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Table 1 Potassium modulation of arterial smooth muscle tone

From: Science Review: Vasopressin and the cardiovascular system part 2 – clinical physiology

 

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

  1. 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 (KV); ATP-sensitive K+ 2+-activated K+ channels (KATP); Ca channels (BKCa); and inward rectifier (KIR) 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 KV and KATP channels, and yet vasodilation of other vascular beds through KATP channels. KATP channels are particularly important in vasodilatory shock states and are hyperpolarized by pathologic conditions such as hypoxia, acidosis, and increased nitric oxide [13]. KATP channels can be depolarized (closed) by vasoconstrictors such as vasopressin and angiotensin II [16]. GRP, gene-related protein.