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The effects of oestrogen on renal and systemic haemodynamics in the rat : influence of intrarenal vasoactive substances and plasma volume statusEvans, John Kenrick January 1986 (has links)
No description available.
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The role of the hypothalamic paraventricular nucleus in the cardiovascular responses to elevations in body temperature.Cham, Joo Lee, julie.cham@rmit.edu.au January 2008 (has links)
The hypothalamic paraventricular nucleus (PVN) is known to be a major integrative region within the forebrain. It is composed of functionally different subgroups of neurons, including the parvocellular neurons that project to important autonomic targets in the brainstem e.g. the rostral ventrolateral medulla (RVLM) and the intermediolateral cell column (IML) of the spinal cord, where the sympathetic preganglionic motor-neurons are located. These regions are critical in cardiovascular regulation; hence, these projections are likely to mediate the effects of the PVN on sympathetic nerve activity and hence may contribute to the cardiovascular changes induced by physiological stimuli such as elevations in body temperature. The neurotransmitter such as nitric oxide (NO) is important in cardiovascular regulation and it is now emerging as a major focus of investigation in thermoregulation. One of the most striking accumulations of NO containing-neurons is in the PVN where it appears to be playing an important role in cardiovascular regulation and body fluid homeostasis. The results of the work show; 1. That spinally-projecting and nitrergic neurons in the PVN may contribute to the central pathways activated by exposure to a hot environment. 2. Suggests that nitrergic neurons and spinally- projecting neurons in the brainstem may make a small contribution to the central pathways mediating the reflex responses initiated by hyperthermia. 3. The present study also illustrates that these PVN neurons projecting to the RVLM may make a smaller contribution than the spinal-projecting neurons in the PVN to the cardiovascular responses initiated by heat. 4. The results of my studies showed that the microinjection of muscimol to inhibit the neuronal activity in the PVN abolished the reflex decrease in renal blood flow following an elevation of core body temperature. In addition, this effect was specific to the PVN, since microinjections of muscimol into areas outside the PVN were not effective. These findings demonstrate that the PVN is critical for this reflex cardiovascular response initiated by hyperthermia. In conclusion, PVN is critical for the reflex decrease in renal blood flow during elevations in core body temperature. We hypothesise that projections from the PVN to the spinal cord and the RVLM contribute to the reflex cardiovascular responses. Additionally, nitrergic neurons in the PVN may contribute but the physiological role of those neurons in the reflex responses elicited by hyperthermia needs to be investigated.
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Renal blood flow and the pathophysiology of acute kidney injuryProwle, John Richard January 2013 (has links)
No description available.
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Renal perfusion in experimental sepsis: impact on kidney metabolism and the role of renal autoregulationPost, Elmar 20 February 2018 (has links)
The etiology of renal dysfunction in sepsis is currently attributed to altered perfusion, microcirculatory abnormalities and cellular alterations. To clarify these mechanisms, we characterized the changes in renal perfusion and cortex metabolism in a large animal model of sepsis. In this model, sepsis was associated with metabolic alterations that may reflect early induction of cortical glycolysis. Septic shock was associated with reduced renal perfusion and decreased cortical and medullary blood flow, followed by signs of anaerobic metabolism in the cortex when flow reductions became critical. Attempts to correct renal hypoperfusion and alleviate the associated perfusion/metabolism mismatch with fenoldopam or renal denervation were unsuccessful. In the final study we focussed on the role of renal autoregulation in experimental sepsis and septic shock. Evidence suggests that higher blood pressure targets are needed in patients with impaired renal autoregulation and septic shock, but the effects of vasopressors should also be considered. We therefore investigated the effects of arginine vasopressin and norepinephrine on renal autoregulation in ovine septic shock. In experimental septic shock, arginine vasopressin was associated with a lower autoregulatory threshold than norepinephrine. As vasopressors may have different effects on renal autoregulation, individualized therapy of blood pressure management in patients with septic shock should take into account drug-specific effects. / Doctorat en Sciences médicales (Médecine) / info:eu-repo/semantics/nonPublished
