Autoregulation and non‐homeostatic behaviour of renal blood flow in conscious dogs.

Persson, Pontus B.; Ehmke, Heimo; Kirchheim, H. R.; Janssen, Bart; Baumann, J.; Just, Armin; Nafz, B.

doi:10.1113/jphysiol.1993.sp019554

Cited by 32 publications

(19 citation statements)

References 21 publications

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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: 78%

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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Section: Consequences Of Impaired Renal Autoregulation On Volume Homesupporting

confidence: 78%

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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“…Pressure autoregulation of blood flow has long been recognized as an important factor in volume-dependent forms of hypertension (Guyton, Granger & Coleman, 1971), and the conscious areflexic rat has successfully been used to quantify autoregulatory responses to changes in blood volume (Hinojosa-Laborde, Greene & Cowley, 1988;Hinojosa-Laborde, Frohlich & Cowley, 1991). However, as far as we know, there have been no previous studies describing the spontaneous occurrence of short-term autoregulatory changes in the systemic or regional circulations of conscious animals, although in some (Persson et al 1993), but not all (Skarlatos et al 1993), studies an autoregulatory-like pressure-flow pattern was suggested in the renal circulation of conscious dogs. The latency of autoregulatory responses suggested by the present experiments is much shorter than that measured in vitro (VanBavel, Giezeman, Mooij & Spaan, 1991) or in vivo in anaesthetized animals (Borgdorff, 1983).…”

Section: Discussionmentioning

confidence: 93%

Short‐term haemodynamic variability in the conscious areflexic rat

Létienne

Barrès

Cerutti

et al. 1998

The Journal of Physiology

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Similtaneous measurements of arterial pressure and cardiac output (n= 8), mesenteric blood flow (n= 7) or hindquarters (n= 8) blood flow were performed during 1 h periods in conscious rats, before and after acute pharmacological blockade of the autonomic, renin‐angiotensin and vasopressin systems. In the latter condition (areflexic state), arterial pressure was maintained with a continuous infusion of noradrenaline. In the areflexic state, spontaneous fluctuations in arterial pressure were markedly exaggerated, especially depressor episodes. At the onset of these falls in arterial pressure, there was an abrupt and transient decrease in stroke volume and cardiac output. Systemic vasodilatation then developed while cardiac output returned to normal. Regional vasodilatations were also delayed from the onset of the falls in arterial pressure and were usually large enough to maintain blood flow. Both time and frequency domain analyses confirmed that changes in systemic and regional vascular conductances lagged by about 1 s behind arterial pressure changes. These results indicate that, in the absence of neurohumoral influences, autoregulatory‐like mechanisms become dominant in the control of systemic and regional circulations and contribute to exaggeration of the spontaneous short‐term variability of arterial pressure.

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“…While renal blood flow significantly increased in response to hypervolaemia and isovolaemic anaemia, total renal oxygen supply remained at its baseline level in all three experimental groups. Data are represented as a percentage of control, because baseline renal blood flows varied considerably from dog to dog (from 144 to 426 ml min-') as observed in a previous investigation from this laboratory (Persson et al 1993). The absolute control values of renal blood flow were 261 + 19 ml min-(hypovolaemia; n = 6), 319 + 35 ml min-' (hypervolaemia; n = 6), and 245 + 11 ml min-' (isovolaemic anaemia; n = 4).…”

Section: Time Controlmentioning

confidence: 99%

Modulation of erythropoietin formation by changes in blood volume in conscious dogs.

Ehmke

Just

Eckardt

et al. 1995

The Journal of Physiology

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1. A possible influence of the filling of the circulatory system on the plasma concentration of erythropoietin, which is the major regulator of erythrocyte formation, was investigated in conscious dogs. 2. Over an experimental period of 5 h, the animals were subjected to either haemorrhage (hypovolaemia), blood volume expansion (hypervolaemia), or exchange transfusion of blood with dextran (isovolaemic anaemia). 3. A reduction of blood volume by 20 % induced by haemorrhage increased plasma erythropoietin levels -1 5-fold in the absence of significant changes in haematocrit. 4. An expansion of blood volume by 12 % induced by an intravenous infusion of dextran did not change plasma erythropoietin levels, although the haematocrit decreased by 0 04. 5. A reduction of the haematocrit by 0-12 in the absence of changes in blood volume induced by an isovolaemic exchange transfusion (dextran vs. blood) increased plasma erythropoietin levels -3-fold. 6. 7.Total renal oxygen supply did not change in any of the three experimental protocols. These data indicate that in dogs the erythropoietin production rate is modulated by changes in blood volume, and suggest a possible role of erythropoietin in the regulation of blood volume.The cardiovascular system responds very sensitively to small alterations in blood volume. Studies in dogs have shown that an expansion of blood volume by less than 10 % caused by an elevated renal reabsorption of fluid is sufficient to raise blood pressure by 20-30 mmHg within a few days

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Autoregulation and non‐homeostatic behaviour of renal blood flow in conscious dogs.

Cited by 32 publications

References 21 publications

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

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

Short‐term haemodynamic variability in the conscious areflexic rat

Modulation of erythropoietin formation by changes in blood volume in conscious dogs.

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