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      Sodium balance, circadian BP rhythm, heart rate variability, and intrarenal renin–angiotensin–aldosterone and dopaminergic systems in acute phase of ARB therapy

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          We have revealed that even in humans, activated intrarenal renin–angiotensin–aldosterone system ( RAAS) enhances tubular sodium reabsorption to facilitate salt sensitivity and nondipper rhythm of blood pressure ( BP), and that angiotensin receptor blocker ( ARB) could increase daytime urinary sodium excretion rate ( U N aV) to produce lower sodium balance and restore nondipper rhythm. However, the sympathetic nervous system and intrarenal dopaminergic system can also contribute to renal sodium handling. A total of 20 patients with chronic kidney disease (61 ± 15 years) underwent 24‐h ambulatory BP monitoring before and during two‐day treatment with ARB, azilsartan. Urinary angiotensinogen excretion rate ( U AGTV , μg/ gCre) was measured as intrarenal RAAS; urinary dopamine excretion rate ( U DAV , pg/ gCre) as intrarenal dopaminergic system; heart rate variabilities (HRV, calculated from 24‐h Holter‐ ECG) of non‐Gaussianity index λ 25s as sympathetic nerve activity; and power of high‐frequency ( HF) component or deceleration capacity ( DC) as parasympathetic nerve activity. At baseline, glomerular filtration rate correlated inversely with U AGTV ( r = −0.47, P = 0.04) and positively with U DAV ( r = 0.58, P = 0.009). HF was a determinant of night/day BP ratio ( β = −0.50, F = 5.8), rather than DC or λ 25s. During the acute phase of ARB treatment, a lower steady sodium balance was not achieved. Increase in daytime U N aV preceded restoration of BP rhythm, accompanied by decreased U AGTV ( r = −0.88, P = 0.05) and increased U DAV ( r = 0.87, P = 0.05), but with no changes in HRVs. Diminished sodium excretion can cause nondipper BP rhythm. This was attributable to intrarenal RAAS and dopaminergic system and impaired parasympathetic nerve activity. During the acute phase of ARB treatment, cooperative effects of ARB and intrarenal dopaminergic system exert natriuresis to restore circadian BP rhythm.

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          Deceleration capacity of heart rate as a predictor of mortality after myocardial infarction: cohort study.

          Decreased vagal activity after myocardial infarction results in reduced heart-rate variability and increased risk of death. To distinguish between vagal and sympathetic factors that affect heart-rate variability, we used a signal-processing algorithm to separately characterise deceleration and acceleration of heart rate. We postulated that diminished deceleration-related modulation of heart rate is an important prognostic marker. Our prospective hypotheses were that deceleration capacity is a better predictor of risk than left-ventricular ejection fraction (LVEF) and standard deviation of normal-to-normal intervals (SDNN). We quantified heart rate deceleration capacity by assessing 24-h Holter recordings from a post-infarction cohort in Munich (n=1455). We blindly validated the prognostic power of deceleration capacity in post-infarction populations in London, UK (n=656), and Oulu, Finland (n=600). We tested our hypotheses by assessment of the area under the receiver-operator characteristics curve (AUC). During a median follow-up of 24 months, 70 people died in the Munich cohort and 66 in the London cohort. The Oulu cohort was followed-up for 38 months and 77 people died. In the London cohort, mean AUC of deceleration capacity was 0.80 (SD 0.03) compared with 0.67 (0.04) for LVEF and 0.69 (0.04) for SDNN. In the Oulu cohort, mean AUC of deceleration capacity was 0.74 (0.03) compared with 0.60 (0.04) for LVEF and 0.64 (0.03) for SDNN (p<0.0001 for all comparisons). Stratification by dichotomised deceleration capacity was especially powerful in patients with preserved LVEF (p<0.0001 in all cohorts). Impaired heart rate deceleration capacity is a powerful predictor of mortality after myocardial infarction and is more accurate than LVEF and the conventional measures of heart-rate variability.
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            Angiotensin II directly stimulates ENaC activity in the cortical collecting duct via AT(1) receptors.

