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Toshiro Fujita - One of the best experts on this subject based on the ideXlab platform.
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Review Article Insulin Resistance, Obesity, Hypertension, and Renal Sodium Transport
2015Co-Authors: Shoko Horita, George Seki, Hideomi Yamada, Masashi Suzuki, Kazuhiko Koike, Toshiro FujitaAbstract:Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Sodium transport through various nephron segments is quite important in regulating sodium Reabsorption and blood pressure. Among several regulators of this process, insulin acts on almost all the nephron segments and is a strong enhancer of sodium Reabsorption. Sodium-proton exchanger type 3 (NHE3) is a main regulator of sodium Reabsorption in the luminal side of proximal tubule. In the basolateral side of the proximal tubule, sodium-bicarbonate cotransporter (NBCe1) mediates sodium and bicarbonate exit from tubular cells. In the distal nephron and the connecting tubule, epithelial sodium channel (ENaC) is of great importance to sodium Reabsorption. NHE3, NBCe1, and ENaC are all regulated by insulin. Recently with-no-lysine (WNK) kinases, responsible for familial hypertension, stimulating sodium Reabsorption in the distal nephron, have been found to be also regulated by insulin. We will discuss the regulation of renal sodium transport by insulin and its roles in the pathogenesis of hypertension in insulin resistance. 1
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insulin resistance obesity hypertension and renal sodium transport
International Journal of Hypertension, 2011Co-Authors: Shoko Horita, George Seki, Hideomi Yamada, Masashi Suzuki, Kazuhiko Koike, Toshiro FujitaAbstract:Sodium transport through various nephron segments is quite important in regulating sodium Reabsorption and blood pressure. Among several regulators of this process, insulin acts on almost all the nephron segments and is a strong enhancer of sodium Reabsorption. Sodium-proton exchanger type 3 (NHE3) is a main regulator of sodium Reabsorption in the luminal side of proximal tubule. In the basolateral side of the proximal tubule, sodium-bicarbonate cotransporter (NBCe1) mediates sodium and bicarbonate exit from tubular cells. In the distal nephron and the connecting tubule, epithelial sodium channel (ENaC) is of great importance to sodium Reabsorption. NHE3, NBCe1, and ENaC are all regulated by insulin. Recently with-no-lysine (WNK) kinases, responsible for familial hypertension, stimulating sodium Reabsorption in the distal nephron, have been found to be also regulated by insulin. We will discuss the regulation of renal sodium transport by insulin and its roles in the pathogenesis of hypertension in insulin resistance.
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angiotensin ii blockade restores albumin Reabsorption in the proximal tubules of diabetic rats
Hypertension Research, 2003Co-Authors: Akihiro Tojo, Maristela L Onozato, Hidetake Kurihara, Tatsuo Sakai, Atsuo Goto, Toshiro FujitaAbstract:The kidney plays an important role in protein metabolism. The albumin Reabsorption in the proximal tubule is disturbed in the early stage of diabetic nephropathy. We evaluated the effects of angiotensin converting enzyme inhibitor (ACEI) and angiotensin II type 1 receptor blocker (ARB) on albumin Reabsorption and expression of megalin, an endocytosis receptor for albumin, in proximal tubules of streptozotocin (STZ)-induced diabetic-rats. Diabetic rats at the second week after STZ injection were treated with quinapril (3mg/kg/day) or candesartan (0.05mg/kg/day) for 2 weeks. The tubular Reabsorption of fluorescein isothiocyanate (FITC)-labeled albumin was evaluated by immunogold electron microscopy, and megalin expression was investigated by immunohistochemistry and Western blotting. Reabsorption of FITC-labeled albumin and megalin expression were prominently inhibited in the proximal convoluted tubules of diabetic rats compared to the controls. Both quinapril and candesartan restored albumin Reabsorption in the proximal tubule due to normalization of megalin expression. Urinary albumin excretion was significantly reduced by both ACEI and ARB treatment. Angiotensin II infusion decreased megalin expression and albumin Reabsorption in the proximal tubule. In conclusion, angiotensin II blockade restored albumin Reabsorption via amelioration of megalin expression in the proximal tubules of early stage diabetic rats. (Hypertens Res 2003; 26: 413-419)
Narihiko Kondo - One of the best experts on this subject based on the ideXlab platform.
