Lercanidipine HCl, Enalapril (as maleate)
Indications
Lercanidipine HCl, Enalapril (as maleate) is used for:
LERCANIDIPINE
For the treatment of hypertension, management of angina pectoris and raynaud's syndrome
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
For the treatment of hypertension, management of angina pectoris and raynaud's syndrome
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
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of Lercanidipine HCl, Enalapril (as maleate) :
Mechanism of Action
LERCANIDIPINE
By deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum, lercanidipine inhibits the influx of extracellular calcium across the myocardial and vascular smooth muscle cell membranes the decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload
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
By deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum, lercanidipine inhibits the influx of extracellular calcium across the myocardial and vascular smooth muscle cell membranes the decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload
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