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Pathophysiology of Unilateral Ischemia-Reperfusion Injury: Importance of Renal Counterbalance and Implications for the AKI-CKD TransitionPolichnowski, Aaron J., Griffin, Karen A., Licea-Vargas, Hector, Lan, Rongpei, Picken, Maria M., Long, Jainrui, Williamson, Geoffrey A., Rosenberger, Christian, Mathia, Susanne, Venkatachalam, Manjeri A., Bidani, Anil K. 01 May 2020 (has links)
Unilateral ischemia-reperfusion (UIR) injury leads to progressive renal atrophy and tubulointerstitial fibrosis (TIF) and is commonly used to investigate the pathogenesis of the acute kidney injury-chronic kidney disease transition. Although it is well known that contralateral nephrectomy (CNX), even 2 wk post-UIR injury, can improve recovery, the physiological mechanisms and tubular signaling pathways mediating such improved recovery remain poorly defined. Here, we examined the renal hemodynamic and tubular signaling pathways associated with UIR injury and its reversal by CNX. Male Sprague-Dawley rats underwent left UIR or sham UIR and 2 wk later CNX or sham CNX. Blood pressure, left renal blood flow (RBF), and total glomerular filtration rate were assessed in conscious rats for 3 days before and over 2 wk after CNX or sham CNX. In the presence of a contralateral uninjured kidney, left RBF was lower (P < 0.05) from 2 to 4 wk following UIR (3.6 + 0.3 mL/min) versus sham UIR (9.6 + 0.3 mL/min). Without CNX, extensive renal atrophy, TIF, and tubule dedifferentiation, but minimal pimonidazole and hypoxia-inducible factor-1α positivity in tubules, were present at 4 wk post-UIR injury. Conversely, CNX led (P < 0.05) to sustained increases in left RBF (6.2 ∓ 0.6 mL/min) that preceded the increases in glomerular filtration rate. The CNX-induced improvement in renal function was associated with renal hypertrophy, more redifferentiated tubules, less TIF, and robust pimonidazole and hypoxia-inducible factor-1α staining in UIR injured kidneys. Thus, contrary to expectations, indexes of hypoxia are not observed with the extensive TIF at 4 wk post-UIR injury in the absence of CNX but are rather associated with the improved recovery of renal function and structure following CNX.
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Renal dysfunction associated with infrarenal cross clamping of the aorta during major vascular surgeryVan der Merwe, Wynand Louw 03 1900 (has links)
Dissertation (MD)--Stellenbosch University, 2000. / ENGLISH ABSTRACT: Acute renal failure still is, with the exception of cardiac deaths, the most important
pathological process associated with perioperative mortality in patients operated for
abdominal aortic aneurysms. The intraoperative change in renal blood flow (RBF) and
glomerular function have been investigated in human and animal models, particularly
over the past 15 years. Despite large variation in study populations, measurement
techniques and study designs in general, a significant body of evidence has developed
which suggests infrarenal aortic clamp-induced renal ischemia to be the cause of
postoperative acute renal failure when this complication does occur.
It is rather surprizing then that, despite some recent studies which have reported on
various pharmacological interventions to prevent intraoperative renal ischemia (with
variable success), very little has apparently been done to unravel the pathogenesis
and exact pathophysiology of this potentially lethal complication. Although a number of
investigators suggest the possibility of hormonal involvement (particularly reninangiotensin,
antidiuretic hormone (ADH) and catecholamines) in the process, the exact
role of these mediators have not been explored (or reported) in a structured fashion.
In an initial human study, renal hemodynamics and function were measured from the
preoperative period, during the intraoperative phase and at least until 4 hours after
aortic unclamping. To investigate the possibility of a temporal relationship between
renal changes and fluctuations in hormonal concentrations, plasma concentrations of
relevant hormones were determined at every sampling period where renal parameters
were measured.
The decrease in RBF and glomerular filtration rate (GFR) which we demonstrated to
coincide with infrarenal aortic cross clamping, is consistent with results previously
published. We demonstrated persistence of the impairment of these parameters as
long as 4 hours into the postoperative phase; which has previously only been reported
for the period until immediately after aortic unclamping with the abdomen still open.
