Eppur Si Muove: The dynamic nature of physiological control of renal blood flow by the renal sympathetic nerves

Schiller, Alicia M.; Pellegrino, Peter R.; Zucker, Irving H.

doi:10.1016/j.autneu.2016.08.003

Cited by 12 publications

(12 citation statements)

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“…For example, tumor necrosis factor α is produced by neurons, astrocytes, and microglia and contributes to the development of the hippocampus, ionic homeostasis, and synaptic plasticity and also to the initiation and progression of some neuronal diseases (Park and Bowers 2010). Further investigation is required to elucidate the physiological functions of IL-36γ in the kidneys through the function of nerves, and these studies should particularly focus on representative sympathetic nerve activity such as the regulation of renal blood flow (Schiller et al 2017).…”

Section: Discussionmentioning

confidence: 99%

Compartmentalization of interleukin 36 subfamily according to inducible and constitutive expression in the kidneys of a murine autoimmune nephritis model

et al. 2021

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The interleukin (IL) 36 subfamily belongs to the IL-1 family and is comprised of agonists (IL-36α, IL-36β, IL-36γ) and antagonists . We previously reported IL-36α overexpression in renal tubules of chronic nephritis mice. To understand the localization status and biological relationships among each member of the IL-36 subfamily in the kidneys, MRL/MpJ-Fas lpr/lpr mice were investigated as autoimmune nephritis models using pathology-based techniques. MRL/MpJ-Fas lpr/lpr mice exhibited disease onset from 3 months and severe nephritis at 6-7 months (early and late stages, respectively). Briefly, IL-36γ and IL-36Ra were constitutively expressed in murine kidneys, while the expression of IL-36α, IL-36β, IL-36Ra, and IL-38 was induced in MRL/MpJ-Fas lpr/lpr mice. IL-36α expression was significantly increased and localized to injured tubular epithelial cells (TECs). CD44 + -activated parietal epithelial cells (PECs) also exhibited higher IL-36α-positive rates, particularly in males. IL-36β and IL-38 are expressed in interstitial plasma cells. Quantitative indices for IL-36α and IL-38 positively correlated with nephritis severity. Similar to IL-36α, IL-36Ra localized to TECs and PECs at the late stage; however, MRL/MpJ-Fas lpr/lpr and healthy MRL/MpJ mice possessed IL-36Ra + smooth muscle cells in kidney arterial tunica media at both stages. IL-36γ was constitutively expressed in renal sympathetic axons regardless of strain and stage. IL-36 receptor gene was ubiquitously expressed in the kidneys and was induced proportional to disease severity. MRL/MpJ-Fas lpr/lpr mice kidneys possessed significantly upregulated IL-36 downstream candidates, including NF-κB-or MAPK-pathway organizing molecules. Thus, the IL-36 subfamily contributes to homeostasis and inflammation in the kidneys, and especially, an IL-36α-dominant imbalance could strongly impact nephritis deterioration. KeywordsNephritis • Systemic autoimmune disease • Chronic kidney disease • Inflammatory cytokine • Interleukin 36 Abbreviations Actb Beta-actin α-SMA Alpha smooth muscle actin BUN Blood urea nitrogen CKD Chronic kidney disease Cr Creatinine dsDNA Double-stranded DNA DT Distal tubule GO Gene ontology HNF-4α Hepatic nuclear factor 4, alpha

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Section: Discussionmentioning

confidence: 99%

Compartmentalization of interleukin 36 subfamily according to inducible and constitutive expression in the kidneys of a murine autoimmune nephritis model

et al. 2021

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“…Sympathetic nerve fibers innervate vascular smooth muscle cells of renal arteries and arterioles and renin-secreting cells of the juxtaglomerular apparatus. [ 52 ] Experimental stimulation of distal transected ends of the renal sympathetic nerve generate renal vasoconstriction, enhance renin release, and reduce glomerular filtration rate and renal plasma flow. [ 52 ] We tabularly summarize the effects of afferent and/or efferent arteriolar constriction or dilation upon glomerular filtration rate, renal plasma flow, filtration fraction, peritubular capillary hydrostatic pressure, and proximal convoluted tubular reabsorption of sodium.…”

Section: Discussionmentioning

confidence: 99%

“…[ 52 ] Experimental stimulation of distal transected ends of the renal sympathetic nerve generate renal vasoconstriction, enhance renin release, and reduce glomerular filtration rate and renal plasma flow. [ 52 ] We tabularly summarize the effects of afferent and/or efferent arteriolar constriction or dilation upon glomerular filtration rate, renal plasma flow, filtration fraction, peritubular capillary hydrostatic pressure, and proximal convoluted tubular reabsorption of sodium. [ 55 ] Constriction of either the afferent or efferent arteriole achieves potent reduction of peritubular capillary hydrostatic pressure, favoring reabsorption of sodium, with filtration fraction insignificantly modified.…”

