Angiotensin II stimulation of Na(+)-H+ exchange in proximal tubule cells

Saccomani, G.; Mitchell, Kenneth D.; Navar, L. Gabriel

doi:10.1152/ajprenal.1990.258.5.f1188

Cited by 89 publications

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“…This effect is mediated mainly by influencing the proximal sodium-hydrogen exchanger on the luminal membrane and the sodium-bicarbonate cotransporter on the basolateral membrane. Studies in isolated proximal tubular cells showed that Ang II stimulates Na + /H + exchanger via AT1 receptors [66]. Although some AT2 receptors have been confirmed on proximal tubules [20], most functional studies suggest that the major effects of Ang II on proximal tubules are via AT1 receptors [67].…”

Section: Tubular Function Of Ras Angiotensin IImentioning

confidence: 99%

Renal Renin-Angiotensin System

Ichihara

Kobori

Nishiyama

et al. 2004

Contributions to Nephrology

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The cardinal role of the intrarenal renin-angiotensin system (RAS) in the control of sodium excretion and the pathophysiology of hypertension continues to receive increased attention. In addition to its very powerful vasoconstrictor action, angiotensin (Ang) II exerts important actions on tubular transport function and several recent studies have emphasized the potential importance of actions of angiotensin peptides on receptors localized to the luminal membranes of both proximal and distal nephron segments. Furthermore, a strong case is being developed supporting the importance of local mechanisms regulating the activity of the RAS. This is due to the fact that all components of the RAS are strongly expressed in the kidneys.

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Section: Tubular Function Of Ras Angiotensin IImentioning

confidence: 99%

Renal Renin-Angiotensin System

Ichihara

Kobori

Nishiyama

et al. 2004

Contributions to Nephrology

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“…Among the neurohumoral systems modulating renal sodium excretion, the renin angiotensin aldosterone system (RAAS) is a potential contributor to diuretic resistance in CHF. The RAAS produces renal sodium retention via several mechanisms [10][11][12] and increased circulating levels of various components comprising this system have been noted in decompensated CHF [13,14]. In severe CHF characterized by hyponatraemia, Dzau & Hollenberg showed that interruption of the RAAS axis for several days with captopril increased frusemide-induced natriuresis [15].…”

Section: Introductionmentioning

confidence: 99%

The renin angiotensin aldosterone system and frusemide response in congestive heart failure.

Reed

Greene

Ryan

et al. 1995

Brit J Clinical Pharma

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1. To test the hypothesis that basal renin angiotensin aldosterone system (RAAS) activity impairs the acute natriuretic response to frusemide in patients with mild or moderate congestive heart failure (CHF), we studied eight adult volunteers with preserved renal function, stable New York Heart Association Class II or III CHF, and echocardiographic evidence of left ventricular dysfunction due to myocardial infarction, hypertension, or both causes. 2. All patients received three dosing regimens administered in random order: (a) intravenous frusemide: 40 mg bolus then 40 mg h‐1 for 3 h, (b) captopril: two 12.5 mg oral doses separated by 2 h, (c) combined dosing: the first captopril dose preceded the frusemide bolus by 30 min. Sodium balance on an 80 mmol day‐1 sodium diet was documented prior to each dosing regimen. Sodium excretion was quantitated in urine collected at intervals until 3.5 h after initiating drug administration. During this time, urine output was replaced intravenously with an equivalent volume of 0.45% saline. 3. Captopril significantly lowered plasma angiotensin converting enzyme (ACE) activity and plasma aldosterone concentration, and raised inulin clearance. The drug had essentially no effect on the time course of magnitude of frusemide's natriuretic effect. Maximal fractional sodium excretion during frusemide infused by itself and in combination with captopril was 24.7 +/‐ 1.9% vs 28.2 +/‐ 3.8%, respectively (difference 3.5%; 95% CI, ‐4.0 to 11.0%; P > 0.05). Cumulative sodium excretion ending at 3.5 h was 429 +/‐ 53 mmol when frusemide was given alone and 455 +/‐ 69 mmol when captopril was added (difference, 26 mmol; CI, ‐121 to 174 mmol; P > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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“…7 Studies in isolated proximal tubular cells showed that Ang II stimulates Na ϩ /H ϩ exchanger via AT 1 receptor. 8 Peti-Peterdi et al 9 demonstrated that Ang II directly stimulates epithelial sodium channel activity in the cortical collecting duct via AT 1 receptors. Furthermore, epithelial sodium channel gene expression in the cortical collecting duct is also upregulated by Ang II.…”