The persistence of a depressed GFR until the time of discharge of patients is cause for
concern, particularly in patients with compromised renal function prior to surgery. Of the measured hormones with a potential influence on RBF and nephron function,
renin was the only mediator where changes in plasma concentrations coincided with
the depression of RBF and GFR after aortic cross clamping. The design of our study
did not allow us to conclude whether the concomitant increase in angiotensin II was
primarily responsible for the change in renal hemodynamics, or whether the raised
renin (and angiotensin) levels were stimulated by the decrease in RBF induced by
another mechanism.
In another patient group, we demonstrated that the combination of mannitol and
dopamine provided no protection against the deleterious effects of aortic cross
clamping. In fact, the high urine volumes produced under the influence of these
agents (which did not correlate with RBF at the corresponding periods), is likely to
prompt a false sense of security. Given the lack of any objective benefit afforded by
these agents, their use in these clinical circumstances should be discouraged.
The animal studies were aimed at elucidation of the exact role of angiotensin in the
pathogenesis and pathophysiology of the renal changes associated with infrarenal
aortic clamping, as well as the interaction of angiotensin with other modulators for
which an interactive relationship had been described previously under other
experimental and/or clinical circumstances.
The first study showed that, although renin (and thus angiotensin) concentrations were
high after aortic unclamping, the hormone had no pathogenic or pathophysiological
role of significance in the observed renal changes during this period (since blocking
angiotensin II activation by the prevention of renin release, or by inhibiting the
conversion enzyme, did not prevent a substantial decrease in RBF or GFR during that
period). Preventing angiotensin II activation did, however, prevent renal changes
during aortic clamping. This beneficial effect did not establish a primary role for
angiotensin during that period, since the favourable influence could also (at least
partially) be explained by prevention of the permissive influence of angiotensin on
other vasoconstrictors and/or other vasodilatory influences of ACE inhibition and [1-
blockade which are unrelated to angiotensin. This study did indicate that (at least
partially) different mechanisms are responsible for the renal changes seen during
aortic clamping, and after aortic unclamping. The second study explored the role of calcium in the renal pathophysiological changes
during aortic clamping and after unclamping. The protective influence effected by
the administration of a Ca2
+ -blocker suggest the dependence of the renal
vasoconstrictive and glomerular pathophysiological process( es) on the cellular influx of
Ca2
+ through voltage-gated channels. It unfortunately provides no definitive insight
into the primary instigators of these processes. However, it does offer a clinically
useful method of preventing these changes and protecting the kidney against ischemic
injury during abdominal aortic surgery.
The third component of the animal studies demonstrates the importance of the
protective effect of renal prostaglandins during the specific experimental (and probably
also the clinical) circumstances. Again, it does not provide definitive information on the
mediators responsible for the renal changes, since the deleterious effects of numerous
endogenous substances have previously been shown to be counterbalanced by
intrarenal synthesis of prostaglandins under various experimental and clinical
circumstances. The extent of the pathophysiological and ultrastructural changes which
occurred under the influence of a NSAID does, however, suggest that these drugs
should not be used under these clinical circumstances.
The last component of the study provides evidence that angiotensin only plays a
secondary/supplementary role in the renal pathophysiological process even during
aortic clamping. This may explain the contradictory evidence regarding the potential
beneficial effect of ACE inhibition (on renal hemodynamics and glomerular function)
during abdominal aortic surgery (Licker et al. 1996, Colson et al. 1992a). Based on
our studies, ACE inhibition can not be supported for this purpose. / AFRIKAANSE OPSOMMING: Akute nierversaking is met die uitsondering van kardiale sterftes, steeds die
belangrikste patologiese proses wat geassosieer is met perioperatiewe mortaliteit in
pasiënte wat opereer word vir abdominale aorta aneurismes. Die intraoperatiewe
veranderinge in renale bloedvloei (NBV) en glomerulêre funksie is die afgelope 15 jaar
ondersoek en gerapporteer in pasiënte- sowel as diere-modelle. Ten spyte van groot
variasies in studie-populasies, meettegnieke en ontwerp van studies in die algemeen,
dui 'n wesenlike hoeveelheid getuienis daarop dat infrarenale klemming van die aorta
renale isgemie induseer, wat die oorsaak is van postoperatiewe akute nierversaking
wanneer hierdie komplikasie voorkom.
