Vasodilators

Pharmacodynamics

The drug class of vasodilators treat hypertension by directly vasodilating blood vessels in the periphery. Vasodilators decrease resistance in the blood vessels resulting in a decrease in blood pressure (Walter, Waldmann, & Nieberding, 1988). Direct-acting vasodilators dilate arterioles specifically, without having a dilating effect on the venous system (Cohn, Mcinnes, & Shepherd, 2011). Although, many antihypertensive drugs ultimately produce vasodilation through a cascade of events, this class antihypertensive drugs produce vasodilation by acting directly on the smooth muscle of the vasculature in the periphery (pharmacotherapy Hypertension carter ) Specifically, direct-acting vasodilators stimulate intracellular components by activating phosphorylation of cyclic-adenosine monophosphate (cAMP) and cyclic-guanosine monophosphate (cGMP) (Walter, Waldmann, & Nieberding, 1988). These cyclic second-messengers inhibit smooth muscle contraction, as well as platelet aggregation (Walter, Waldmann, & Nieberding, 1988).

Pharmacokinetics

However, direct vasodilators are usually not the first in line in the treatment of hypertension. This class of drugs have a fairly short half-life, which requires frequent doses throughout the day (Patel & Jneid, 2018). This class of drugs are primarily metabolized by the liver and excreted via the kidneys (Cohn, Mcinnes, & Shepherd, 2011). While vasodilators are successful in controlling hypertension, these medications possess a myriad of side effects. Reflex tachycardia is the primary adverse effect of these drugs, as a consequence of the medication induced baroreflex response compensating for the sudden medication decrease in vascular resistance. Other less serious side effects include orthostatic hypotension, dizziness, weakness, fluid retention and nausea (Ciccone, 2016). PTs should be mindful of potential implications of adverse effects of these drugs or contraindications to therapy in patients.

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