Spontaneous renal blood flow autoregulation curves in conscious sinoaortic baroreceptor-denervated rats

Pires, S.L.S.; Julien, Claude; Chapuis, Bruno; Sassard, J; Barrès, Christian

doi:10.1152/ajprenal.0186.2001

Cited by 22 publications

(26 citation statements)

References 28 publications

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“…A striking time-associated variability of RBF was observed at any given BP in individual rats in the present study, which has also been observed previously (58,70,81). Nevertheless, despite this variability in RBF, the BP-RBF bin analysis in the present study (Fig.…”

Section: Discussionsupporting

confidence: 90%

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Polichnowski

Griffin

Long

et al. 2013

American Journal of Physiology-Renal Physiology

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Polichnowski AJ, Griffin KA, Long J, Williamson GA, Bidani AK. Blood pressure-renal blood flow relationships in conscious angiotensin II-and phenylephrine-infused rats. Am J Physiol Renal Physiol 305: F1074 -F1084, 2013. First published July 3, 2013 doi:10.1152/ajprenal.00111.2013.-Chronic ANG II infusion in rodents is widely used as an experimental model of hypertension, yet very limited data are available describing the resulting blood pressurerenal blood flow (BP-RBF) relationships in conscious rats. Accordingly, male Sprague-Dawley rats (n ϭ 19) were instrumented for chronic measurements of BP (radiotelemetry) and RBF (Transonic Systems, Ithaca, NY). One week later, two or three separate 2-h recordings of BP and RBF were obtained in conscious rats at 24-h intervals, in addition to separate 24-h BP recordings. Rats were then administered either ANG II (n ϭ 11, 125 ng·kg Ϫ1 ·min Ϫ1 ) or phenylephrine (PE; n ϭ 8, 50 mg·kg Ϫ1 ·day Ϫ1 ) as a control, ANG IIindependent, pressor agent. Three days later the BP-RBF and 24-h BP recordings were repeated over several days. Despite similar increases in BP, PE led to significantly greater BP lability at the heart beat and very low frequency bandwidths. Conversely, ANG II, but not PE, caused significant renal vasoconstriction (a 62% increase in renal vascular resistance and a 21% decrease in RBF) and increased variability in BP-RBF relationships. Transfer function analysis of BP (input) and RBF (output) were consistent with a significant potentiation of the renal myogenic mechanism during ANG II administration, likely contributing, in part, to the exaggerated reductions in RBF during periods of BP elevations. We conclude that relatively equipressor doses of ANG II and PE lead to greatly different ambient BP profiles and effects on the renal vasculature when assessed in conscious rats. These data may have important implications regarding the pathogenesis of hypertension-induced injury in these models of hypertension.hypertension; hemodynamics; blood pressure variability INCREASED ACTIVITY OF THE renin-angiotensin-aldosterone system (RAAS) (40,56,73) is postulated to be a major contributor to chronic kidney disease progression through both blood pressure (BP)-dependent and -independent mechanisms (7,28,39,73). Accordingly, chronic ANG II infusion is extensively used to investigate mechanisms that mediate renal damage in hypertensive states characterized by enhanced RAAS activation (3,20,42,65,71). Renal parenchymal injury with significant tubulointerstitial fibrosis and a propensity to develop salt-sensitive hypertension has been observed after ANG II infusions (44, 57). Both barotrauma and renal vasoconstrictionmediated tissue ischemia have been postulated to initiate the pathogenic cascades that lead to renal injury after chronic ANG II infusions. However, despite its wide use, there is a paucity of experimental data describing the BP-renal blood flow (RBF) relationships in conscious ANG II-infused animals, and the relative contribution of these two initiating mechanisms ...

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Section: Discussionsupporting

confidence: 90%

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Polichnowski

Griffin

Long

et al. 2013

American Journal of Physiology-Renal Physiology

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“…7, which depicts the variations in RBF and BP seen over a 2-h period in a conscious, unrestrained rat. Similar observations are reported by other laboratories (120,123,142,143). Such temporal variability may reflect the influence of neurohormonal and metabolic inputs (Fig.…”