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the sweat glands maximum ion Reabsorption rates following heat acclimation in healthy older adults
Experimental Physiology, 2021Co-Authors: Nicola Gerrett, Tatsuro Amano, Yoshimitsu Inoue, Narihiko KondoAbstract:New Findings: What is the central question to this study? Do the sweat glands’ maximum ion Reabsorption rates increase following heat acclimation in healthy older individuals and is this associated with elevated aldosterone concentrations? What is the main finding and its importance? Sweat gland maximum ion Reabsorption rates improved heterogeneously across body sites, which occurred without any changes in aldosterone concentration following a controlled hyperthermic heat acclimation protocol in healthy older individuals. Abstract: We examined whether the eccrine sweat glands’ ion Reabsorption rates improved following heat acclimation (HA) in older individuals. Ten healthy older adults (>65 years) completed a controlled hyperthermic (+0.9°C rectal temperature, Tre) HA protocol for nine non-consecutive days. Participants completed a passive heat stress test (lower leg 42°C water submersion) pre-HA and post-HA to assess physiological regulation of sweat gland ion Reabsorption at the chest, forearm and thigh. The maximum ion Reabsorption rate was defined as the inflection point in the slope of the relation between galvanic skin conductance and sweat rate (SR). We explored the responses again after a 7-day decay. During passive heating, the Tb thresholds for sweat onset on the chest and forearm were lowered after HA (P 0.05). Any changes observed were lost during the decay. Pilocarpine-induced sudomotor responses to iontophoresis did not change after HA (P ≥ 0.801). Maximum ion Reabsorption rate was only enhanced at the chest (P = 0.001) despite unaltered aldosterone concentration after HA. The data suggest that this adaptation is lost after 7 days’ decay. The HA protocol employed in the present study induced partial adaptive sudomotor responses. Eccrine sweat gland ion Reabsorption rates improved heterogeneously across the skin sites. It is likely that aldosterone secretion did not alter the chest sweat ion Reabsorption rates observed in the older adults.
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the influence of local skin temperature on the sweat glands maximum ion Reabsorption rate
European Journal of Applied Physiology, 2019Co-Authors: Nicola Gerrett, Tatsuro Amano, Yoshimitsu Inoue, George Havenith, Narihiko KondoAbstract:Changes in mean skin temperature (Tsk) have been shown to modify the maximum rate of sweat ion Reabsorption. This study aims to extend this knowledge by investigating if modifications could also be caused by local Tsk. The influence of local Tsk on the sweat gland maximum ion Reabsorption rates was investigated in ten healthy volunteers (three female and seven male; 20.8 ± 1.2 years, 60.4 ± 7.7 kg, 169.4 ± 10.4 cm) during passive heating (water-perfused suit and lower leg water immersion). In two separate trials, in a randomized order, one forearm was always manipulated to 33 °C (Neutral), whilst the other was manipulated to either 30 °C (Cool) or 36 °C (Warm) using water-perfused patches. Oesophageal temperature (Tes), forearm Tsk, sweat rate (SR), galvanic skin conductance (GSC) and salivary aldosterone concentrations were measured. The sweat gland maximum ion Reabsorption rates were identified using the ∆SR threshold for an increasing ∆GSC. Thermal [Tes and body temperature (Tb)] and non-thermal responses (aldosterone) were similar across all conditions (p > 0.05). A temperature-dependent response for the sweat gland maximum ion Reabsorption rates was evident between 30 °C (0.18 ± 0.10 mg/cm2/min) and 36 °C (0.28 ± 0.14 mg/cm2/min, d = 0.88, p 0.05. The data indicate that small variations in local Tsk may not affect the sweat gland maximum ion Reabsorption rates but when the local Tsk increases by > 6 °C, ion Reabsorption rates also increase.