            Angiotensin II (AngII) helps to regulate overall renal tubular reabsorption of salt and water, yet its effects in the distal nephron have not been well studied. The purpose of these studies was to determine whether AngII stimulates luminal Na(+) transport in the cortical collecting duct (CCD). Intracellular Na(+) concentration ([Na(+)](i)), as a reflection of Na(+) transport across the apical membrane, was measured with fluorescence microscopy using sodium-binding benzofuran isophthalate (SBFI) in isolated, perfused CCD segments dissected from rabbit kidneys. Control [Na(+)](i), during perfusion with 25 mM NaCl and a Na(+)-free solution in the bath containing the Na(+)-ionophore monensin (10 microM, to eliminate basolateral membrane Na(+) transport) averaged 19.3 +/- 5.2 mM (n = 16). Increasing luminal [NaCl] to 150 mM elevated [Na(+)](i) by 9.87 +/- 1.5 mM (n = 7; P < 0.05). AngII (10(-9) M) added to the lumen significantly elevated baseline [Na(+)](i) by 6.3 +/- 1.0 mM and increased the magnitude (Delta = 25.2 +/- 3.7 mM) and initial rate ( approximately 5 fold) of change in [Na(+)](i) to increased luminal [NaCl]. AngII when added to the bath had similar stimulatory effects; however, AngII was much more effective from the lumen. Thus, AngII significantly increased the apical entry of Na(+) in the CCD. To determine if this apical entry step occurred via the epithelial Na(+) channel (ENaC), studies were performed using the specific ENaC blocker, benzamil hydrochloride (10(-6) M). When added to the perfusate, benzamil almost completely inhibited the elevations in [Na(+)](i) to increased luminal [NaCl] in both the presence and absence of AngII. These results suggest that AngII directly stimulates Na(+) channel activity in the CCD. AT(1) receptor blockade with candesartan or losartan (10(-6) M) prevented the stimulatory effects of AngII. Regulation of ENaC activity by AngII may play an important role in distal Na(+) reabsorption in health and disease.
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              Sodium-potassium-adenosinetriphosphatase-dependent sodium transport in the kidney: hormonal control.

               E Féraille,  A Doucet (2000)
              Tubular reabsorption of filtered sodium is quantitatively the main contribution of kidneys to salt and water homeostasis. The transcellular reabsorption of sodium proceeds by a two-step mechanism: Na(+)-K(+)-ATPase-energized basolateral active extrusion of sodium permits passive apical entry through various sodium transport systems. In the past 15 years, most of the renal sodium transport systems (Na(+)-K(+)-ATPase, channels, cotransporters, and exchangers) have been characterized at a molecular level. Coupled to the methods developed during the 1965-1985 decades to circumvent kidney heterogeneity and analyze sodium transport at the level of single nephron segments, cloning of the transporters allowed us to move our understanding of hormone regulation of sodium transport from a cellular to a molecular level. The main purpose of this review is to analyze how molecular events at the transporter level account for the physiological changes in tubular handling of sodium promoted by hormones. In recent years, it also became obvious that intracellular signaling pathways interacted with each other, leading to synergisms or antagonisms. A second aim of this review is therefore to analyze the integrated network of signaling pathways underlying hormone action. Given the central role of Na(+)-K(+)-ATPase in sodium reabsorption, the first part of this review focuses on its structural and functional properties, with a special mention of the specificity of Na(+)-K(+)-ATPase expressed in renal tubule. In a second part, the general mechanisms of hormone signaling are briefly introduced before a more detailed discussion of the nephron segment-specific expression of hormone receptors and signaling pathways. The three following parts integrate the molecular and physiological aspects of the hormonal regulation of sodium transport processes in three nephron segments: the proximal tubule, the thick ascending limb of Henle's loop, and the collecting duct.

                Author and article information

                Physiol Rep
                Physiol Rep
                Physiological Reports
                John Wiley and Sons Inc. (Hoboken )
                02 June 2017
                June 2017
                : 5
                : 11 ( doiID: 10.1002/phy2.2017.5.issue-11 )
                [ 1 ] Department of Cardio‐Renal Medicine and HypertensionNagoya City University Graduate School of Medical Sciences NagoyaJapan
                [ 2 ] Department of BiochemistryNagoya City University Graduate School of Medical Sciences NagoyaJapan
                [ 3 ] Department of Mechanical Science and BioengineeringOsaka University OsakaJapan
                [ 4 ] Department of Physical and Health EducationUniversity of Tokyo Graduate School of Education TokyoJapan
                [ 5 ]International University of Health and Welfare TokyoJapan
                [ 6 ] Department of Medical EducationNagoya City University Graduate School of Medical Sciences NagoyaJapan
                Author notes
                [* ] Correspondence

                Michio Fukuda, Director, Division of Nephrology and Dialysis Center, Associate Professor, Department of Cardio‐Renal Medicine and Hypertension, Nagoya City University Graduate School of Medical Sciences, 467‐8601 Nagoya, Japan. Tel: +81‐52‐853‐8221; Fax: +81‐52‐852‐3796, E‐mail: m-fukuda@ 123456med.nagoya-cu.ac.jp

                © 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                Page count
                Figures: 2, Tables: 5, Pages: 13, Words: 9672
                Original Research
                Original Research
                Custom metadata
                June 2017
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.1.1 mode:remove_FC converted:14.06.2017


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