Section: Consequences Of Impaired Renal Autoregulation On Volume Homesupporting

confidence: 89%

Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms

Loutzenhiser

Griffin²,

Bidani³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

238

244

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dani. Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms. Am J Physiol Regul Integr Comp Physiol 290: R1153-R1167, 2006. doi:10.1152/ajpregu.00402.2005.-When the kidney is subjected to acute increases in blood pressure (BP), renal blood flow (RBF) and glomerular filtration rate (GFR) are observed to remain relatively constant. Two mechanisms, tubuloglomerular feedback (TGF) and the myogenic response, are thought to act in concert to achieve a precise moment-by-moment regulation of GFR and distal salt delivery. The current view is that this mechanism insulates renal excretory function from fluctuations in BP. Indeed, the concept that renal autoregulation is necessary for normal renal function and volume homeostasis has long been a cornerstone of renal physiology. This article presents a very different view, at least regarding the myogenic component of this response. We suggest that its primary purpose is to protect the kidney against the damaging effects of hypertension. The arguments advanced take into consideration the unique properties of the afferent arteriolar myogenic response that allow it to protect against the oscillating systolic pressure and the accruing evidence that when this response is impaired, the primary consequence is not a disturbed volume homeostasis but rather an increased susceptibility to hypertensive injury. It is suggested that redundant and compensatory mechanisms achieve volume regulation, despite considerable fluctuations in distal delivery, and the assumed moment-by-moment regulation of renal hemodynamics is questioned. Evidence is presented suggesting that additional mechanisms exist to maintain ambient levels of RBF and GFR within normal range, despite chronic alterations in BP and severely impaired acute responses to pressure. Finally, the implications of this new perspective on the divergent roles of the myogenic response to pressure vs. the TGF response to changes in distal delivery are considered, and it is proposed that in addition to TGF-induced vasoconstriction, vasodepressor responses to reduced distal delivery may play a critical role in modulating afferent arteriolar reactivity to integrate the regulatory and protective functions of the renal microvasculature. renal microcirculation; afferent arteriole; myogenic; tubuloglomerular feedback ONE OF THE MOST STRIKING CHARACTERISTICS of the renal circulation is the ability of the kidney to maintain a constant renal blood flow (RBF) and glomerular filtration rate (GFR) as renal perfusion pressure is altered. The dual regulation of both RBF and GFR is achieved by proportionate changes in the preglomerular resistance and is believed to be mediated by two mechanisms, tubuloglomerular feedback (TGF) and the renal myogenic response. TGF involves a flow-dependent signal that is sensed at the macula densa and alters tone in the adjacent segment of the afferent arteriole via a mechanism that remains controversial but likely involves adenosine and/or ATP (30,80,144). The myo...

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“…This occurs via dilation or constriction in response to alterations in blood pressure, which incite changes in circumferential wall tension. The active myogenic response closely follows an initial passive distension, as has been observed in a multitude of experimental studies (5,11,19,26,27,30,32,39,45,58,61,63).…”

Section: Vessel Modelsupporting

confidence: 69%

“…9B), with a non-zero gradient of flow with respect to pressure in the autoregulatory range due to the omission of TGF from the model. This corresponds well to data from the experimental scenario that most closely simulates the condition of purely myogenic renal autoregulation (45). To prevent bias, this data set was not used to determine the parameters used in the mathematical system.…”

Section: Whole-organ Autoregulationmentioning

confidence: 57%

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Dynamic myogenic autoregulation in the rat kidney: a whole-organ model

Kleinstreuer¹,

Todem²,

Plank³

et al. 2008

American Journal of Physiology-Renal Physiology

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Kleinstreuer N, David T, Plank MJ, Endre Z. Dynamic myogenic autoregulation in the rat kidney: a whole-organ model. Am J Physiol Renal Physiol 294: F1453-F1464, 2008. First published March 19, 2008 doi:10.1152/ajprenal.00426.2007.-A transient 1D mathematical model of whole-organ renal autoregulation in the rat is presented, examining the myogenic response on multiple levels of the renal vasculature. Morphological data derived from micro-CT imaging were employed to divide the vasculature via a Strahler ordering scheme. A previously published model of the myogenic response based on wall tension is expanded and adapted to fit the response of each level, corresponding to a distally dominant resistance distribution with the highest contributions localized to the afferent arterioles and interlobular arteries. The mathematical model was further developed to include the effects of in vivo viscosity variation and flow-induced dilation via endothelial nitric oxide production. Computer simulations of the autoregulatory response to pressure perturbations were examined and compared with experimental data. The model supports the hypothesis that change in circumferential wall tension is the catalyst for the myogenic response. The model provides a basis for examining the steady state and transient characteristics of the whole-organ renal myogenic response in the rat, as well as the modulatory influences of metabolic and hemodynamic factors.renal; myogenic response THE MYOGENIC RESPONSE, a pressure-induced constriction or dilation of the vasculature first discovered 100 years ago by Bayliss, is now known to exist throughout the body (28). It is crucial in establishing basal arterial tone and maintaining a relatively constant blood supply to major organs, a phenomenon known as autoregulation (13). There are two key autoregulatory mechanisms in the kidney, the tubuloglomerular feedback (TGF) loop, which monitors NaCl delivery and filtration rate and adjusts afferent arteriolar resistance accordingly, and the myogenic response, which is the focus of current research and exists to varying degrees throughout the renal vasculature. Together, these two mechanisms account for ϳ90% of renal autoregulation, with 50% attributed to the myogenic component (30,31,39). The estimation of this regulatory balance is based on an assumed linearity of the system and is subject to variations due to observed nonlinear interactions among mechanisms (41,42,62). Other possible mechanisms, with less impact and longer time courses, could be attributed to metabolic catalysts, sympathetic stimulation, or various other causes.The myogenic response features predominantly in the small arteries and arterioles which make up the majority of peripheral resistance in the vasculature; this adjusts the vascular smooth muscle (VSM) tone, and hence diameter, to provide dynamic regulation of blood flow. The cellular mechanisms by which the myogenic response operates have been extensively studied (13,23,26,50,52). There is general agreement that an alteration in circumf...

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Spontaneous renal blood flow autoregulation curves in conscious sinoaortic baroreceptor-denervated rats

Cited by 22 publications

References 28 publications

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Renal autoregulation: new perspectives regarding the protective and regulatory roles of the underlying mechanisms

Dynamic myogenic autoregulation in the rat kidney: a whole-organ model

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