Nicola Gerrett - One of the best experts on this subject based on the ideXlab platform.
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the sweat glands maximum ion Reabsorption rates following heat acclimation in healthy older adults
Experimental Physiology, 2021Co-Authors: Nicola Gerrett, Tatsuro Amano, Yoshimitsu Inoue, Narihiko KondoAbstract:New Findings: What is the central question to this study? Do the sweat glands’ maximum ion Reabsorption rates increase following heat acclimation in healthy older individuals and is this associated with elevated aldosterone concentrations? What is the main finding and its importance? Sweat gland maximum ion Reabsorption rates improved heterogeneously across body sites, which occurred without any changes in aldosterone concentration following a controlled hyperthermic heat acclimation protocol in healthy older individuals. Abstract: We examined whether the eccrine sweat glands’ ion Reabsorption rates improved following heat acclimation (HA) in older individuals. Ten healthy older adults (>65 years) completed a controlled hyperthermic (+0.9°C rectal temperature, Tre) HA protocol for nine non-consecutive days. Participants completed a passive heat stress test (lower leg 42°C water submersion) pre-HA and post-HA to assess physiological regulation of sweat gland ion Reabsorption at the chest, forearm and thigh. The maximum ion Reabsorption rate was defined as the inflection point in the slope of the relation between galvanic skin conductance and sweat rate (SR). We explored the responses again after a 7-day decay. During passive heating, the Tb thresholds for sweat onset on the chest and forearm were lowered after HA (P 0.05). Any changes observed were lost during the decay. Pilocarpine-induced sudomotor responses to iontophoresis did not change after HA (P ≥ 0.801). Maximum ion Reabsorption rate was only enhanced at the chest (P = 0.001) despite unaltered aldosterone concentration after HA. The data suggest that this adaptation is lost after 7 days’ decay. The HA protocol employed in the present study induced partial adaptive sudomotor responses. Eccrine sweat gland ion Reabsorption rates improved heterogeneously across the skin sites. It is likely that aldosterone secretion did not alter the chest sweat ion Reabsorption rates observed in the older adults.
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the influence of local skin temperature on the sweat glands maximum ion Reabsorption rate
European Journal of Applied Physiology, 2019Co-Authors: Nicola Gerrett, Tatsuro Amano, Yoshimitsu Inoue, George Havenith, Narihiko KondoAbstract:Changes in mean skin temperature (Tsk) have been shown to modify the maximum rate of sweat ion Reabsorption. This study aims to extend this knowledge by investigating if modifications could also be caused by local Tsk. The influence of local Tsk on the sweat gland maximum ion Reabsorption rates was investigated in ten healthy volunteers (three female and seven male; 20.8 ± 1.2 years, 60.4 ± 7.7 kg, 169.4 ± 10.4 cm) during passive heating (water-perfused suit and lower leg water immersion). In two separate trials, in a randomized order, one forearm was always manipulated to 33 °C (Neutral), whilst the other was manipulated to either 30 °C (Cool) or 36 °C (Warm) using water-perfused patches. Oesophageal temperature (Tes), forearm Tsk, sweat rate (SR), galvanic skin conductance (GSC) and salivary aldosterone concentrations were measured. The sweat gland maximum ion Reabsorption rates were identified using the ∆SR threshold for an increasing ∆GSC. Thermal [Tes and body temperature (Tb)] and non-thermal responses (aldosterone) were similar across all conditions (p > 0.05). A temperature-dependent response for the sweat gland maximum ion Reabsorption rates was evident between 30 °C (0.18 ± 0.10 mg/cm2/min) and 36 °C (0.28 ± 0.14 mg/cm2/min, d = 0.88, p 0.05. The data indicate that small variations in local Tsk may not affect the sweat gland maximum ion Reabsorption rates but when the local Tsk increases by > 6 °C, ion Reabsorption rates also increase.
