Role of Hepatic Receptors in Controlling Body Fluid Homeostasis.

Morita, Hironobu; Matsuda, Tsunenori; Tanaka, Kunihiko; Hara, Hiroshi

doi:10.2170/jjphysiol.45.355

Cited by 19 publications

(13 citation statements)

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“…The surge of glucagon disagrees with the previous canine studies in which portal glucagon did not increase in either method of delivery over 3 h (14,22). Presumably, the instantaneous glucagon response to isotonic saline via the portal route is due to the stress or the load of the isotonic saline at 1.0 ml/h in rats, since putative baroreceptors have been reported to exist in the hepatoportal region (23). Because glucose infusion with insulin release could have suppressed the glucagon release, the difference in portal glucagon between Po and Pe may also be partly attributed to the animals being stressed.…”

contrasting

confidence: 94%

Characterization of the portal signal during 24-h glucose delivery in unrestrained, conscious rats

Ogihara¹,

Kawamura²,

Kasuga³

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

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To characterize the "portal signal" during physiological glucose delivery, liver glycogen was measured in unrestrained rats during portal (Po) and peripheral (Pe) constant-rate infusion, with minimal differences in hepatic glucose load (HGL) and portal insulin between the delivery routes. Hepatic blood flows were measured by Doppler flowmetry during open surgery. Changes in hepatic glucose, portal insulin, glucagon, lactate, and free fatty acid concentrations were generally similar in either delivery except for glucagon at 4 h. Hepatic glycogen, however, increased continuously in Po and was higher than Pe at 8 and 24 h, although it decreased to the level of Pe upon the removal of Po at 8 h. There was a near-linear relationship between hepatic glycogen and HGL in either delivery, with the slope being twice as high in Po and the intercepts converging to basal HGL. The hepatic response to Po did not alter upon 80% replacement by Pe. These results suggest that negative arterial-portal glucose gradients increase the rate of hepatic glycogen synthesis against the incremental HGL in an all-or-nothing mode.hepatic glycogen synthesis; hepatic glucose load; negative arterialportal glucose gradients; nonsteady state IT HAS BEEN WELL DOCUMENTED that portal glucose delivery (Po) creates an important signal to enhance net hepatic glucose uptake (NHGU) or hepatic glycogen deposition in rodents (6, 9, 33), dogs (1-3, 14, 24, 25, 29 -31), and humans (8). Evidence has shown that NHGU is dependent on hepatic glucose load (HGL), plasma insulin concentration, and negative arterial-portal (A-P) glucose gradients. Adkins et al. (1) and have shown that a negative A-P gradient might serve as the portal signal, whereas Pagliassotti et al. (31) found that the magnitude of NHGU is dependent on the magnitude of the A-P gradients. On the other hand, Myers and colleagues (24,25) demonstrated that NHGU is linearly related to HGL, whereas it is curvilinearly related to the plasma insulin concentration, and that the hepatic response to Po results in a leftward shift in the dose-response relationship. These results have been obtained under hyperglycemic hyperinsulinemic and/or pancreatic clamp conditions, where the concentration of plasma glucose, that of insulin, or the negative A-P gradients were varied while the other two conditions were held fixed. Therefore, the relationship within these parameters remains unsettled in the nonsteady hyperglycemic state. Moore et al. (22) showed that, even in the absence of somatostatin and fixed hormone concentrations, the portal signal acts to stimulate NHGU during glucose infusion at a constant rate in dogs. In a similar experiment, we (28) also observed that there was a linear relationship between NHGU and HGL in either method of delivery, with the slope being four times steeper in Po and the HGL intercepts converging to near-basal values. We hypothesized from these results that the portal signal might increase the slope for NHGU against HGL.Therefore, the aim of the present study was to prove the hypo...

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contrasting

confidence: 94%

Characterization of the portal signal during 24-h glucose delivery in unrestrained, conscious rats

Ogihara¹,

Kawamura²,

Kasuga³

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

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“…The sensory function of the liver and its contribution to the maintenance of body-fluid homeostasis through the hepatorenal reflex has been suggested in animals and humans. 3,4,25,26 The present study provides a novel negative-feedback mechanism for the liver to regulate the balance of body blood volume by sensing the changes in its portal blood flow and then initiating a hepatorenal reflex to regulate renal water-sodium excretion. By sensing the changes in PVBF, the flow-related hepatorenal reflex may adjust the rate of urine production in a manner that tends to normalize portal blood flow.…”

Section: Discussionmentioning

confidence: 94%

“…An activated hepatorenal reflex, with an increased discharge from both hepatic afferent and renal efferent nerves, triggered through the activation of chemo-or mechanoreceptors in the hepatic portal circulation, has been suggested to activate renal sympathetic nerves. [1][2][3][4][5] This would lead to a reduction of urine flow rate. In this regard, previous studies have concluded that the increase in intrahepatic sinusoidal pressure was the event responsible for triggering the hepatorenal reflex in cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

“…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.…”

mentioning

confidence: 99%

“…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.…”

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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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Contribution of hepatic adenosine A1 receptors to renal dysfunction associated with acute liver injury in rats†

et al. 2006

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Acute liver injury is associated with renal insufficiency, whose mechanism may be related to activation of the hepatorenal reflex. We previously showed that intrahepatic adenosine is involved in activation of the hepatorenal reflex to restrict urine production in both healthy rats and in rats with cirrhosis. The aim of the present study was to test the hypothesis that activation of intrahepatic adenosine receptors is involved in the pathogenesis of the renal insufficiency seen in acute liver injury. Acute liver injury was induced by intraperitoneal injection of thioacetamide (TAA, 500 mg/kg) in rats. The animals were instrumented 24 hours later to monitor systemic, hepatic, and renal circulation and urine production. Severe liver injury developed following TAA insult, which was associated with renal insufficiency, as demonstrated by decreased (approximately 25%) renal arterial blood flow, a lower (approximately 30%) glomerular filtration rate, and decreased urine production. Further, the increase in urine production following volume expansion challenge was inhibited. Intraportal, but not intravenous, administration of a nonselective adenosine receptor antagonist, 8-phenyltheophylline, improved urine production. To specify receptor subtype, the effects of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, an adenosine A(1) receptor antagonist) and 3,7-dimethyl-1-propargylxanthine (DMPX, an adenosine A(2) receptor antagonist) were compared. Intraportal but not intravenous administration of DPCPX greatly improved impaired renal function induced by acute liver injury, and this beneficial effect was blunted in rats with liver denervation. In contrast, neither intraportal nor intravenous administration of DMPX showed significant improvement in renal function. In conclusion, an activated hepatorenal reflex, triggered by intrahepatic adenosine A(1) receptors, contributed to the pathogenesis of the water and sodium retention associated with acute liver injury.

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Role of Hepatic Receptors in Controlling Body Fluid Homeostasis.

Cited by 19 publications

References 0 publications

Characterization of the portal signal during 24-h glucose delivery in unrestrained, conscious rats

Characterization of the portal signal during 24-h glucose delivery in unrestrained, conscious rats

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

Contribution of hepatic adenosine A1 receptors to renal dysfunction associated with acute liver injury in rats†

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