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Hydrochlorothiazide-Lisinopril Information

What's inside Hydrochlorothiazide-Lisinopril

Hydrochlorothiazide-Lisinopril Active Ingredients: hydrochlorothiazide, lisinopril, details.
Hydrochlorothiazide-Lisinopril Dosages & Strengths
Strength Format Route Strength Class
Hydrochlorothiazide-Lisinopril 25 mg-20 mg tablet oral 1.0 each OTC
Hydrochlorothiazide-Lisinopril 12.5 mg-10 mg tablet oral 1.0 each OTC
Hydrochlorothiazide-Lisinopril 25 mg-20 mg tablet oral 1.0 each OTC
Hydrochlorothiazide-Lisinopril 12.5 mg-10 mg tablet oral 1.0 each OTC

Recent Hydrochlorothiazide-Lisinopril Side Effects

Posted by amykev1107 4 days ago
It must be the HCTZ... I was on Lisinopril 20mg for a month with little avail to my bp. I'm 25 and prior to taking it I was a...

Posted by djg315 29 days ago
I'm 36 and have been on this med for about 1.5 years. I've had some mild sporadic side effects on going but thought they wer...

Posted by r50880 about 1 month ago
I've been on Lisinopril-HCTZ for about 9 months now. I stumbled across this website because I was wondering if perhaps incre...


Hydrochlorothiazide-Lisinopril Chemical Information

hydrochlorothiazide - The hydrogenated derivative of chlorothiazide, a thiazide diuretic with antihypertensive and anti-urolithic effects. This agent binds to the electroneutral Na-K-Cl cotransporter (NKCC) and thereby impairs Na+, K+ and Cl- reabsorption on the luminal membrane of the early segment in the distal convoluted tubule in the kidney. This leads to an increase in urinary excretion of sodium, chloride, potassium, bicarbonate and water subsequently reducing plasma and extracellular fluid volume leading to a reduction in blood pressure. Hydrochlorothiazide also decreases urinary calcium and uric acid excretion by direct action on the distal tubule.

lisinopril - A synthetic peptide derivate and long-acting angiotensin-converting enzyme (ACE) inhibitor with antihypertensive activity. Lisinopril specifically and competitively inhibits angiotensin-converting enzyme thereby decreasing the formation of the potent vasoconstrictor angiotensin II. This leads to a diminished vasopressor activity. In addition, angiotensin II-stimulated aldosterone secretion by adrenal cortex is decreased which results in a decrease of sodium and water retention and an increase of serum potassium.





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