Renal microvascular effects of vasopressin and vasopressin antagonists

Edwards, Ruth; Trizna, Walter; Kinter, Lewis B.

doi:10.1152/ajprenal.1989.256.2.f274

Cited by 101 publications

(86 citation statements)

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“…Although the renal effects of AVP are complex, the observed improvement in renal blood flow was likely secondary to nitric oxidemediated afferent arteriolar vasodilatation and selective efferent arteriolar vasoconstriction (4,25). However, with higher exogenous AVP doses, profound vasoconstriction and decreased renal blood flow should be expected (8).…”

Section: Discussionmentioning

confidence: 99%

Vasopressin vs. norepinephrine in endotoxic shock: systemic, renal, and splanchnic hemodynamic and oxygen transport effects

Guzmán

Rosado

Kruse

2003

Journal of Applied Physiology

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vs. norepinephrine in endotoxic shock: systemic, renal, and splanchnic hemodynamic and oxygen transport effects. J Appl Physiol 95: 803-809, 2003; 10.1152/ japplphysiol.00017.2003.-The effects of intravenous norepinephrine (NE, group 1) and vasopressin (AVP, group 2) infusions on systemic, splanchnic, and renal circulations were studied in anesthetized dogs under basal conditions and during endotoxic shock. Under basal conditions, AVP infusion induced a 12 Ϯ 7% drop in left ventricular stroke work, a 45 Ϯ 5% fall in portal venous blood flow, and a 31 Ϯ 13% decrease in intestinal mucosal blood flow (P Ͻ 0.05). AVP also decreased splanchnic oxygen delivery (DO 2) and increased splanchnic and renal oxygen extraction significantly during basal conditions. Except for more pronounced bradycardia among animals in group 2, the systemic and splanchnic changes were comparable between study groups during endotoxic shock. AVP infusion restored renal blood flow and DO 2 in endotoxic shock compared with animals resuscitated with NE, which had persistently low renal blood flow and DO 2. Our data demonstrate that, in contrast to NE, administration of AVP effectively restores renal blood flow and DO2 with comparable systemic and splanchnic hemodynamic and metabolic effects in endotoxin-induced circulatory shock.vasopressors; resuscitation; blood flow SEPTIC SHOCK IS A FORM OF distributive circulatory collapse caused by severe infections (6,22). The hallmark of clinical septic shock is marked peripheral arteriolar vasodilatation, which results in low systemic vascular resistance, elevated cardiac output, hypotension, and inadequate tissue perfusion. Although the mechanism of the vasodilatation of septic shock remains incompletely understood, growing evidence implicates abnormalities of vasomotor regulation (11, 31). In addition, inappropriately low plasma vasopressin levels have been suggested as contributory to the hypotension in advanced vasodilatory septic shock (10).Therapy for septic shock typically includes administration of intravenous fluids, antibiotics, and vasopressor agents (33). However, development of adrenergic hyposensitivity with gradual loss of catecholamine pressor responsiveness resulting in refractory hypotension is a frequent clinical challenge (2, 21). Arginine vasopressin (AVP), a potent endogenous vasoconstrictor, has been proposed as a vasopressor alternative or adjuvant to conventional catecholamine treatment for management of septic shock (16,23,29). In this setting, AVP infusion improved mean arterial blood pressure, facilitated withdrawal of catecholamine vasopressor support, and improved some measures of renal function (16,23,29). However, organ-specific heterogeneity in the vascular responsiveness to AVP has been described. For example, AVP causes cerebral and pulmonary vasodilatation (9, 30), whereas increases in systemic vascular resistance and reduction of skeletal muscle and skin blood flow have been described as well (5). The effects of AVP on intestinal and renal blood flow during sepsis-ind...

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Section: Discussionmentioning

confidence: 99%

Vasopressin vs. norepinephrine in endotoxic shock: systemic, renal, and splanchnic hemodynamic and oxygen transport effects

Guzmán

Rosado

Kruse

2003

Journal of Applied Physiology

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“…Activation of V 2 receptors, which are present only in the kidneys, leads to incorporation of aquaporins into the distal tubules and collecting ducts, thereby increasing the retention of free water by the kidneys (94,97,98). Low doses of vasopressin have been shown to produce a diuresis in humans (99)(100)(101), likely because of efferent arteriolar vasoconstriction (102). At higher doses, vasopressin can produce renal afferent vasoconstriction (103,104) and eventually decreased urine output, most likely because of a combination of V 1 -mediated reductions in renal blood flow and V 2 -mediated free water retention (105).…”

Section: Vasopressor Selectionmentioning

confidence: 99%

AKI Associated with Cardiac Surgery

Thiele¹,

Isbell²,

Rosner

2015

Clinical Journal of the American Society of Nephrology

261

198

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Approximately 18% of patients undergoing cardiac surgery experience AKI (on the basis of modern standardized definitions of AKI), and approximately 2%-6% will require hemodialysis. The development of AKI after cardiac surgery portends poor short-and long-term prognoses, with those developing RIFLE failure or AKI Network stage III having an almost 2-fold increase in the risk of death. AKI is caused by a variety of factors, including nephrotoxins, hypoxia, mechanical trauma, inflammation, cardiopulmonary bypass, and hemodynamic instability, and it may be affected by the clinician's choice of fluids and vasoactive agents as well as the transfusion strategy used. The risk of AKI may be ameliorated by avoidance of nephrotoxins, achievement of adequate glucose control preoperatively, and use of goal-directed therapy hemodynamic strategies. Remote ischemic preconditioning is an exciting future strategy, but more work is needed before widespread implementation. Unfortunately, there are no pharmacologic agents known to reduce the risk of AKI or treat established AKI.

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“…111 The mechanisms of the diuretic effect of vasopressin have not been fully explained. Possible mechanisms include downregulation of the V2R, 102 NO-mediated afferent arteriolar vasodilation, selective efferent arteriolar vasoconstriction, 103 and OTRactivated natriuresis. 105 Higher levels of vasopressin (pressor doses), however, cause a dose-dependent fall in renal blood flow (afferent arteriole and medulla most sensitive), glomerular filtration rate, and sodium excretion.…”

Section: Renal Effects Of Vasopressinmentioning

confidence: 99%