Section: Discussionmentioning

confidence: 99%

Trimethoprim-sulfamethoxazole-induced hyponatremia in an elderly lady with Achromobacter xylosoxidans pneumonia

Ghali

Kim

2020

Medicine

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Rationale: Hyponatremia occurs frequently in the hospital setting and may be attributable to a host of etiologies. Drugs are frequently implicated. Trimethoprim-sulfamethoxazole (TMP/SMX) represents a well-recognized pharmacologic precipitant of drug-induced hyponatremia, with several reports extant in the retrievable literature. Nephrologists thus debate the mechanisms giving rise to TMP/SMX-induced hyponatremia and the precise mechanism by which treatment with TMP/SMX generates reductions of serum sodium concentration remain controversial. The agent has a well-known effect of antagonizing the effects of aldosterone upon the distal nephron. Renal salt wasting and the syndrome of inappropriate antidiuretic hormone secretion represent implicated mechanistic intermediaries in TMP/SMX-induced hyponatremia. Patient concerns: The patient endorsed no explicit concerns. Diagnoses: We describe the case of an 83-year-old female clinically diagnosed with pneumonia found to have an initial serum sodium in the range of 130 to 134 mEq/L consistent with mild hyponatremia upon admission. Sputum cultures grew Achromobacter xylosoxidans susceptible to TMP/SMX. The patient's serum sodium concentration precipitously decline following institution of treatment with TMP/SMX to 112 to 114 mEq/L during the course of 5 days. Interventions: Severe hyponatremia proved recalcitrant to initial therapy with supplemental salt tabs and standard doses of the vasopressin receptor antagonist tolvaptan. Outcomes: Escalating doses of tolvaptan increased the patient's sodium to 120 to 124 mEq/L. The patient was transferred to another hospital for further management. During her stay, the patient did not exhibit frank or obvious clinical features consistent with hyponatremia nor readily appreciable evidence of volume depletion. Lessons: TMP/SMX represents a frequent, though underreported cause of hyponatremia in the hospital setting several authors believe natriuresis may represent the most common mechanism underlying TMP/SMX-induced hyponatremia. Evidence implicating natriuresis to be mechanistic in TMP/SMX-induced hyponatremia include clinically appreciable hypovolemia and resolution of hyponatremia with oral or intravenous salt repletion. Salt repletion failed to monotherapeutically enhance our patient's hyponatremiadisfavoring renal salt wasting as originately mechanistic. Contemporaneous refractoriness of serum sodium to fluid restriction nor standard doses of tolvaptan confounded our initial attempts to mechanistically attribute the patient's hyponatremia to a specific cause. Clinical euvolemia and rapid response of hyponatremia to exceptionally high doses of tolvaptan strongly favors syndrome of inappropriate antidiuretic hormone to represent the chief mechanism by which TMP/SMX exacerbates hyponatremia.

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“…The kidneys receive 20-25% of the total cardiac output (CO) of the human body, approximately between 1,000 and 1,200 milliliters of blood per minute, oxygen is distributed in a heterogeneous manner, mainly through the cortex where it reaches a concentration 10 times higher than in the renal medulla. Faced with an abrupt transitory drop in RBF, intrinsic and neurohumoral self-regulatory mechanisms cause proportional changes in glomerular filtration in a way that can lead to the diagnosis of AKI [20]. This can occur as a consequence of 1) Hypovolemia, 2) Hypotension, 3) Renal venous congestion [21][22][23].…”

Section: Renal Response To An Ischemic Insultmentioning

confidence: 99%

Acute Kidney Injury in the Perioperative Period: Beyond the Obvious

Escarramán¹,

Guerrero²,

Meade³

et al. 2021

Int J Anesthetic Anesthesiol

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Acute kidney injury (AKI) represents a great challenge for the anesthesiologist during the perioperative period, since its presence directly impacts in patients mortality and morbidity, even after its resolution as a result of multiples factors. Furthermore, it is characterized by coexisting with a great variety of systemic alterations, which add special difficulty to its study and understanding. During perioperative period there may be ischemic insult and non-ischemic insult, on the other hand, volume overload (hypervolemia) can also cause alteration on kidney function by modifying the consumption and delivery of renal oxygen. Throughout, some of the most important points for understanding this topic are presented in the present paper.

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Eppur Si Muove: The dynamic nature of physiological control of renal blood flow by the renal sympathetic nerves

Cited by 12 publications

References 42 publications

Compartmentalization of interleukin 36 subfamily according to inducible and constitutive expression in the kidneys of a murine autoimmune nephritis model

Compartmentalization of interleukin 36 subfamily according to inducible and constitutive expression in the kidneys of a murine autoimmune nephritis model

Trimethoprim-sulfamethoxazole-induced hyponatremia in an elderly lady with Achromobacter xylosoxidans pneumonia

Acute Kidney Injury in the Perioperative Period: Beyond the Obvious

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