Table 1.

Potassium modulation of arterial smooth muscle tone

	Vasoconstriction: close		Vasodilation: open
Channel	Effector	Artery	Effector	Artery
KV	Angiotensin II	Pulmonary	Prostacyclin	Cerebral
	Histamine	Coronary	β-Adrenoreceptor	Portal vein, cerebral
	Hypoxia	Pulmonary
KATP	Vasopressin	Mesenteric	Adenosine	Coronary
	Angiotensin II	Mesenteric and coronary	Calcitonin-GRP	Mesenteric, coronary and renal
	Endothelin	-	Acidosis, lactate	Cerebral
	Norepinephrine	-	Nitric oxide	-
	Histamine	-	Vasactive intestinal peptide	-
	Serotonin	-	Prostacyclin	-
	Neuropeptide Y	-	Hypoxia	Coronary
	Hypoxia	Pulmonary
BKCa	Angiotensin II	Coronary	β-Adrenoreceptor	Coronary, aorta
	Thromboxane a2 agonist	Coronary	Nitric oxide	Basilar
	Endothelin	Coronary	Atrial natriuretic peptide
			C-type natriuretic peptide
KIR			Potassium	Cerebral, coronary

K⁺ channels contribute importantly to the resting membrane potential of smooth muscle and thus regulate the intracellular calcium level. When K⁺ channels are closed (depolarized), voltage-gated calcium channels open and cytosolic calcium concentrations rise, leading to vasoconstriction. Agents that open (hyperpolarize) K⁺ channels cause vasodilation through inactivation of voltage-gated calcium channels and a decrease in intracellular calcium concentration [13]. Four types of K⁺ channel have been described in vascular smooth muscle: voltage-activated K⁺ channels (K_V); ATP-sensitive K^{+ 2+}-activated K⁺ channels (K_ATP); Ca channels (BK_Ca); and inward rectifier (K_IR) channels [16]. The table summarizes what is known regarding the modulation of K⁺ channels by vasoconstrictors and vasodilators on the various vascular beds. Note that hypoxia causes vasoconstriction of the pulmonary vasculature through K_V and K_ATP channels, and yet vasodilation of other vascular beds through K_ATP channels. K_ATP channels are particularly important in vasodilatory shock states and are hyperpolarized by pathologic conditions such as hypoxia, acidosis, and increased nitric oxide [13]. K_ATP channels can be depolarized (closed) by vasoconstrictors such as vasopressin and angiotensin II [16]. GRP, gene-related protein.