Bradykinin and hypoxemia-induced renal changes in the newborn rabbit

Tóth-Heyn, Péter; Viani, M. Thonney; Guignard, Jean‐Pierre

doi:10.1007/s004670050469

Cited by 5 publications

(4 citation statements)

References 20 publications

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“…As previously shown in newborn rabbits (4,(7)(8)(9)(10)(11)19), as well as lambs and puppies (33)(34)(35), acute normocapnic hypoxemia in the present study was associated with a significant drop in GFR, together with a concomitant decrease in RBF, MAP, and diuresis, and a significant increase in RVR. Administration of the specific A 1 antagonist DPCPX totally prevented the well-documented hypoxemia-induced fall in GFR and diuresis; both parameters were not modified from the control period to the experimental hypoxemia plus DPCPX periods, although MAP remained significantly decreased.…”

Section: Map Heart Rate (Hr) Hematocrit (Htc) Plasma Protein Levsupporting

confidence: 88%

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Renal Effects of Adenosine A1-Receptor Blockade with 8-Cyclopentyl-1,3-Dipropylxanthine in Hypoxemic Newborn Rabbits

et al. 2003

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The key role of intrarenal adenosine in mediating the hypoxemic acute renal insufficiency in newborn rabbits has been well demonstrated using the nonspecific adenosine antagonist theophylline. The present study was designed to define the role of adenosine A 1 receptors during systemic hypoxemia by using the specific A 1 -receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). Renal function parameters were assessed in 31 anesthetized and mechanically ventilated newborn rabbits. In normoxia, DPCPX infusion induced a significant increase in diuresis (ϩ44%) and GFR (ϩ19%), despite a significant decrease in renal blood flow (RBF) (Ϫ22%) and an increase in renal vascular resistance (RVR) (ϩ37%). In hypoxemic conditions, diuresis (Ϫ19%), GFR (Ϫ26%), and RBF (Ϫ35%) were decreased, whereas RVR increased (ϩ33%). DPCPX administration hindered the hypoxemia-induced decrease in GFR and diuresis. However, RBF was still significantly decreased (Ϫ27%), whereas RVR increased (ϩ22%). In all groups, the filtration fraction increased significantly. The overall results support the hypothesis that, in physiologic conditions, intrarenal adenosine plays a key role in regulating glomerular filtration in the neonatal period through preferential A 1 -mediated afferent vasoconstriction. During a hypoxemic stress, the A 1 -specific antagonist DPCPX only partially prevented the hypoxemiainduced changes, as illustrated by the elevated RVR and drop in RBF. These findings imply that the contribution of intrarenal adenosine to the acute adverse effects of hypoxemia might not be solely mediated via the A 1 receptor. Adenosine is ubiquitous in the kidney. Intrarenal adenosine vasoconstricts the preglomerular vessels via the A 1 receptors, while dilating the efferent arterioles via the A 2 receptors. It thus affects GFR as well as RBF and its distribution within the kidney. In addition to its vascular actions, intrarenal adenosine modulates renal mechanisms, including TGF, renin release, and the tubular handling of electrolytes and water. Intrarenal adenosine also appears to be an important hemodynamic mediator in some models of vasomotor nephropathy, such as those induced by intramuscular glycerol injection (1), contrast media (2), cisplatin (3), or hypoxemia (4).In animal models as in humans, hypoxemia can lead to functional renal insufficiency (5-7). In the newborn rabbit, acute normocapnic hypoxemia induces renal hypoperfusion with decreased GFR and RBF (4, 7-9). The underlying mechanism of this hypoxemia-induced vasomotor nephropathy still remains controversial. The chemoreceptor-mediated reflex and/or the activation of vasoactive factors such as angiotensin II (AII) (9), endothelin (10), nitric oxide (8), or bradykinin (11) have been suggested to play a role.We previously demonstrated that the administration of theophylline, a nonspecific antagonist to adenosine receptors, ameliorates the hypoxemia-induced renal hemodynamic changes seen in the newborn rabbit model (4). Moreover, in neonates with respiratory distress syndrome (12)

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Section: Map Heart Rate (Hr) Hematocrit (Htc) Plasma Protein Levsupporting

confidence: 88%

“…The underlying mechanism of this hypoxemia-induced vasomotor nephropathy still remains controversial. The chemoreceptor-mediated reflex and/or the activation of vasoactive factors such as angiotensin II (AII) (9), endothelin (10), nitric oxide (8), or bradykinin (11) have been suggested to play a role.…”

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confidence: 99%

Renal Effects of Adenosine A1-Receptor Blockade with 8-Cyclopentyl-1,3-Dipropylxanthine in Hypoxemic Newborn Rabbits

et al. 2003

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“…Clinically, acute hypoxemia causes a decrease in glomerular filtration rate and renal blood flow in newborns 36 . Streitman et al .…”

Section: Discussionmentioning

confidence: 99%

Developmental changes in cyclo‐oxygenase mRNA induction by hypoxia in rat kidney

Ogawa

Tomomasa

Morikawa

2002

Pediatrics International

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“…Icatibant did not modify the hypoxemia-induced vasoconstriction, an observation indicating that renal kallikrein was not stimulated by hypoxemia (fig. 2) [25]. As icatibant did aggravate the hypoxemic vasoconstriction, hypoxemia seems to inhibit bradykinin production.…”

Section: Role Of Bradykinin During Neonatal Hypoxemiamentioning

confidence: 99%