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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.