Arginine Vasopressin-lnduced Renal Vasodilation Mediated by Nitric Oxide

Rudichenko, V M; Beierwaltes, William H.

doi:10.1159/000159082

Cited by 67 publications

(34 citation statements)

References 19 publications

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“…These observations were consistent with the direct observations that AVP stimulated NO production in the epithelial cells of inner medullary collecting ducts (IMCD) as determined by fluorescent microscopy (67) and other reports that AVP stimulated increases of urinary cGMP concentrations (103) and that the inhibition of NOS acutely enhanced systemic pressor responses to AVP (35,109).…”

Section: Acute Counterregulatory Action Of Renal Medullary No On Circsupporting

confidence: 91%

Role of renal NO production in the regulation of medullary blood flow

Cowley

Mori

Mattson

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

175

202

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. Role of renal NO production in the regulation of medullary blood flow. Am J Physiol Regul Integr Comp Physiol 284: R1355-R1369, 2003 10.1152/ajpregu.00701.2002The unique role of nitric oxide (NO) in the regulation of renal medullary function is supported by the evidence summarized in this review. The impact of reduced production of NO within the renal medulla on the delivery of blood to the medulla and on the long-term regulation of sodium excretion and blood pressure is described. It is evident that medullary NO production serves as an important counterregulatory factor to buffer vasoconstrictor hormoneinduced reduction of medullary blood flow and tissue oxygen levels. When NO synthase (NOS) activity is reduced within the renal medulla, either pharmacologically or genetically [Dahl salt-sensitive (S) rats], a super sensitivity to vasoconstrictors develops with ensuing hypertension. Reduced NO production may also result from reduced cellular uptake of L-arginine in the medullary tissue, resulting in hypertension. It is concluded that NO production in the renal medulla plays a very important role in sodium and water homeostasis and the long-term control of arterial pressure. renal medulla; Dahl salt-sensitive rats; hypertension; L-arginine THE RENAL MEDULLARY CIRCULATION is now recognized to be of importance for reasons that extend far beyond providing the economy of countercurrent exchange to concentrate large volumes of filtrate to produce small volumes of concentrated urine. It is now recognized that medullary blood flow (MBF) can play an important role in determining long-term levels of arterial pressure and that 15-30% reductions of blood flow to the renal medulla in the face of imperceptibly small changes of total renal blood flow can lead to the development of hypertension (16,21). Evidence is reviewed showing that nitric oxide (NO) plays a unique role in the acute and chronic regulation of renal MBF, sodium homeostasis, and arterial pressure. More specifically, the role of NO in the regulation of MBF, in linking tubular metabolic needs with delivery of nutrients and as a counterregulatory system to protect the medulla from the consequences of underperfusion, are the focus of this review. The influence of NO on the renal cortex and such issues that relate to pressure-natriuresis, autoregulation of total renal blood flow, tubuloglomerular feedback, and glomerular filtration rate (GFR) regulation are important subjects of renal function that either have been reviewed by others (2,29,43,55,96) or are beyond the scope of this relatively brief review.

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Section: Acute Counterregulatory Action Of Renal Medullary No On Circsupporting

confidence: 91%

Role of renal NO production in the regulation of medullary blood flow

Cowley

Mori

Mattson

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

175

202

View full text Add to dashboard Cite

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“…In addition, Stadlbauer et al [18] implied that vasopressin may be beneficial when continuous bleeding injuries occur, because it simply shifts blood away from the injury, i.e., from the site of bleeding. Besides the facts described above, exogenous vasopressin administered at subpressor doses induces significant renal vasodilation mediated by nitric oxide [15]. Thus, vasopressin may act as a vasopressor to recover preload more efficiently in redistribution of blood flow than catecholamine with the least complications in terms of vital organs such as the brain, kidney, and lung.…”

Section: Discussionmentioning

confidence: 98%

Vasopressor Therapy Using Vasopressin Prior to Crystalloid Resuscitation in Irreversible Hemorrhagic Shock under Isoflurane Anesthesia in Dogs