Dit is verbasend dat, ten spyte van sommige onlangse studies wat rapporteer oor 'n
verskeidenheid farmakologiese ingrepe om intraoperatiewe renale isgemie te voorkom
(met wisselende sukses), baie min oënskynlik gedoen is om die patogenese en die
presiese patofisiologie van hierdie potensieel dodelike komplikasie te ontrafel. Hoewel
verskeie outeurs die moontlikheid van hormonale betrokkenheid (veral renienangiotensien,
antidiuretiese hormoon en katekolamiene) in hierdie proses suggereer, is
die presiese rol van hierdie mediators nog nie op 'n gestruktureerde wyse ondersoek
(of rapporteer) nie.
In ons aanvanklike pasiënte-studie is renale hemodinamika en -funksie gemeet vanaf
die preoperatiewe periode, gedurende die intra-operatiewe fase en tot minstens vier
uur na ontklemming van die aorta. Serumkonsentrasies van relevante hormone is
bepaal tydens elke metingsperiode waar renale parameters gemeet is, ten einde die
moontlikheid van 'n temporale verwantskap tussen renale veranderinge en variasies in
hormoonkonsentrasies te ondersoek.
Die vermindering in NBV en glomerulêre filtrasiespoed (GFS) wat ons aangetoon het
om saam te val met infrarenale aortaklemming, stem ooreen met resultate wat tevore
deur ander navorsers publiseer is. Ons het aangetoon dat die inkorting van hierdie
parameters voortduur tot minstens vier uur na aorta-ontklemming. Hierdie
veranderinge is tevore slegs rapporteer vir periodes tot kort na aorta-ontklemming voor
sluiting van die buikwond. Die feit dat die GFS steeds verlaag is met ontslag van hierdie pasiënte, skep rede tot kommer, veral in pasiënte wat alreeds ingekorte
nierfunksie het voor die chirurgiese prosedure.
Van die gemete hormone wat moontlik 'n invloed sou kon uitoefen op NBV eh
nefronfunksie, was renien die enigste waarvan verandering in plasmakonsentrasies
saamgeval het met die onderdrukking van NBV en GFS na aortaklemming. Die
ontwerp van ons studie het ons nie toegelaat om 'n besliste uitspraak te maak of die
geassosieerde verhoging in angiotensien II primêr verantwoordelik was vir die
verandering in renale hemodinamika, of dat die verhoogde renien (en angiotensien)
bloedvlakke moontlik sekondêr stimuleer is deur die verandering in NBV wat deur 'n
ander meganisme induseer is.
In 'n ander pasiëntegroep het ons aangetoon dat die kombinasie van mannitol en
dopamien geen beskerming verleen het teen die nadelige effekte van aorta-klemming
nie. Die groot volumes uriene wat uitgeskei is onder die invloed van hierdie middels
(wat nie korreleer het met NBV tydens ooreenstemmende periodes nie), het
inderwaarheid 'n ontoepaslike gerustheid uitgelok. Weens die ooglopende gebrek aan
objektiewe voordeel wat verleen word deur hierdie middels, behoort hulle gebruik
tydens hierdie kliniese omstandighede ontmoedig te word.
Die doel van die diere studies was die identifisering van die presiese rol van
angiotensien in die patogenese en patofisiologie van die renale veranderinge
geassosieer met infrarenale aortaklemming, sowel as die interaksie van angiotensien
met ander modulators waarvoor 'n interaktiewe verwantskap voorheen beskryf is onder
eksperimentele en/of kliniese omstandighede.
