Vasoconstrictors comprise a class of endogenous compounds and vasopressor drugs which increase arterial blood pressure by two mechanisms: (1) increasing systemic vascular resistance (SVR) in the high resistance, low capacitance arteries and arterioles, and (2) increasing venous pressure and preload in the low resistance, high capacitance veins and venules (Table 169-1).
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TABLE 169-1 Vasoconstrictor Drugs
|Adrenergic ||Nonadrenergic |
|Ephedrine ||Vasopressin |
|Phenylephrine ||Methylene blue |
|Norepinephrine ||Angiotensin II |
|Epinephrine || |
|Dopamine || |
Vascular tone is mediated by multiple receptor subtypes located on smooth muscle cells, the most significant being the adrenergic receptors. The sympathetic nervous system regulates vascular tone by releasing catecholamines which bind to adrenergic receptor targets. Of the four main adrenergic receptors (alpha and beta subtypes), the alpha-1 receptor is responsible for peripheral vasoconstriction. In fact, it is the most predominant receptor subtype located on vascular smooth muscle. Binding of adrenergic vasoconstrictors such as phenylephrine to the alpha-1 receptor initiates a G-protein-coupled signal transduction cascade that leads to vascular smooth muscle contraction, particularly of cutaneous and mesenteric beds. Activation of adenylate cyclase and phospholipase C second messenger systems promote calcium release from the sarcoplasmic reticulum. Intracellular calcium–calmodulin complexes then stimulate kinases which phosphorylate myosin, allow actin and myosin to interact, and cause muscle contraction.
Although the sympathetic nervous system has the most predominant role in vasoconstriction, there are also nonadrenergic cellular mechanisms responsible for maintaining vascular tone.
Vascular smooth muscle contains vasopressin V1 receptors which serve as targets for the endogenous hormone, arginine vasopressin (AVP) or antidiuretic hormone (ADH). Activation of the V1 receptor leads to smooth muscle contraction through the phospholipase C system.
Nitric oxide (NO) released from vascular endothelial cells diffuses into the smooth muscle and activates guanylate cyclase, the enzyme which synthesizes cyclic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP). High cGMP levels inhibit calcium influx, activate K+ channels, and hyperpolarize the muscle cell, leading to vasodilation.
Vascular smooth muscle contains angiotensin II (AT) receptors, the most important being subtype 1 (AT1). Binding of angiotensin II to the AT1 receptor causes vasoconstriction through the G-protein-phospholipase C pathway.
Pharmacological vasoconstriction is often necessary to correct states of low SVR, such as anesthetic-induced vasodilation. First-line adrenergic drugs (eg, phenylephrine, norepinephrine) are usually effective. Vasoplegia, or vasoplegic syndrome, describes the vasodilatory shock state when vascular tone is profoundly decreased and unresponsive to traditional sympathomimetic drugs. This syndrome is characterized by severe hypotension refractory to adrenergic vasoconstrictors and fluid resuscitation, very low SVR, tachycardia, high cardiac output, and low cardiac filling pressures (Table 169-2). In the differential diagnosis of hypotension, vasoplegia is often a diagnosis of exclusion.
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