Yoo

Kim

Eom

et al. 2007

The Journal of Veterinary Medical Science

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ABSTRACT. In the present study, we tested the hypothesis that vasopressin administration prior to crystalloid resuscitation can be used to improve hemodynamic and oxygen delivery functions. Hemorrhagic shock was experimentally induced by maintaining mean arterial pressure at 60 mmHg for 30 min in sixteen healthy dogs weighing from 8 to 10.6 kg. Vasopressin was administered and then volume resuscitation was performed for the 6 dogs of V-C group, while vasopressin was administered at the end of volume resuscitation in the 5 dogs of C-V group. The control group (n=5) was administered 0.4 IU/kg of vasopressin after induction of shock without fluid resuscitation. In all groups, hemodynamic parameters were measured pre-and post-hemorrhage and for 60 min after fluid resuscitation. The dogs in V-C group had substantially increased systolic arterial pressure (SAP) for 60 min and improved pulmonary capillary wedge pressure (PCWP), cardiac output (CO), oxygen delivery, and oxygen consumption indexes compared with C-V and control groups. Diastolic pressure and systemic vascular resistance was significantly lower in the V-C group than those in the C-V and control groups (P<0.05). In the V-C group, there was effective and rapid restoration of the SAP, CO, PCWP, and oxygen delivery parameters after treatment. This study indicates that vasopressin administration before crystalloid resuscitation is a more efficient way of improving hemodynamic and oxygen delivery functions in hemorrhagic shock in dogs.

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“…Although divergent renal hemodynamic responses to AVP have been reported concerning species, the route of administration, and dose, a similar decrease in RVR with increased RBF has been observed in rat. The renal vasodilation seems to be mediated by a V 2 and/or oxytocin receptor and NO production (38,39). AVP infusion up to 0.4 U/min has no effect in normal humans and a marked pressor response in septic shock (40).…”

Section: Discussionmentioning

confidence: 99%

Maintenance of Renal Vascular Reactivity Contributes to Acute Renal Failure during Endotoxemic Shock

Boffa

Arendshorst

2005

Journal of the American Society of Nephrology

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Septic shock is characterized by hypotension and decreased systemic vascular resistance and impaired vascular reactivity. Renal vasoconstriction markedly contrasts with sepsis-induced generalized systemic vasodilation, which is strongly dependent on nitric oxide. Whether maintained renal vascular reactivity to vasoconstrictors contributes to the decrease in renal blood flow (RBF) and GFR observed during LPS-induced sepsis was tested by assessment of the acute effects of pressor agents on mean arterial pressure (MAP) and renal hemodynamics in endotoxemic and control mice. LPS-injected mice displayed lower MAP, RBF, and GFR than controls (P < 0.001). Despite a lower MAP, basal renal vascular resistance (RVR) was higher during endotoxemia (P < 0.02). Angiotensin II infusion produced a weaker MAP response in septic mice (24 versus 37%; P < 0.005), suggesting impaired vasoconstriction and hyporeactivity. A similar MAP increase was observed between groups during norepinephrine (NE) infusion. The MAP increase to nitric oxide synthase inhibition by N G -nitro-L-arginine methyl ester (L-NAME) was much greater in LPS-treated mice (41 versus 15%, P ‫؍‬ 0.01), indicating a strong influence of nitric oxide in sepsis. In contrast, the RBF and RVR responses to angiotensin II, NE, or L-NAME were similar in both groups. Moreover, vasopressin produced greater changes in MAP, RBF, and RVR in septic mice than in controls. Among the vasoconstrictor challenges, only NE ameliorated the decrease in GFR 14 h after LPS injection. The in vivo results demonstrate that the renal microvasculature displays a normal or enhanced reactivity to constrictor agents as compared with nonrenal circulatory beds. Such responsiveness may contribute to reduced RBF and GFR during endotoxemia.

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Arginine Vasopressin-lnduced Renal Vasodilation Mediated by Nitric Oxide

Cited by 67 publications

References 19 publications

Role of renal NO production in the regulation of medullary blood flow

Role of renal NO production in the regulation of medullary blood flow

Vasopressor Therapy Using Vasopressin Prior to Crystalloid Resuscitation in Irreversible Hemorrhagic Shock under Isoflurane Anesthesia in Dogs

Maintenance of Renal Vascular Reactivity Contributes to Acute Renal Failure during Endotoxemic Shock

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