Die eerste studie het getoon dat alhoewel renien (en dus angiotensien) konsentrasies
hoog was na aorta-ontklemming, die hormone geen betekenisvolle patogenetiese of
patofisiologiese rol in die waargenome renale veranderinge gedurende hierdie
periode het nie (aangesien blokkade van angiotensien aktivering deur voorkoming van
renien vrystelling, of deur inhibisie van angiotensien omsettingsensiem (AOE), nie 'n
daling in NBV of GFS kon voorkom nie). Voorkoming van angiotensien II aktivering het
egter wel renale verandering voorkom gedurende aortaklemming. Dié voordelige
effek het nie 'n primêre rol vir angiotensien gedurende die periode bevestig nie,
aangesien die gunstige invloed ook (ten minste gedeeltelik) verduidelik kon word deur
die voorkoming van die fassiliterende invloed van angiotensien op ander vasokonstriktore en/of ander vasodilator-invloede van die onderdrukking van AOE en
ïs-blokkers (wat geen verband het met angiotensien of die blokkade daarvan nie). Die
studie het aangetoon dat (ten minste gedeeltelik) verskillende meganismes
verantwoordelik is vir renale veranderinge wat gesien is gedurende aortaklemming
en na -ontklemming.
Die tweede studie het die rol van kalsium in die renale patofisiologiese veranderinge
gedurende aortaklemming en na ontklemming ondersoek. Die beskermende
invloed wat deur die toediening van Ca2
+ -blokkers bewerkstellig is, het bevestig dat die
renale vasokonstriktoriese en glomerulêre patofisiologiese prosesse afhanklik is van
sellulêre influks van kalsium deur spannings-afhanklike kannale. Dit het ongelukkig
geen definitiewe insig verleen ten opsigte van die primêre inisieerders van die proses
nie. Dit verskaf nogtans 'n bruikbare kliniese metode om daardie veranderinge te
voorkom en die niere teen isgemiese besering gedurende abdominale aorta-chirurgie
te beskerm.
Die derde komponent van die diere-studies demonstreer die belangrikheid van die
beskermende effek van renale prostaglandiene tydens die spesifieke eksperimentele
(en waarskynlik ook die kliniese) omstandighede. Weereens gee dit nie definitiewe
inligting oor die bemiddelaars wat verantwoordelik is vir die renale veranderinge nie,
aangesien die skadelike effekte van verskeie endogene stowwe voorheen aangetoon
is om beperk of voorkom te word deur die intrarenale vrystelling van prostaglandiene.
Die omvang van die patofisiologiese en ultrastrukturele veranderinge wat ontstaan het
onder die invloed van nie-steroïed anti-inflammatoriese middels (wat gebruik is om
prostaglandien sintese te inhibeer), dui aan dat hierdie middels vermy moet word
onder soortelyke kliniese omstandighede.
Die laaste komponent van die studie verskaf 'n sterk aanduiding dat angiotensien slegs
'n sekondêre/aanvullende rol speel in die renale patofisiologiese proses, selfs
gedurende aortaklemming. Dit mag die weersprekende getuienis oor die potensiële
voordeel van AOE onderdrukking (op renale hemodinamika en glomerulêre funksie)
gedurende abdominale aortachirurgie (Licker et al. 1996, Colson et al. 1992a) verklaar.
Gebaseer op ons studies, kan AOE onderdrukking nie ondersteun word vir hierdie doel
nie.
