Potential mechanisms mediating postprandial renal hyperemia and hyperfiltration

Premen, A. J.

doi:10.1096/fasebj.2.2.3277887

Cited by 53 publications

(31 citation statements)

References 35 publications

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“…The PVBF increases postprandially. 27 Whether the correspondent postprandial diuresis may, in part, result from the increases in PVBF is unclear. The effect of increased PVBF on renal function has not, however, been assessed, but a lack of baseline effect caused by hepatic denervation or adenosine receptor blockade in rats with normal PVBF suggests a lack of basal reflex tone.…”

Section: Discussionmentioning

confidence: 99%

Decreases in portal flow trigger a hepatorenal reflex to inhibit renal sodium and water excretion in rats: Role of adenosine

2002

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The regulation of renal sodium and water excretion through a hepatorenal reflex activated by the changes in hemodynamics of the portal circulation has been suggested. We hypothesize that the changes in intrahepatic blood flow and flow-related intrahepatic adenosine are involved in the control of renal water and sodium excretion by triggering a hepatorenal reflex. Anesthetized rats were instrumented to monitor the systemic, hepatic, and renal circulation. A vascular shunt connecting the portal vein and central vena cava was established to allow for control of the portal venous blood flow (PVBF). Urine was collected from the bladder. The effects of decreased PVBF on renal water and sodium excretion were compared in normal and hepatic denervated rats. T he liver is involved in the regulation of renal excretion of sodium and water. [1][2][3][4][5] In this regard, the existence of a hepatorenal reflex to regulate urine production has been suggested. Lang et al. observed in a rat model that infusion of glutamine into the liver induced a hepatic and renal nerve-dependent reduction in renal glomerular filtration rate (GFR), renal plasma flow, and urine production. Other studies have also suggested that the activation of hepatic afferent nerves could result in the activation of renal sympathetic nerves to regulate renal function in health and diseases. [6][7][8][9][10] The changes in the hemodynamics of hepatic portal circulation have been considered as the major event in triggering the hepatorenal reflex. Theoretically, both increased portal veous blood pressure (PVP) and decreased portal venous blood flow (PVBF) could be the initial event that triggers the hepatorenal reflex. [3][4][5][6] Previous studies have been interpreted to indicate that PVP is the major event responsible for the triggering of the observed activation of the hepatorenal reflex. However, the maneuvers used in those studies to increase PVP unavoidably decreased or even stopped intrahepatic PVBF, leaving the issue unresolved. Moreover, an increased PVP as the trigger of the hepatorenal reflex would represent a positive-feedback mechanism, in which fluid retention would lead to an elevated PVP in healthy livers that would then result in more fluid retention. Little is known about the contribution of decreased intrahepatic PVBF in the regulation of renal water and sodium excretion.Thus, we tested the hypothesis that intrahepatic PVBF is involved in the regulation of renal water and sodium excretion. The experiments were performed in two different animal models: intrahepatic PVBF was reduced either by the portacaval shunt or by ligation of the superior mesenteric artery (SMA). The results revealed that renal water and sodium excretion were significantly decreased after reducing intrahepatic PVBF. The mechanism may relate to the flow-dependent accumulation of adenosine within the liver, triggering a hepatorenal reflex. Materials and Methods Surgical PreparationMale Sprague-Dawley rats weighing 260 to 300 g were maintained in the animal house under contro...

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Section: Discussionmentioning

confidence: 99%

Decreases in portal flow trigger a hepatorenal reflex to inhibit renal sodium and water excretion in rats: Role of adenosine

2002

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“…Indeed, the postprandial state is characterized by decreased catecholamine and increased insulin, secretin, and cholecystokinin secretion, which increase GFR and thereby decrease sodium, calcium, and phosphorus reabsorption. [23][24][25] Although further studies are needed to explore this hypothesis, we speculate that increased urinary calcium and phosphorus excretion in the early postprandial period is nonspecific and could represent an innate, loosely regulated renal adaptation that prevents rapid and potentially dangerous increases in serum calcium and phosphorus (and potassium) levels that would otherwise be induced by dietary intake.…”

