MOA of agents

inhibits angiotensin-converting enzyme, which prevents conversion of angiotensin I to angiotensin II, resulting in decreased renin activity and reduced aldosterone secretion.

ace-i

blocks vasoconstriction and aldosterone-secreting effects of angiotensin-II

Angiotensin II Receptor Antagonist (ARB)

Bind to the alpha site of L-type calcium channels and inhibit calcium ions from entering "slow channels" or select voltage-sensitive areas of CV smooth muscle and myocardium during depolarization (HTN); amlodipine acts directly on vascular smooth muscle for peripheral arterial vasodilation, DHP CCBs are most selective to arterioles

Dihydropyridine Calcium Channel Blocker

Inhibit L- type calcium channels resulting in decreased intracellular calcium into the smooth muscle, decreasing contractility

Non-Dihydropyridine Calcium Channel Blocker

Competitively bind to the beta receptor and blocks beta-adrenergic stimulation; Decreases cAMP, which decreases sodium and calcium currents

Beta-Blocker

Blocks Alpha 1-adrenergic receptors in prostatic stromal tissue and competitively inhibits postsynaptic alpha-1 adrenergic receptors causing vasodilation

Alpha-1 blocker

Blocks alpha-1/beta-1/beta-2- adrenergic receptors and reduces elevated renins

Alpha-1/Beta-blocker

Stimulates alpha-2 receptors in the brain to cause a decreased sympathetic outflow

Central alpha-2 agonist

Relaxes smooth muscle in arteries to dilate arterioles; may inhibit calcium release from sarcoplasmic reticulum and inhibit myosin phosphorylation in arterial smooth muscle; May also lead to hyperpolarization of arteriole smooth muscle by stimulation of potassium channels, and stimulates NO formation

Direct Arterial Vasodilator

Inhibition of NKCC transporter leads to a collapse of the corticopapillary interstitial osmotic gradient, significantly reducing the ability of the kidney to concentrate the urine. Additionally, inhibition of the NKCC increases the sodium load delivered to the late distal segments causing increased activity of the Na/K-ATPase and potassium exchange into the urine.

Loop Diuretics

Sulfonamide-derived diuretic that inhibits reabsorption of sodium and chloride in distal convoluted tubule, increases potassium excretion. Stimulates increased compensatory activity of the sodium-calcium exchanger (NCX) leading to increased calcium absorption.

Thiazide Diuretics

Blocks epithelial sodium channels in late distal convoluted tubule and collecting duct, inhibiting sodium reabsorption from lumen. Reduces intracellular sodium, decreases Na/K ATPase activity, which leads to potassium retention

Potassium Sparing Diuretic

Competes with aldosterone for mineralocorticoid receptor in distal renal tubules; may block effect of aldosterone on arteriolar smooth muscle. Increases the level and activity of the Na/K-ATPase, ENaC, and ROMK channel proteins. This leads to increased sodium reabsorption and potassium loss.

Mineralocorticoid (Aldosterone) Antagonist

depletes norepinephrine from sympathetic nerve endings and blocks transport of norepinephrine into its storage granules 

Peripheral Sympathetic Inhibitor

decreases plasma renin activity and inhibits conversion of angiotensinogen to angiotensin I

Direct Renin Inhibitor