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Macula Densa Derived Nitric Oxide and Kidney FunctionOllerstam, Anna January 2002 (has links)
<p>The kidney is the major organ regulating the extracellular fluid volume and thereby the arterial blood pressure. The neuronal isoform of nitric oxide synthase (nNOS) in the kidney is predominantly located in the macula densa cells. These cells are sensors for both renin release and the tubuloglomerular feedback mechanism (TGF), which is an important regulator of the glomerular filtration rate and afferent arteriole tone. The aim of this investigation was to elucidate the function of nNOS in the macula densa cells.</p><p>Acute nNOS inhibition in rats resulted in an increased TGF responsiveness and unchanged blood pressure while, after chronic inhibition, the TGF was normalised and the blood pressure was elevated. The plasma renin concentration was elevated in rats on long-term low salt diet, but was not significantly affected by chronic nNOS inhibition. On the other hand, nNOS inhibition for four days increased plasma renin concentration in rats treated with a low salt diet. The renal vasculature of rats exhibits a diminished renal blood flow and intracellular Ca2+ response to angiotensin II after one week blockade of nNOS while angiotensin II’s effect on the renal blood flow was abolished after four weeks treatment. Acute extracellular volume expansion diminish the TGF sensitivity thus assisting the elimination of excess fluid but after acute addition of nNOS inhibitor to volume expanded rats the TGF sensitivity restored.</p><p>In conclusion, the results from the present study suggest an important role for nNOS in the macula densa cells in the regulation of the arterial blood pressure and the modulation of the TGF response.</p>
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Macula Densa Derived Nitric Oxide and Kidney FunctionOllerstam, Anna January 2002 (has links)
The kidney is the major organ regulating the extracellular fluid volume and thereby the arterial blood pressure. The neuronal isoform of nitric oxide synthase (nNOS) in the kidney is predominantly located in the macula densa cells. These cells are sensors for both renin release and the tubuloglomerular feedback mechanism (TGF), which is an important regulator of the glomerular filtration rate and afferent arteriole tone. The aim of this investigation was to elucidate the function of nNOS in the macula densa cells. Acute nNOS inhibition in rats resulted in an increased TGF responsiveness and unchanged blood pressure while, after chronic inhibition, the TGF was normalised and the blood pressure was elevated. The plasma renin concentration was elevated in rats on long-term low salt diet, but was not significantly affected by chronic nNOS inhibition. On the other hand, nNOS inhibition for four days increased plasma renin concentration in rats treated with a low salt diet. The renal vasculature of rats exhibits a diminished renal blood flow and intracellular Ca2+ response to angiotensin II after one week blockade of nNOS while angiotensin II’s effect on the renal blood flow was abolished after four weeks treatment. Acute extracellular volume expansion diminish the TGF sensitivity thus assisting the elimination of excess fluid but after acute addition of nNOS inhibitor to volume expanded rats the TGF sensitivity restored. In conclusion, the results from the present study suggest an important role for nNOS in the macula densa cells in the regulation of the arterial blood pressure and the modulation of the TGF response.
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Aspects of Regulation of GFR and Tubular Function in the Diabetic Kidney : Roles of Adenosine, Nitric Oxide and Oxidative StressPersson, Patrik January 2013 (has links)
Diabetic nephropathy is the main cause for initiation of renal replacement therapy and early symptoms in patients include increased glomerular filtration rate (GFR), decreased oxygen tension and albuminuria, followed by a progressive decline in GFR and loss of kidney function. Experimental models of diabetes display increased GFR, decreased tissue oxygenation and nitric oxide bioavailability. These findings are likely to be intertwined in a mechanistic pathway to kidney damage and this thesis investigated their roles in the development of diabetic nephropathy. In vivo, diabetes-induced oxidative stress stimulates renal tubular Na+ transport and in vitro, proximal tubular cells from diabetic rats display increased transport-dependent oxygen consumption, demonstrating mechanisms contributing to decreased kidney oxygenation. In control animals, endogenous adenosine reduces vascular resistance of the efferent arteriole via adenosine A2-receptors resulting in reduced filtration fraction. However, in diabetes, adenosine A2-signalling is dysfunctional resulting in increased GFR via increased filtration fraction. This is caused by reduced adenosine A2a receptor-mediated vasodilation of efferent arterioles. The lack of adenosine-signaling in diabetes is likely due to reduced local adenosine concentration since adenosine A2a receptor activation reduced GFR only in diabetic animals by efferent arteriolar vasodilation. Furthermore, sub-optimal insulin treatment also alleviates increased filtration pressure in diabetes. However, this does not affect GFR due to a simultaneously induction of renal-blood flow dependent regulation of GFR by increasing the filtration coefficient. In diabetes, there is decreased bioavailability of nitric oxide, resulting in alterations that may contribute to diabetes-induced hyperfiltration and decreased oxygenation. Interestingly, increased plasma concentration of l-arginine, the substrate for nitric oxide production, prevents the development of increased GFR and proteinuria, but not increased oxygen consumption leading to sustained intra-renal hypoxia in diabetes. This thesis concludes that antioxidant treatment directed towards the NADPH oxidase as well maneuvers to promote nitric oxide production is beneficial in diabetic kidneys but is targeting different pathways i.e. transport-dependent oxygen consumption in the proximal tubule by NADPH oxidase inhibition and intra-renal hemodynamics after increased plasma l-arginine. Also, the involvement and importance of efferent arteriolar resistance in the development of diabetes-induced hyperfiltration via reduced adenosine A2a signaling is highlighted.
