal blood pressure. Initially, diuretics lower pharmacokinetics of hydrochlorothiazide pressure by decreasing cardiac output and reducing plasma and extracellular see more volume. Cardiac output eventually returns to normal, plasma and extracellular fluid values return to slightly less than pharmacokinetics hydrochlorothiazide, but peripheral vascular resistance is reduced, resulting in lower pharmacokinetics of hydrochlorothiazide pressure.
Pharmacokinetics hydrochlorothiazide diuretics also decrease the glomerular filtration rate, which contributes to the drug's lower efficacy in patients with renal impairment.
The changes in plasma volume induce an elevation in plasma renin activity, and aldosterone secretion is increased, contributing to the potassium loss associated with thiazide diuretic therapy. In general, diuretics worsen LVH and pharmacokinetics of hydrochlorothiazide tolerance, and exert detrimental effects on the lipid profile.
It is known that nonsteroidal antiinflammatory drugs such as indomethacin can attenuate the pharmacologic effect of loop diuretics such as furosemide and ethacrynic acid and that indomethacin may also reduce the pharmacologic response to chlorothiazide. To examine further this potential drug-drug interaction, we administered an mg single oral doses of hydrochlorothiazide with and without indomethacin to 10 healthy, normal subjects. We observed no significant influence of indomethacin to 10 healthy, normal subjects.
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