Renal sympathetic nerve activity and natriuresis during water immersion in conscious dogs

Miki, Kenju; Hayashida, Yoshiaki; Sagawa, Sueko; Shiraki, Keizō

doi:10.1152/ajpregu.1989.256.2.r299

Cited by 52 publications

(67 citation statements)

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“…Our results are contrary to those in conscious monkeys, in which the renal response to volume loading is abolished by renal denervation (Peterson, Chase & Gray, 1984). They are also contrary to the results obtained in dogs subjected to head-out immersion (Miki, Hayshida, Sagawa & Shiraki, 1989 (Majid & Karim, 1995) (1995), as in our chronic preparation, also used chloralose. On the other hand, Emmeluth, Goetz, Drummer, Gerzer, Forssmann & Bie (1993) recently reported a persistent natriuresis in conscious trained dogs with renal denervation when isotonic volume expansion was carried out over 100min.…”

Section: Discussioncontrasting

confidence: 99%

Natriuresis caused by blood volume expansion in dogs is not mediated by the renal nerves

Drake-Holland¹,

Song²,

Belcher³

et al. 1996

Experimental Physiology

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SUMMARYThe influence of renal denervation on the renal response to rapid blood volume expansion was investigated by measurement of urine volume, sodium and osmolar excretion rates, sodium p-aminohippurate and free water clearances, and systemic haemodynamic and plasma hormone (atrial natriuretic peptide, arginine vasopressin and plasma renin activity (PRA)) changes in ten control and ten renal-denervated chloralose-anaesthetized mongrel dogs. Following renal denervation, blood volume expansion caused a similar increase in sodium excretion to that in the control group. Renal denervation resulted in systemic vasodilatation and decreased PRA. During fluid loading the right atrial pressure and pulmonary capillary wedge pressure were significantly higher in the control group. In the control group, volume expansion caused a large fall in PRA, whereas in the renal-denervated dogs, PRA remained suppressed. We conclude, from the fact that natriuresis is preserved after renal denervation, that this response is not mediated by a reflex with efferent limb in the renal nerves.

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Section: Discussioncontrasting

confidence: 99%

Natriuresis caused by blood volume expansion in dogs is not mediated by the renal nerves

Drake-Holland¹,

Song²,

Belcher³

et al. 1996

Experimental Physiology

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“…62 Therefore, it is possible that the cardiopulmonary volume receptor is unloaded, and the renal sympathetic nerve is then reflexively activated. 63 Consistent with this, an increase in the central blood volume with no effect on the total blood volume, induced by head-out water immersion, which is known to reduce renal sympathetic nerve activity via the cardiopulmonary volume receptor, 64,65 significantly improves the renal excretory function. 66 Increased hepatic portal pressure is the other factor responsible for the increased renal sympathetic nerve activity.…”

Section: Liver Cirrhosismentioning

confidence: 71%

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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“…9 Conscious dogs subjected to head-out water immersion exhibit an increase in cardiac filling pressure that produces a sustained reflex decrease in RSNA, leading to a natriuresis in the absence of changes in GFR or RBF; the natriuresis is abolished by renal denervation. 10 Conscious dogs subjected to head-up tilt exhibit a decrease in both arterial and cardiac filling pressure that produces a sustained reflex increase in RSNA, leading to an antinatriuresis in the absence of changes in GFR or RBF; the antinatriuresis is abolished by renal denervation. 11 It also became evident from observations in humans that intact renal sympathetic innervation was important in ensuring a normal renal response to dietary sodium restriction.…”

mentioning

confidence: 99%

Neural Control of the Kidney

DiBona

2003

Hypertension

159

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Abstract-This article provides a chronological perspective on the development of knowledge concerning the neural control of renal function and is divided into three parts: the past, the present, and the future. The PastResearch in the area of the neural control of renal function was not very active for the first half of the 20th century. This can be attributed to 2 factors. First, the renowned renal physiologist, Homer Smith, rendered an opinion that the renal nerves were of little functional consequence. [1][2][3] This was based on his interpretation of experiments involving renal denervation in anesthetized and surgically operated animals. He criticized this approach, as he believed that the starting level of renal sympathetic nerve activity (RSNA) would be quite elevated, owing to the associated stress, so that "denervation hyperemia and diuresis appear to be a release from enhanced vasoconstriction engendered by anesthesia and traumatic operative procedures." 3 Second, there was a lack of convincing evidence that the renal innervation extended beyond the renal vasculature to either the tubules or the juxtaglomerular apparatus. The demonstration by Luciano Barajas 4 that all segments of the renal tubule (as well as the juxtaglomerular apparatus) were innervated by norepinephrine-containing renal sympathetic nerve terminals that make contact with the renal tubular epithelial cell basement membrane paved the way for increased research activity in this area. This critical observation reconfirmed once again the important relationship between structure and function.Given the powerful influence of changes in renal hemodynamics (ie, arterial pressure, glomerular filtration rate [GFR] and renal blood flow [RBF]) on urinary sodium excretion (U Na V), it was evident that the influence of changes in RSNA on U Na V must be examined in experimental protocols in which these variables remained constant. By using electrical stimulation of the efferent renal sympathetic nerves at frequencies just subthreshold for decreases in RBF, it was shown that a reversible decrease in U Na V occurred in the absence of changes in GFR (ie, filtered sodium load), RBF, and arterial pressure. 5 These results indicated that lowfrequency renal sympathetic nerve stimulation increased overall renal tubular sodium reabsorption via a direct action on the renal tubule, independent of changes in renal hemodynamics. Additional experiments demonstrated that this effect occurred in the proximal convoluted tubule, the thick ascending limb of Henle's loop, the distal convoluted tubule, and the collecting duct. 6,7 Subsequent work (reviewed in DiBona and Kopp 8 ) showed that this was owing to the release of norepinephrine from renal sympathetic nerve terminals with stimulation of postsynaptic ␣ 1 -adrenoceptors located on the basolateral membrane of renal tubular epithelial cells throughout the nephron. Subsequent intracellular signaling events resulted in an increase in activity of the sodium pump (Na ϩ ,K ϩ -ATPase), with increased transepithelial sod...

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Renal sympathetic nerve activity and natriuresis during water immersion in conscious dogs

Cited by 52 publications

References 0 publications

Natriuresis caused by blood volume expansion in dogs is not mediated by the renal nerves

Natriuresis caused by blood volume expansion in dogs is not mediated by the renal nerves

Negative feedforward control of body fluid homeostasis by hepatorenal reflex

Neural Control of the Kidney

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