Section: Clinical Research Wwwjasnorgmentioning

confidence: 97%

Postprandial Mineral Metabolism and Secondary Hyperparathyroidism in Early CKD

Isakova¹,

Gutiérrez²,

Shah³

et al. 2008

Journal of the American Society of Nephrology

142

124

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Normophosphatemia and normocalcemia are maintained in chronic kidney disease (CKD) by increased levels of fibroblast growth factor-23 (FGF-23) and parathyroid hormone (PTH), but the stimuli for secretion of these hormones in early CKD are incompletely understood. Most human physiologic studies have focused on random or fasting measurements of phosphorus, calcium, FGF-23, and PTH, but in this study, the hypothesis was that measurements in the postprandial state may reveal intermittent stimuli that lead to increased FGF-23 and PTH levels. The 4-h postprandial response in 13 patients with CKD and fasting normophosphatemia and normocalcemia (mean GFR 41 Ϯ 8 ml/min per m 2 ) was compared with 21 healthy volunteers. Compared with healthy subjects, fasting patients with CKD had significantly higher levels of FGF-23 and fractional excretion of phosphorus; lower fractional excretion of calcium; and no difference in serum calcium, phosphorus, and PTH levels. After standardized meals, urinary phosphorus excretion in both groups increased despite unchanged serum phosphorus and FGF-23 levels. Postprandial urinary calcium excretion also increased in both groups, and this was accompanied by significantly reduced serum calcium and increased PTH levels in patients with CKD only; therefore, FGF-23 does not seem to be an acute postprandial regulator of phosphaturia in CKD or in health, but inappropriate postprandial calciuria with episodic, relative hypocalcemia may represent a previously unreported mechanism of secondary hyperparathyroidism in CKD.

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“…This decrease in filtration fraction is caused by preferential efferent arteriolar vasodilatation, causing an increase in renal blood flow, a decrease in renal vascular resistance and little effect on glomerular filtration rate (Wang, Y.-W. et al, 1992). The restoration or potentiation of the tubuloglomerular feedback mechanism by dopamine probably plays a significant role in the reversal of hyperfiltration in these models (Premen, 1988;Schnermann et al, 1990).…”

Section: Glycerol-induced Arfmentioning

confidence: 99%

Regional haemodynamic effects of dopamine and its prodrugs l‐dopa and gludopa in the rat and in the glycerol‐treated rat as a model for acute renal failure

Drieman

Kan

Thijssen

et al. 1994

British J Pharmacology

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1 In this study the renal selectivity of dopamine and its prodrugs L-dopa and gludopa, with respect to their effects on regional blood flow, vascular resistance and central haemodynamics was investigated in normal rats and in rats with glycerol-induced acute renal failure (ARF). 2 In normal, anaesthetized rats, dopamine as well as its prodrugs caused a dose-dependent reduction of vascular resistance in the kidney (RR), mesentery (MR) and hindquarters (HQR) (dose range: dopamine: 0. 1-5 ftmol kg-' h-i; L-dopa and gludopa: 1 -200 pmol kg'-h-'). Blood pressure and heart rate were affected at the highest dose only. 3 Administration of glycerol induced a preferential renal vasoconstriction; renal blood flow (-60%) and vascular resistance (+ 190%) were significantly more affected than MR (+40%) and HQR (+ 60%). This was only ameliorated by a low rate (10 pmol kg-' h-') infusion of gludopa: the glycerolinduced reduction of renal flow and increase in RR were significantly attenuated. A high dose of gludopa (100 gmol kg-' h-') or any dose of L-dopa or dopamine did not induce this beneficial effect. The glycerol-induced increase in MR and HQR was not attenuated by any of the treatments used. 4 The results indicate that gludopa is not renally selective at a pharmacodynamic level in normal, anaesthetized rats. Contrary to this, a low dose of gludopa does cause a renal selective vasodilatation and reduction of RR in rats with glycerol-induced ARF. This difference could be explained by a difference in renal vascular tone between normal rats and glycerol-induced ARF rats. A high dose of gludopa does not cause these renal-selective effects: renal resistance and renal flow are at the same level as following glycerol and saline. This is probably due to the systemic effects of the released dopamine.

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Potential mechanisms mediating postprandial renal hyperemia and hyperfiltration

Cited by 53 publications

References 35 publications

Decreases in portal flow trigger a hepatorenal reflex to inhibit renal sodium and water excretion in rats: Role of adenosine

Decreases in portal flow trigger a hepatorenal reflex to inhibit renal sodium and water excretion in rats: Role of adenosine

Postprandial Mineral Metabolism and Secondary Hyperparathyroidism in Early CKD

Regional haemodynamic effects of dopamine and its prodrugs l‐dopa and gludopa in the rat and in the glycerol‐treated rat as a model for acute renal failure

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