Relationship Between Activation of the Sympathetic Nervous System and Renal Blood Flow Autoregulation in Cirrhosis

Stadlbauer, Vanessa; Wright, Gavin; Banaji, Murad; Mukhopadhya, Ashis; Mookerjee, Rajeshwar P.; Moore, Kevin; Jalan, Rajiv

doi:10.1053/j.gastro.2007.10.055

Cited by 179 publications

(131 citation statements)

References 38 publications

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“…Although relatively few studies have evaluated this pathway in cirrhotic patients, improved renal function and lowered noradrenaline overflow from the kidney have been observed when the intrahepatic pressure is reduced in cirrhotic patients. 69,70 These observations are consistent with the notion that the hepatoportal baroreflex contributes to increased renal sympathetic nerve activity.…”

Section: Liver Cirrhosissupporting

confidence: 89%

Negative feedforward control of body fluid homeostasis by hepatorenal reflex

Morita

Abe

2011

Hypertens Res

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The liver, well known for its role in metabolism, clearance and storage can also be regarded as a sensory organ. The liver is an ideal place to monitor the quality and quantity of absorbed substances, because portal blood delivers substances absorbed from the intestine to the liver and these substances circulate in the hepatic vasculature before substances enter the systemic circulation. Sodium (Na + )-sensitive mechanism exists in the liver; it is stimulated by the increase in Na + concentration in the portal vein, and then hepatorenal reflex is triggered. Renal sympathetic nerve activity is reflexively decreased and urinary Na + excretion is increased. This Na + -sensitive hepatorenal reflex has a significant role in post-prandial natriuresis. However, the long-term role of this reflex in Na + homeostasis may be less important, probably because of the desensitization of Na + -sensitive mechanisms. Na + -K + -2Cl -cotransporter (NKCC1) is involved in the hepatoportal Na + -sensitive mechanism, and NKCC1 expression is reduced if the hepatoportal region is exposed to high Na + concentrations for a long time. This situation occurs when animals intake a high-sodium chloride diet for a long time. Liver cirrhosis also impairs the Na + -sensitive hepatorenal reflex. Hepatoportal baroreceptor-induced renal sympathetic excitation and the impaired Na + -sensitive hepatorenal reflex may partially explain the Na + retention in liver cirrhosis. Keywords: hepatorenal reflex; hepatic afferent nerve; liver cirrhosis; post-prandial natriuresis; renal sympathetic nerve It is well documented that the mammalian liver is not only a metabolic, clearance and storage organ but also contains many receptors, including osmoreceptors, 1,2 baroreceptors 3,4 and ionic receptors. [5][6][7] Given the roles that these receptors have in the systemic circulation, it is possible that they are also involved in the regulation of body fluid homeostasis. A growing body of evidence suggests that the osmoreceptors and ionic receptors in the liver and its vasculature detect a variety of physiological events and are responsible for the activation of a number of physiological responses, which may have important roles in the regulation of body fluid homeostasis. The important features of the hepatic sensor mechanism are: (1) substances consumed orally are absorbed from the intestine into the blood, circulate in the hepatic vasculature and then enter the systemic circulation; and (2) the portal venous blood flow is 20-25% of the cardiac output. Because of these features, the hepatic osmoreceptors and ionic receptors have advantages over those receptors located in the systemic circulation. First, the hepatic receptors are triggered by changes in portal venous osmolality and ionic concentration before any changes occur in the systemic blood, and then reflexively regulate renal excretion and intestinal absorption. 7-10 Second, the concentrations of the absorbed substances in the hepatoportal region and the changes in them are 4-5 times greater than those in th...

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Section: Liver Cirrhosissupporting

confidence: 89%

Negative feedforward control of body fluid homeostasis by hepatorenal reflex

Morita

Abe

2011

Hypertens Res

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“…In patients with decompensated cirrhosis, the main abnormality causing renal dysfunction is systemic and splanchnic vasodilatation secondary to portal (or sinusoidal) hypertension that leads to decreased effective arterial blood volume and activation of neurohormonal systems, the rennin-angiotensin aldosterone (RAAS), the sympathetic nervous system, and non-osmotic release of antidiuretic hormone, resulting in sodium and water retention [76][77][78]. Eventhough the systemic hemodynamic alterations in ACLF are similar to patients with decompensated cirrhotics [79], the pathogenesis of renal dysfunction in ACLF is quite different in these patients as a major role is played by SIRS and subsequent sepsis [80].…”