Yawara Niijima - One of the best experts on this subject based on the ideXlab platform.
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lower renal threshold for glucose Reabsorption in type 1 diabetes mellitus t1dm may explain the smaller contribution of sglt2 inhibitors to the improvement of plasma glucose control compared with t2dm
Diabetes Therapy, 2019Co-Authors: Aya Osaki, Tsugumichi Saito, Eijiro Yamada, Yawara Niijima, Yoko Shimoda, Junichi Okada, Yasuyo Nakajima, Atsushi OzawaAbstract:Previously, we reported that the renal threshold for glucose Reabsorption can be measured as the lowest plasma glucose level that correlates with the first detectable appearance of urine glucose. These data revealed significant variations among patients with type 2 diabetes mellitus (T2DM), and there was a significant negative correlation between the renal threshold for glucose Reabsorption and HbA1c levels following treatment with the sodium-glucose co-transporter 2 (SGLT2) inhibitor ipragliflozin. Recently approved SGLT inhibitors may not show the same efficacy in patients with T1DM as in those with T2DM unless the renal threshold for glucose Reabsorption shows similar levels between the two groups. SGLT2 inhibitors improve plasma glucose control in patients with T2DM by reducing glucose Reabsorption via the epithelial cells of the proximal tubule. The renal threshold for glucose Reabsorption was defined as the minimum blood glucose concentration that results in the presence of measurable glycosuria in at least 12 measurements. The renal threshold for glucose Reabsorption in patients with T2DM [n = 64; 201.8 ± 33.6 (range 121–268) mg/dL] was significantly higher than that in patients with T1DM [n = 33; 171.0 ± 33.0 (range 76–259) mg/dL; p = 0.00022]. The renal threshold for glucose Reabsorption in patients with T1DM was near the normal range and significantly lower than that in patients with T2DM. The efficacy of the SGLT2 inhibitor was better in patients with a higher renal threshold for glucose Reabsorption. Thus, these results indicate that it is advisable to estimate the renal threshold for glucose Reabsorption prior to initiating SGLT2 inhibitor therapy in patients with T1DM.
Elaine M. Worcester - One of the best experts on this subject based on the ideXlab platform.
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pathophysiology based treatment of idiopathic calcium kidney stones
Clinical Journal of The American Society of Nephrology, 2011Co-Authors: Fredric L Coe, Andrew P. Evan, Elaine M. WorcesterAbstract:Summary Idiopathic calcium oxalate (CaOx) stone-formers (ICSFs) differ from patients who make idiopathic calcium phosphate (CaP) stones (IPSFs). ICSFs, but not IPSFs, form their stones as overgrowths on interstitial apatite plaque; the amount of plaque covering papillary surface is positively correlated with urine calcium excretion and inversely with urine volume. The amount of plaque predicts the number of recurrent stones. The initial crystal overgrowth on plaque is CaP, although the stone is mainly composed of CaOx, meaning that lowering supersaturation (SS) for CaOx and CaP is important for CaOx stone prevention. IPSFs, unlike ICSFs, have apatite crystal deposits in inner medullary collecting ducts, which are associated with interstitial scarring. ICSFs and IPSFs have idiopathic hypercalciuria, which is due to decreased tubule calcium Reabsorption, but sites of abnormal Reabsorption may differ. Decreased Reabsorption in proximal tubules (PTs) delivers more calcium to the thick ascending limb (TAL), where increased calcium Reabsorption can load the interstitium, leading to plaque formation. The site of abnormal Reabsorption in IPSFs may be the TAL, where an associated defect in bicarbonate Reabsorption could produce the higher urine pH characteristic of IPSFs. Preventive treatment with fluid intake, protein and sodium restriction, and thiazide will be effective in ICSFs and IPSFs by decreasing urine calcium concentration and CaOx and CaP SS and may also decrease plaque formation by increased PT calcium Reabsorption. Citrate may be detrimental for IPSFs if urine pH rises greatly, increasing CaP SS. Future trials should examine the question of appropriate treatment for IPSFs.
