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Circulation. 1997;95:1108-1110

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(Circulation. 1997;95:1108-1110.)
© 1997 American Heart Association, Inc.


Articles

Role of Vasopressin Deficiency in the Vasodilation of Septic Shock

Ian A. Reid, PhD

the Department of Physiology, University of California San Francisco.

Correspondence to Ian A. Reid, PhD, Department of Physiology, University of California San Francisco, San Francisco, CA 94143-0444. E-mail ianreid@itsa.ucsf.edu


Key Words: Editorials • shock • vasopressin • blood pressure • vasodilation


*    Introduction
 
Septic shock is a form of distributive shock most commonly caused by infection with gram-negative bacteria.1 2 The hallmark of septic shock is marked peripheral arteriolar vasodilation, which results in low systemic vascular resistance, high cardiac output, severe hypotension, and inadequate tissue perfusion. Therapy typically includes administration of fluids and vasopressor agents.

The mechanism of the vasodilation of septic shock remains incompletely understood, but considerable evidence implicates abnormalities of vasodilator mechanisms. Much attention has been focused on bacterial lipopolysaccharide or endotoxin, the administration of which reproduces many of the cardiovascular alterations that occur in septic shock.3 Endotoxin stimulates the synthesis of tumor necrosis factor, interleukin 1, and other cytokines, and these substances in turn increase the generation of the vasodilator nitric oxide. Thus, inhibition of nitric oxide synthase reverses endotoxin- or cytokine-induced hypotension in experimental animals4 5 6 7 and increases systemic vascular resistance and blood pressure in patients with septic shock who have not responded to conventional therapy.8 In addition to increased generation of nitric oxide, there may also be activation of the vascular ATP-sensitive K+ channel in septic shock.9 Opening of this channel hyperpolarizes vascular smooth muscle and reduces Ca2+ entry through voltage-gated Ca2+ channels, thereby inducing vasodilation.

There may also be abnormalities in vasoconstrictor mechanisms in septic shock. In this issue, Landry and associates10 present evidence that deficiency of vasopressin, now recognized as an important vasoconstrictor peptide, contributes to the hypotension of septic shock.


*    Vasopressin
 
Vasopressin is a peptide hormone that is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus . . . [Full Text of this Article]




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