Antihypertensives Flashcards
Chlortalidone
Thaizide diuretic
Moderately potent diuretics; they inhibit reabsorption of sodium and chloride in the proximal (diluting) segment of the distal convoluted tubule, increasing the delivery of sodium to the collecting tubules and producing a corresponding increase in potassium excretion.
When used in recommended low doses for hypertension, thiazides lower BP mostly by a vasodilator effect.
Hydrochlorothiazide
Thaizide diuretic
Moderately potent diuretics; they inhibit reabsorption of sodium and chloride in the proximal (diluting) segment of the distal convoluted tubule, increasing the delivery of sodium to the collecting tubules and producing a corresponding increase in potassium excretion.
When used in recommended low doses for hypertension, thiazides lower BP mostly by a vasodilator effect.
Amiloride
Potassium sparring diuretic
Amiloride is a weak potassium-sparing diuretic; it inhibits sodium reabsorption in the distal tubule by blocking sodium channels. As a result, it interferes with sodium/potassium exchange and reduces urinary potassium excretion.
Indapamide
Thaizide diuretic
Moderately potent diuretics; they inhibit reabsorption of sodium and chloride in the proximal (diluting) segment of the distal convoluted tubule, increasing the delivery of sodium to the collecting tubules and producing a corresponding increase in potassium excretion.
When used in recommended low doses for hypertension, thiazides lower BP mostly by a vasodilator effect.
Captopril
ACE inhibitors
ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. They reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Enalapril
ACE inhibitors
ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. They reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Fosinopril
ACE inhibitors
ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. They reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Lisinopril
ACE inhibitors
ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. They reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Perindopril
ACE inhibitors
ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. They reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Quinapril
ACE inhibitors
ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. They reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Ramipril
ACE inhibitors
ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. They reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Tranolapril
ACE inhibitors
ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin. They reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Candesartan
ARB2 blocker/Sartan
Competitively block binding of angiotensin II to type 1 angiotensin (AT1) receptors. They reduce angiotensin II-induced vasoconstriction, sodium reabsorption and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Eprosartan
ARB2 blocker/Sartan
Competitively block binding of angiotensin II to type 1 angiotensin (AT1) receptors. They reduce angiotensin II-induced vasoconstriction, sodium reabsorption and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Irbesartan
ARB2 blocker/Sartan
Competitively block binding of angiotensin II to type 1 angiotensin (AT1) receptors. They reduce angiotensin II-induced vasoconstriction, sodium reabsorption and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Losartan
ARB2 blocker/Sartan
Competitively block binding of angiotensin II to type 1 angiotensin (AT1) receptors. They reduce angiotensin II-induced vasoconstriction, sodium reabsorption and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Olmesartan
ARB2 blocker/Sartan
Competitively block binding of angiotensin II to type 1 angiotensin (AT1) receptors. They reduce angiotensin II-induced vasoconstriction, sodium reabsorption and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Telmisartan
ARB2 blocker/Sartan
Competitively block binding of angiotensin II to type 1 angiotensin (AT1) receptors. They reduce angiotensin II-induced vasoconstriction, sodium reabsorption and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Valsartan
ARB2 blocker/Sartan
Competitively block binding of angiotensin II to type 1 angiotensin (AT1) receptors. They reduce angiotensin II-induced vasoconstriction, sodium reabsorption and aldosterone release. They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
Amlodipine
Dihydropyridine Calcium channel blocker
Dihydropyridines act mainly on arteriolar smooth muscle to reduce peripheral vascular resistance and BP. They have minimal effect on myocardial cells
Block inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L‑type calcium channels.
Act on coronary arteriolar smooth muscle to reduce vascular resistance and myocardial oxygen requirements, relieving angina symptoms.
Clevidipine
Dihydropyridine Calcium channel blocker
Dihydropyridines act mainly on arteriolar smooth muscle to reduce peripheral vascular resistance and BP. They have minimal effect on myocardial cells.
Block inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L‑type calcium channels.
Act on coronary arteriolar smooth muscle to reduce vascular resistance and myocardial oxygen requirements, relieving angina symptoms.
Diltiazem
Non-dihydropyridine Calcium channel blocker
Non-dihydropyridines: diltiazem and verapamil act on cardiac and arteriolar smooth muscle. They reduce cardiac contractility, heart rate and conduction, with verapamil having the greater effect. Diltiazem has a greater effect on arteriolar smooth muscle than verapamil.
Block inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L‑type calcium channels.
Act on coronary arteriolar smooth muscle to reduce vascular resistance and myocardial oxygen requirements, relieving angina symptoms.
Felodipine
Dihydropyridine Calcium channel blocker
Dihydropyridines act mainly on arteriolar smooth muscle to reduce peripheral vascular resistance and BP. They have minimal effect on myocardial cells.
Block inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L‑type calcium channels.
Act on coronary arteriolar smooth muscle to reduce vascular resistance and myocardial oxygen requirements, relieving angina symptoms.
Lercanidipine
Dihydropyridine Calcium channel blocker
Dihydropyridines act mainly on arteriolar smooth muscle to reduce peripheral vascular resistance and BP. They have minimal effect on myocardial cells.
Block inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L‑type calcium channels.
Act on coronary arteriolar smooth muscle to reduce vascular resistance and myocardial oxygen requirements, relieving angina symptoms.