Cardiovascular Pharmacology Quiz

Endothelin receptor antagonists are used to treat pulmonary hypertension by blocking the effects of endothelin, a potent vasoconstrictor.

Angiotensin II receptor blockers (ARBs) like sartans inhibit the AT1 receptor, reducing blood pressure by decreasing plasma volume.

Statins are HMG-CoA reductase inhibitors, responsible for lowering cholesterol levels by inhibiting an enzyme in the cholesterol synthesis pathway.

Acetazolamide is a carbonic anhydrase inhibitor that reduces fluid buildup by interfering with its production.

Alirocumab is a PCSK9 inhibitor that helps reduce LDL cholesterol levels by increasing the number of LDL receptors on liver cells.

Aliskiren is a renin release inhibitor, used to lower blood pressure by preventing the production of angiotensin.

Amiloride is an ENaC inhibiting potassium-sparing diuretic, removing sodium while conserving potassium to lower blood pressure.

Amlodipine is a vascular L-type calcium channel blocker, decreasing heart rate and force, relaxing blood vessels, and lowering blood pressure.

Angiotensinogen, a precursor protein, is converted to angiotensin I, and then angiotensin II, a potent vasoconstrictor, increasing blood pressure.

A smaller vascular radius leads to increased resistance and higher blood pressure, making it harder for blood to flow.

Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE).

Nitric oxide (NO) is a signaling molecule produced in the body. It helps regulate blood pressure, blood flow, and inflammation.

Angiotensin II binds to angiotensin type 1 (AT1) receptors on blood vessels, leading to vasoconstriction.

Nitric oxide (NO) is produced from the conversion of L-arginine by the enzyme nitric oxide synthase (NOS).

Angiotensin II acts on the adrenal gland to stimulate the release of aldosterone.

Nitric oxide (NO) is a key signaling molecule that promotes vasodilation. It relaxes smooth muscles in blood vessels, leading to increased blood flow.

NO helps prevent platelet aggregation by relaxing blood vessels and inhibiting the activation of platelets.

Aldosterone binds to mineralocorticoid receptors (MR) in the kidneys, promoting sodium and water reabsorption.

The main factors determining arterial pressure are cardiac output, the amount of blood pumped by the heart, and peripheral resistance, the resistance to blood flow in the blood vessels.

The conversion to cGMP is a key step in the NO signaling pathway.

At high doses (above 10 micrograms), dopamine acts on alpha and beta receptors, inducing vasoconstriction.

At low doses (below 2 micrograms), dopamine acts on D2 receptors, promoting vasorelaxation and inhibiting norepinephrine release.

High potency nitrates are bioactivated by aldehyde dehydrogenase in the mitochondria.

High potency nitrates are converted to active metabolites that cause vasodilation.

Bempedoic acid, a lipid-lowering medication, inhibits the enzyme ATP citrate lyase, preventing the formation of malonyl-CoA, which is a key building block in cholesterol synthesis.

Beta blockers, used to manage high blood pressure, lower heart rate and force of contraction by blocking beta-adrenergic receptors, ultimately reducing myocardial oxygen demand and preventing HTN-induced damage.

Bile acid binding resins work by binding to bile acids in the gut, preventing their reabsorption and increasing fecal excretion, causing a compensatory increase in LDL uptake by the liver.

Bumetanide, a loop diuretic, inhibits the Na+/K+/2Cl- cotransporter in the ascending limb of the loop of Henle, increasing sodium and water excretion.

Carbonic anhydrase inhibitors like acetazolamide work by preventing the enzyme carbonic anhydrase from converting carbon dioxide and water into bicarbonate and hydrogen ions, leading to decreased fluid formation.

Carvedilol, a nonselective alpha and beta blocker, works by blocking both alpha and beta receptors, leading to vasodilation (relaxation of blood vessels) and reduced heart rate and force of contraction.

The enzyme carbonic anhydrase type II is found in the cytoplasm of various tissues, and plays a role in the production of bicarbonate.

Carbonic anhydrase type IV is specifically present in the luminal brush border and basolateral membrane of the kidney, playing a crucial role in kidney function.

At high doses, the drug activates through a specific enzyme called CYP450 in the endoplasmic reticulum of cells.

Beta blockers should be avoided in patients with myocardial conduction defects due to their potential to worsen these conditions by slowing the heart rate and conduction.

At high doses, the activation of nitrates occurs via the enzyme CYP450 in the endoplasmic reticulum (ER).

At low doses, high-potency nitrates are activated by aldehyde dehydrogenase in the mitochondria.

The active form of nitrates reacts with either mitochondrial cytochrome oxidase or xanthine oxidase, leading to the formation of nitric oxide (NO).

Nitric oxide (NO) is converted into cyclic guanosine monophosphate (cGMP), which relaxes smooth muscles in blood vessels and prevents platelet aggregation.

At moderate doses (2-5 micrograms), dopamine acts on beta1 receptors, increasing cardiac contractility.

Atenolol is a cardioselective beta blocker, meaning it specifically blocks beta1 receptors.

Inhibiting the release of renin lowers blood pressure by preventing the formation of angiotensin II, a powerful vasoconstrictor.

Angiotensin II receptor blockers (ARBs) inhibit the AT1 receptor, leading to a decrease in plasma volume and lower blood pressure.

Statins, by inhibiting HMG-CoA reductase, decrease cholesterol levels.

Alirocumab is a PCSK9 inhibitor, working by increasing the number of LDL receptors on liver cells, leading to lower LDL cholesterol levels.

A carbonic anhydrase inhibitor that reduces fluid buildup by interfering with its production.

A thiazide diuretic, it increases urinary output by increasing sodium and water excretion.

An ultra short-acting L-type calcium channel blocker.

A bile acid binding resin, it binds to bile acids in the intestines, preventing their reabsorption and reducing cholesterol levels.

A loop diuretic, it blocks the reabsorption of sodium and chloride in the loop of Henle.

A fibric acid derivative, it promotes lipid reduction by activating PPAR-a.

A bile acid binding resin, it binds to bile acids in the intestines, preventing their reabsorption.

A loop diuretic that inhibits sodium and chloride reabsorption in the loop of Henle.

A cardioselective alpha-1 subunit L-type calcium channel blocker that decreases the rate and force of cardiac contraction.

An SGLT2 inhibitor, it works in the kidney by blocking the reabsorption of glucose into the bloodstream.

An angiotensin II receptor blocker (ARB), it blocks the binding of angiotensin II to its receptors in the body.

A V1a/V2 antagonist, it blocks the effects of vasopressin, a hormone that regulates blood pressure.

An alpha 2 agonist, it reduces blood pressure by constricting smooth muscle and decreasing heart rate.

A PCSK9 inhibitor, it helps reduce LDL cholesterol levels by increasing the number of LDL receptors on liver cells.

A cholesterol absorption inhibitor that works in the intestinal lumen, blocking NPC1L1 to reduce chylomicron synthesis and promote LDL receptor generation.