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pathophysiology based treatment of idiopathic calcium kidney stones
PMC, 2011Co-Authors: Fredric L Coe, Andrew P. Evan, Elaine M. WorcesterAbstract:Summary Idiopathic calcium oxalate (CaOx) stone-formers (ICSFs) differ from patients who make idiopathic calcium phosphate (CaP) stones (IPSFs). ICSFs, but not IPSFs, form their stones as overgrowths on interstitial apatite plaque; the amount of plaque covering papillary surface is positively correlated with urine calcium excretion and inversely with urine volume. The amount of plaque predicts the number of recurrent stones. The initial crystal overgrowth on plaque is CaP, although the stone is mainly composed of CaOx, meaning that lowering supersaturation (SS) for CaOx and CaP is important for CaOx stone prevention. IPSFs, unlike ICSFs, have apatite crystal deposits in inner medullary collecting ducts, which are associated with interstitial scarring. ICSFs and IPSFs have idiopathic hypercalciuria, which is due to decreased tubule calcium Reabsorption, but sites of abnormal Reabsorption may differ. Decreased Reabsorption in proximal tubules (PTs) delivers more calcium to the thick ascending limb (TAL), where increased calcium Reabsorption can load the interstitium, leading to plaque formation. The site of abnormal Reabsorption in IPSFs may be the TAL, where an associated defect in bicarbonate Reabsorption could produce the higher urine pH characteristic of IPSFs. Preventive treatment with fluid intake, protein and sodium restriction, and thiazide will be effective in ICSFs and IPSFs by decreasing urine calcium concentration and CaOx and CaP SS and may also decrease plaque formation by increased PT calcium Reabsorption. Citrate may be detrimental for IPSFs if urine pH rises greatly, increasing CaP SS. Future trials should examine the question of appropriate treatment for IPSFs. Clin J Am Soc Nephrol 6: 2083–2092, 2011. doi: 10.2215/CJN.11321210
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evidence for increased postprandial distal nephron calcium delivery in hypercalciuric stone forming patients
American Journal of Physiology-renal Physiology, 2008Co-Authors: Elaine M. Worcester, Kristin J. Bergsland, Joan H Parks, Andrew P. Evan, Fredric L Coe, Lynn R Willis, D Clark, Daniel L GillenAbstract:A main mechanism of idiopathic hypercalciuria (IH) in calcium stone-forming patients (IHSF) is postprandial reduction of renal tubule calcium Reabsorption that cannot be explained by selective reduction of serum parathyroid hormone levels; the nephron site(s) responsible are not as yet defined. Using fourteen 1-h measurements of the clearances of sodium, calcium, and endogenous lithium during a three-meal day in the University of Chicago General Clinical Research Center, we found reduced postprandial proximal tubule Reabsorption of sodium and calcium in IHSF vs. normal subjects. The increased distal sodium delivery is matched by increased distal Reabsorption so that urine sodium excretions do not differ, but distal calcium Reabsorption does not increase enough to match increased calcium delivery, so hypercalciuria results. In fact, urine calcium excretion and overall renal fractional calcium Reabsorption both are high in IHSF vs. normal when adjusted for distal calcium delivery, strongly suggesting a distal as well as proximal reduction of calcium Reabsorption. The combination of reduced proximal tubule and distal nephron calcium Reabsorption in IHSF is a new finding and indicates that IH involves a complex, presumably genetic, variation of nephron function. The increased calcium delivery into the later nephron may play a role in stone formation via deposition of papillary interstitial apatite plaque.