Section: Renal Failurementioning

confidence: 99%

Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific Association for the Study of the Liver (APASL) 2014

et al. 2014

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The first consensus report of the working party of the Asian Pacific Association for the Study of the Liver (APASL) set up in 2004 on acute-on-chronic liver failure (ACLF) was published in 2009. Due to the rapid advancements in the knowledge and available information, a consortium of members from countries across Asia Pacific, ''APASL ACLF Research Consortium (AARC),'' was formed in 2012. A large cohort of retrospective and prospective data of ACLF patients was collated and followed up in this data base. The current ACLF definition was reassessed based on the new AARC data base. These initiatives were concluded on a 2-day meeting in February 2014 at New Delhi and led to the development of the final AARC consensus. Only those statements which were based on the evidence and were unanimously recommended were accepted. These statements were circulated again to all the experts and subsequently presented at the annual conference of the APASL at Brisbane, on March 14, 2014. The suggestions from the delegates were analyzed by the expert panel, and the modifications in the consensus were made. The final consensus and guidelines document was prepared. After detailed deliberations and data analysis, the

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“…These two mechanisms act in concert and that their primary role is to stabilize renal function by preventing pressure-induced fluctuations in RBF, GFR. However, in cirrhosis, this autoregulatory function of kidney is lost and for every given level of renal perfusion pressure, the renal blood flow progressively falls shifting autoregulation curve to the right [41]. Therefore, in end stage cirrhosis, despite of maintenance of renal perfusion pressure, renal blood flow is severely compromised.…”

Section: Excess Vasoconstrictors Versus Insufficient Renal Vasodilatorsmentioning

confidence: 99%

Hepatorenal Syndrome-Current Concepts in Pathophysiology

Mathur¹,

Agarwal²

2017

GHOA

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Hepatorenal syndrome (HRS) is a functional renal impairment that occurs in advanced liver cirrhosis or fulminant hepatic failure due to diminished renal blood flow in histological normal kidneys. The pathophysiologic hallmark of HRS is splanchnic vasodilation and renal vasoconstriction leading to renal hypoperfusion and decline in glomerular filtration rate. Two subtypes of HRS i.e. Type 1 and type 2 have been identified with type 1 carrying poor prognosis.Keywords: Hepatorenal syndrome; Splanchnic vasodilation; Renal vasoconstriction; Glomerular filtration rate kidneys. This pathophysiologic correlation was first described by Hecker and Sherlock in 1958 [1]. The functional nature of HRS was confirmed further by the ability to transplant kidneys from patients with HRS and the normalization of renal function after liver transplantation [2,3]. The pathophysiologic hallmark of HRS is splanchnic vasodilation and renal vasoconstriction which has been established in multiple studies [4][5][6][7][8]. Here we present brief overview of current concepts in pathophysiology of HRS. DefinitionThe hepatorenal syndrome is defined as potentially reversible functional impairment of renal function in a patient who has established or clinically evident acute or chronic liver disease. It is characterized clinically by progressive rise in serum creatinine with or without oliguria and urine sediment is often bland. Two subtypes of HRS have been identified: Type 1 HRS: It is defined as at least a twofold increase in serum creatinine to a level greater than 2.5 mg/dL or by 50% reduction in creatinine clearance to a level <20 ml/min during a period of less than two weeks. It is usually precipitated by infection and has a worse prognosis with median survival of less than 10% at 3 months [9-11]. Type 2 HRS:It is defined as renal impairment that is less severe than that observed with type 1 disease and is characterized by refractory ascites. Pathophysiology-Current ConceptsThe pathophysiologic process of HRS begins early and progresses with worsening liver function and involves multiple interrelated pathways ultimately leading to splanchnic vasodilation and renal vasoconstriction which are the hallmark of HRS. In liver disease, portal hypertension leads to splanchnic vasodilation, which progressively increases with advancing disease causing altered cardiovascular function and hyperdynamic circulation leading to decrease in effective arterial volume with activation of endogenous vasoactive systems. These hemodynamic changes ultimately lead to renal hypoperfusion and decline in glomerular filtration rate (GFR). Figure 1 shows pathophysiology of HRS.

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Relationship Between Activation of the Sympathetic Nervous System and Renal Blood Flow Autoregulation in Cirrhosis

Cited by 179 publications

References 38 publications

Negative feedforward control of body fluid homeostasis by hepatorenal reflex

Negative feedforward control of body fluid homeostasis by hepatorenal reflex

Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific Association for the Study of the Liver (APASL) 2014

Hepatorenal Syndrome-Current Concepts in Pathophysiology

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