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confidence: 99%

AT ₁ Receptor Mediated Augmentation of Intrarenal Angiotensinogen in Angiotensin II-Dependent Hypertension

et al. 2004

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Abstract-Angiotensin (Ang) II-infused hypertensive rats exhibit increases in renal angiotensinogen mRNA and protein, as well as urinary angiotensinogen excretion in association with increased intrarenal Ang II content. The present study was performed to determine if the augmentation of intrarenal angiotensinogen requires activation of Ang II type 1 (AT 1 ) receptors. Male Sprague-Dawley rats (200 to 220 g) were divided into 3 groups: sham surgery (nϭ10), subcutaneous infusion of Ang II (80 ng/min, nϭ11), and Ang II infusion plus AT 1 blocker (ARB), olmesartan (5 mg/d, nϭ12). Ang II infusion progressively increased systolic blood pressure (SBP) compared with sham (178Ϯ8 mm Hg versus119Ϯ4 at day 11). ARB treatment prevented hypertension (113Ϯ6 at day 11). Twenty-four-hour urine collections were taken at day 12, and plasma and tissue samples were harvested at day 13. The Ang IIϩARB group had a significant increase in plasma Ang II compared with Ang II and sham groups (365Ϯ46 fmol/mL versus 76Ϯ9 and 45Ϯ14, respectively). Nevertheless, ARB treatment markedly limited the enhancement of kidney Ang II by Ang II infusion (65Ϯ17 fmol/g in sham, 606Ϯ147 in Ang II group, and 288Ϯ28 in Ang IIϩARB group). Ang II infusion significantly increased kidney angiotensinogen compared with sham (1.69Ϯ0.21 densitometric units versus 1.00Ϯ0.17). This change was reflected by increased angiotensinogen immunostaining in proximal tubules. ARB treatment prevented this increase (1.14Ϯ0.12). Urinary angiotensinogen excretion rates were enhanced 4.7ϫ in Ang II group (4.67Ϯ0.41 densitometric units versus 1.00Ϯ0.21) but ARB treatment prevented the augmentation of urinary angiotensinogen (0.96Ϯ0.23). These data demonstrate that augmentation of intrarenal angiotensinogen in Ang II-infused rats is AT 1 -dependent and provide further evidence that urinary angiotensinogen is closely linked to intrarenal Ang II in Ang II-dependent hypertension. Key Words: angiotensin II Ⅲ angiotensinogen Ⅲ receptors, angiotensin II Ⅲ rats Ⅲ kidney A ngiotensin II (Ang II) plays an important role in proximal tubular reabsorptive function primarily via activation of Ang II type 1 (AT 1 ) receptor at both basolateral and luminal membranes. 1 Although some Ang II type 2 receptors have been confirmed on proximal tubules, 2 most functional studies suggest that the major effects of Ang II on proximal tubules are via AT 1 receptors. 3 Several studies have suggested that Ang II also plays an important role in the regulation of distal tubular reabsorption rate. 4 This effect was blocked by either saralasin or losartan, indicating that this stimulation involves AT 1 receptor activation. 4 These findings, together with the demonstration that AT 1 receptor is present on the luminal membranes of distal nephron segments, 5,6 suggest that luminal Ang II plays an important role in the regulation not only of proximal reabsorption rate but also of distal tubular reabsorptive function. 7 Studies in isolated proximal tubular cells showed that Ang II stimulates Na ϩ /H ϩ exchanger via AT 1 ...

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Angiotensin II stimulation of Na(+)-H+ exchange in proximal tubule cells

Cited by 89 publications

References 0 publications

Renal Renin-Angiotensin System

Renal Renin-Angiotensin System

The renin angiotensin aldosterone system and frusemide response in congestive heart failure.

AT ₁ Receptor Mediated Augmentation of Intrarenal Angiotensinogen in Angiotensin II-Dependent Hypertension

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Angiotensin II stimulation of Na(+)-H+ exchange in proximal tubule cells

Cited by 89 publications

References 0 publications

Renal Renin-Angiotensin System

Renal Renin-Angiotensin System

The renin angiotensin aldosterone system and frusemide response in congestive heart failure.

AT 1 Receptor Mediated Augmentation of Intrarenal Angiotensinogen in Angiotensin II-Dependent Hypertension

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AT ₁ Receptor Mediated Augmentation of Intrarenal Angiotensinogen in Angiotensin II-Dependent Hypertension