Negative feedforward control of body fluid homeostasis by hepatorenal reflex

Morita, Hironobu; Abe, Chikara

doi:10.1038/hr.2011.88

Cited by 10 publications

(11 citation statements)

References 73 publications

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“…Studies have shown that the infusion of water into the portal vein results in greater urinary excretion than infusing the same volume of water into the vena cava, a finding also supported by earlier work (2, 62, 66). These findings highlight another powerful mechanism for maintaining fluid homeostasis, which is known as the hepatorenal reflex.…”

Section: Hepatic Afferent Nervessupporting

confidence: 74%

“…Similar to osmoreception, the hepatic nervous system recognizes changes in ion concentration before they occur in the systemic blood (63). Hepatic nerves have a distinct advantage for the detection of ions compared to other organs since the concentration of absorbed substances in the portal vein is 4–5 times higher than that detected in the systemic blood (62). Thus, the liver is an ideal “predictor” of systemic blood-ion concentration, allowing for predictive compensation of fluid homeostasis.…”

Section: Hepatic Afferent Nervesmentioning

confidence: 99%

“…This reflex is characterized by increased Na + concentration in the portal vein triggering a decrease in renal sympathetic tone and excretion of Na + (Fig. 4) (62). Loss of this reflex may be partially responsible for the increased Na + concentration seen in cirrhotic patients (62).…”

Section: Hepatic Afferent Nervesmentioning

confidence: 99%

“…4) (62). Loss of this reflex may be partially responsible for the increased Na + concentration seen in cirrhotic patients (62). Future research will help uncover whether it is possible to activate the hepatorenal reflex during disease states with high serum Na + concentrations such as hypertension.…”

Section: Hepatic Afferent Nervesmentioning

confidence: 99%

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Hepatic Nervous System and Neurobiology of the Liver

Jensen

Alpini

Glaser

2013

Comprehensive Physiology

143

145

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The liver has a nervous system containing both afferent and efferent neurons that are involved in a number of processes. The afferent arm includes the sensation of lipids, glucose, and metabolites (after eating and drinking) and triggers the nervous system to make appropriate physiological changes. The efferent arm is essential for metabolic regulation, modulation of fibrosis and biliary function and the control of a number of other processes. Experimental models have helped us to establish how: (i) the liver is innervated by the autonomic nervous system; and (ii) the cell types that are involved in these processes. Thus, the liver acts as both a sensor and effector that is influenced by neurological signals and ablation. Understanding these processes hold significant implications in disease processes such as diabetes and obesity, which are influenced by appetite and hormonal signals.

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Section: Hepatic Afferent Nervessupporting

confidence: 74%

Section: Hepatic Afferent Nervesmentioning

confidence: 99%

Section: Hepatic Afferent Nervesmentioning

confidence: 99%

Section: Hepatic Afferent Nervesmentioning

confidence: 99%

See 2 more Smart Citations

Hepatic Nervous System and Neurobiology of the Liver

Jensen

Alpini

Glaser

2013

Comprehensive Physiology

143

145

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“…Although we did not detect liver morphological or functional abnormalities, it is possible that the liver ACE modulates hepatorenal reflexes in the ACE 3/3 mice. While work by others highlights the importance of these reflexes in the regulation of postprandial natriuresis, such a mechanism seems to be less important for longterm sodium homeostasis (39).…”

Section: Figurementioning

confidence: 99%

The absence of intrarenal ACE protects against hypertension

González-Villalobos

Janjoulia²,

Fletcher³

et al. 2013

J. Clin. Invest.

176

210

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Activation of the intrarenal renin-angiotensin system (RAS) can elicit hypertension independently from the systemic RAS. However, the precise mechanisms by which intrarenal Ang II increases blood pressure have never been identified. To this end, we studied the responses of mice specifically lacking kidney angiotensin-converting enzyme (ACE) to experimental hypertension. Here, we show that the absence of kidney ACE substantially blunts the hypertension induced by Ang II infusion (a model of high serum Ang II) or by nitric oxide synthesis inhibition (a model of low serum Ang II). Moreover, the renal responses to high serum Ang II observed in wild-type mice, including intrarenal Ang II accumulation, sodium and water retention, and activation of ion transporters in the loop of Henle (NKCC2) and distal nephron (NCC, ENaC, and pendrin) as well as the transporter activating kinases SPAK and OSR1, were effectively prevented in mice that lack kidney ACE. These findings demonstrate that ACE metabolism plays a fundamental role in the responses of the kidney to hypertensive stimuli. In particular, renal ACE activity is required to increase local Ang II, to stimulate sodium transport in loop of Henle and the distal nephron, and to induce hypertension. IntroductionHypertension affects more than 1.5 billion people worldwide and is a key contributor to stroke and cardiovascular and kidney disease. The importance of the renin-angiotensin system (RAS) in the origins of this disorder is underscored by the blood pressure-lowering effects of angiotensin-converting enzyme (ACE) inhibitors and Ang II receptor blockers. However, plasma renin activity, the clinical index used to determine systemic RAS status, is distributed over a wide range in hypertensive subjects (1, 2). This observation prompts the suggestion that alterations in tissue-specific RAS, not detected by plasma renin activity, may underlie hypertension. The kidneys play a central role in long-term blood pressure control through their regulation of sodium and fluid balance. Because renal salt retention is strongly influenced by Ang II and there is a complete RAS along the nephron, it has been suggested that increased local Ang II formation may induce hypertension. Indeed, using gene-targeted mice, we and others have shown that increased intrarenal Ang II formation results in hypertension (3-6). As a whole, these observations suggest that renal Ang II synthesis has important consequences for nephron function and the development of hypertension. However, precisely how the intrarenal generation of Ang II elevates blood pressure is not known. Therefore, we tested the hypothesis that, in conditions in which the intrarenal RAS becomes activated, local Ang II synthesis enhances sodium and water reabsorption along the nephron. In addition, we postulated that inhibiting intrarenal Ang II formation effectively protects against hypertension.

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