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Impact d’une sténose expérimentale de l’artère rénale sur le débit sanguin rénal et le contenu tissulaire en oxygène / Impact of an experimental renal artery stenosis on renal blood flow and oxygen contentRognant, Nicolas 13 December 2010 (has links)
La sténose de l’artère rénale (SAR) est à l’origine d’une néphropathie dite « ischémique », dont les mécanismes conduisant au développement d’une insuffisance rénale sont mal connus. Il est utile de savoir à partir de quel degré de SAR surviennent des modifications hémodynamiques significatives dans le rein d’aval, et si une SAR chronique et hémodynamiquement significative peut entraîner une hypoxie rénale. Nous avons donc entrepris 2 études afin de préciser le lien entre degré de SAR et baisse du débit sanguin rénal (DSR), et de rechercher l’apparition d’une hypoxie dans le rein situé en aval d’une SAR chronique. Les résultats de la première étude montrent que la baisse du DSR reste modeste tant que le degré de SAR n’a pas dépassé 70%. Ces résultats nous permettent de conclure qu’une SAR de degré inférieur à 70% n’est probablement associée qu’à des modifications hémodynamiques mineures dans le rein d’aval. Dans la deuxième étude, nous avons décrit l’évolution du contenu rénal en oxygène (CRO) sur une période de 4 semaines après induction d’une SAR chez des rats. La méthode utilisée était l’IRM BOLD, qui permet d’étudier le CRO de manière non-invasive en mesurant le paramètre R2* dont la valeur est inversement proportionnelle au CRO. La mesure hebdomadaire de R2* dans le cortex, la médullaire externe et la partie externe de la médullaire externe des reins sténosés et des reins controlatéraux ne variaient pas au cours de l’étude, malgré l’apparition progressive d’une atrophie des reins en aval de la SAR. Ces données tendent à montrer qu’il n’y a pas d’hypoxie rénale dans notre modèle, et que l’atrophie rénale observée n’est donc pas secondaire à l’hypoxie / Renal artery stenosis (RAS) can lead to a so-called “ischemic” nephropathy but the mechanisms responsible for the development of chronic kidney disease in kidney downstream the RAS are largely unknown. There is an interest to know the degree of RAS that involves significant hémodynamic changes in the downstream kidney and if hypoxia occurs in this case. Therefore, we have undertaken two studies in order to describe the link between RAS degree and renal blood flow (RBF) and to search for the development of renal hypoxia in kidney downstream the RAS. Findings of the first study were that only a minor decrease of RBF occurs until the RAS degree reach 70%. We can thus conclude from these results that RAS degree must be at least of 70% to have hemodynamical repercussions in downstream kidney. In the second study, we describe the evolution of renal oxygen content (ROC) before and during 4 weeks after the constitution of RAS. ROC was measured weekly by the MRI BOLD technique, who allows to study ROC non-invasively by measuring the parameter called R2* that is inversely proportional to ROC. The value of R2* in the cortex, the outer medulla and the outer stripe of outer medulla in stenotic kidneys and controlateral kidneys was unchanged instead the development of atrophy of the kidney downstream the RAS. These results suggest that no renal hypoxia occur in this model and that renal atrophy is not caused by hypoxia
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