Enalapril, Hydrochlorothiazide
Indications
Enalapril, Hydrochlorothiazide is used for:
ENALAPRIL
For the treatment of essential or renovascular hypertension and symptomatic congestive heart failure. It may be used alone or in combination with thiazide diuretics
HYDROCHLOROTHIAZIDE
For the treatment of high blood pressure and management of edema
For the treatment of essential or renovascular hypertension and symptomatic congestive heart failure. It may be used alone or in combination with thiazide diuretics
HYDROCHLOROTHIAZIDE
For the treatment of high blood pressure and management of edema
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of Enalapril, Hydrochlorothiazide :
Mechanism of Action
ENALAPRIL
There are two isoforms of ace: the somatic isoform, which exists as a glycoprotein comprised of a single polypeptide chain of 1277; and the testicular isoform, which has a lower molecular mass and is thought to play a role in sperm maturation and binding of sperm to the oviduct epithelium. Somatic ace has two functionally active domains, n and c, which arise from tandem gene duplication. Although the two domains have high sequence similarity, they play distinct physiological roles. The c-domain is predominantly involved in blood pressure regulation while the n-domain plays a role in hematopoietic stem cell differentiation and proliferation. Ace inhibitors bind to and inhibit the activity of both domains, but have much greater affinity for and inhibitory activity against the c-domain. Enalaprilat, the principle active metabolite of enalapril, competes with ati for binding to ace and inhibits and enzymatic proteolysis of ati to atii. Decreasing atii levels in the body decreases blood pressure by inhibiting the pressor effects of atii as described in the pharmacology section above. Enalapril also causes an increase in plasma renin activity likely due to a loss of feedback inhibition mediated by atii on the release of renin and/or stimulation of reflex mechanisms via baroreceptors. Enalaprilat's affinity for ace is approximately 200,000 times greater than that of ati and 300-1000 times greater than that enalapril
HYDROCHLOROTHIAZIDE
Hydrochlorothiazide, a thiazide diuretic, inhibits water reabsorption in the nephron by inhibiting the sodium-chloride symporter (slc12a3) in the distal convoluted tubule, which is responsible for 5% of total sodium reabsorption. Normally, the sodium-chloride symporter transports sodium and chloride from the lumen into the epithelial cell lining the distal convoluted tubule. The energy for this is provided by a sodium gradient established by sodium-potassium atpases on the basolateral membrane. Once sodium has entered the cell, it is transported out into the basolateral interstitium via the sodium-potassium atpase, causing an increase in the osmolarity of the interstitium, thereby establishing an osmotic gradient for water reabsorption. By blocking the sodium-chloride symporter, hydrochlorothiazide effectively reduces the osmotic gradient and water reabsorption throughout the nephron
There are two isoforms of ace: the somatic isoform, which exists as a glycoprotein comprised of a single polypeptide chain of 1277; and the testicular isoform, which has a lower molecular mass and is thought to play a role in sperm maturation and binding of sperm to the oviduct epithelium. Somatic ace has two functionally active domains, n and c, which arise from tandem gene duplication. Although the two domains have high sequence similarity, they play distinct physiological roles. The c-domain is predominantly involved in blood pressure regulation while the n-domain plays a role in hematopoietic stem cell differentiation and proliferation. Ace inhibitors bind to and inhibit the activity of both domains, but have much greater affinity for and inhibitory activity against the c-domain. Enalaprilat, the principle active metabolite of enalapril, competes with ati for binding to ace and inhibits and enzymatic proteolysis of ati to atii. Decreasing atii levels in the body decreases blood pressure by inhibiting the pressor effects of atii as described in the pharmacology section above. Enalapril also causes an increase in plasma renin activity likely due to a loss of feedback inhibition mediated by atii on the release of renin and/or stimulation of reflex mechanisms via baroreceptors. Enalaprilat's affinity for ace is approximately 200,000 times greater than that of ati and 300-1000 times greater than that enalapril
HYDROCHLOROTHIAZIDE
Hydrochlorothiazide, a thiazide diuretic, inhibits water reabsorption in the nephron by inhibiting the sodium-chloride symporter (slc12a3) in the distal convoluted tubule, which is responsible for 5% of total sodium reabsorption. Normally, the sodium-chloride symporter transports sodium and chloride from the lumen into the epithelial cell lining the distal convoluted tubule. The energy for this is provided by a sodium gradient established by sodium-potassium atpases on the basolateral membrane. Once sodium has entered the cell, it is transported out into the basolateral interstitium via the sodium-potassium atpase, causing an increase in the osmolarity of the interstitium, thereby establishing an osmotic gradient for water reabsorption. By blocking the sodium-chloride symporter, hydrochlorothiazide effectively reduces the osmotic gradient and water reabsorption throughout the nephron