Table 2.

Mechanisms of action of the different antihypertensive drug classes.

Antihypertensive Agent	Mechanism of Action
Diuretics	Diuretics produce a negative salt and water balance via similar pathways and prevent sodium retention in the long-term [26]. Several diuretics exist with different potencies and renal sites of action [26]. Loop diuretics (furosemide, bumetanide) exert their mechanism on NKCC transporters (NKCC1 and NKCC2), inhibiting the intracellular Cl- concentration, and Na+ and Cl- reabsorption in the renal tubule [27]. Thiazides act in the cortical diluting segment of the distal renal tubule, inducing diuresis by excreting mainly of sodium and chloride [28], inhibiting the thiazide-sensitive sodium-chloride cotransporter, which reabsorbs 5–10% of the filtered sodium load in the kidney [29].
ACE-inhibitors	RAAS is a key element in BP regulation and homeostasis of the body’s fluid volume. Renin breaks down angiotensinogen into angiotensin. In pulmonary blood vessels, angiotensin I interacts with ACE, which converts angiotensin I (Ang I) into the octapeptide hormone angiotensin II (Ang II) [30]. ACE-inhibitors prevent the conversion of Ang I to Ang II, thus inhibiting aldosterone release, promoting vasodilation [30].
Angiotensin receptor blockers	Ang II acts on the angiotensin II type 1 receptor (AT1R), which triggers vasoconstriction [30]. The AT1R is the principal regulator of BP and fluid volume homeostasis, hereby playing a vital role in cardiovascular and renal pathophysiology. Over-stimulation of the AT1R is implicated in hypertension. AT1R is the primary target receptor for the antihypertensive drug ARBs, therefore over-stimulation can be greatly reduced by treating with ARBs, thus reducing BP [31].
Beta-adrenergic receptor blockers	Stimulation of the $\beta$-adrenergic receptor ($\beta$-AR) by sympathetic neuronal activation (SNS), circulating catecholamines, or adrenergic agonists is proven to increase the heart rate, contraction force, and rate of cardiac relaxation [32]. $\beta$-AR can be divided into three subtypes, ${\beta }_1$-AR, ${\beta }_2$-AR, and ${\beta }_3$-AR, with the expression of mainly ${\beta }_1$-AR (75–80%) and ${\beta }_2$-AR in human cardiac tissue [32]. BARBs bind selectively to $\beta$-ARs, implementing competitive antagonism to the effects of the $\beta$-adrenergic stimuli [33]. Proposed antihypertensive functions of BARBs are [34]: Cardiac output reduction; RAAS inhibition; Plasma volume reduction; Reduction in the peripheral vascular resistance; Vascular compliance improvement; and Baroreceptor resetting.
Calcium channel blockers	Inhibit the flow of extracellular calcium by blocking ion-specific channels extending over the cell wall. Several types of ion-specific calcium channels have been identified; the mechanism of CCB action in humans is located in the L-type channels. Inhibiting calcium influx causes vascular smooth muscles to relax, evoking vasodilation and subsequently lowering the BP [35].