Increased urinary NO2−/NO3− and cyclic guanosine monophosphate levels in patients with bartter's syndrome: Relationship to vascular reactivity

Calò, Lorenzo A.; D’Angelo, Angela; Cantaro, S.; Bordin, Maria Cristina; Favaro, S.; Antonello, Augusto; Borsatti, A.

doi:10.1016/s0272-6386(96)90514-4

Cited by 49 publications

(27 citation statements)

References 23 publications

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“…40 Relationships between EPCs, FMD and HO-1 LA Calò et al in BS/GS patients. 29,30 In addition, despite high levels of Ang II, BS/GS patients have increased FMD and upregulation of NO system, 19,31,32 both of which are consistent with the increased number of EPC cells found in this study. The elevated HO-1 gene expression found in BS/GS patients and the increased levels of EPC observed in this study are consistent with the reports in an animal study that elevating HO-1 increased the numbers of circulating EPCs and bone marrow early and late outgrowth progenitor cells, and enhanced the maturation of bonemarrow-derived progenitor cells.…”

Section: Discussionsupporting

confidence: 86%

“…[16][17][18][19][20] We have documented a blunted Ang II signaling and related pathways [21][22][23][24][25][26][27][28] in BS/GS patients. In addition, we have reported in BS/GS reduced oxidative stress alongside increased HO-1 gene expression, 29,30 upregulation of nitric oxide (NO) system 31,32 and increased NO-dependent vasodilation. 19 BS/GS likely represents a human model of endogenous Ang II type 1 receptor antagonism and produce a mirror image of the alterations found in hypertension.…”

Section: Introductionmentioning

confidence: 97%

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Endothelial progenitor cells relationships with clinical and biochemical factors in a human model of blunted angiotensin II signaling

et al. 2011

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Angiotensin II (Ang II) is essential for endothelial progenitor cells (EPCs) function as Ang-II-induced oxidative stress causes senescence of EPCs and endothelial dysfunction and Ang II type 1 receptor blockers increase EPCs. Moreover, EPCs activity is dependent on nitric oxide (NO) and heme oxygenase (HO)-1 as these correlate with EPCs senescence and are reduced in hypertensives. Bartter's/Gitelman's syndrome patients (BS/GS), have increased Ang II yet normo/hypotension along with blunted Ang II signaling, reduced oxidative stress, increased NO and HO-1, thus presenting a unique system to explore EPC biology and its relationship with vascular clinical and biochemical correlates. Circulating EPCs, NO-dependent vasodilation (flow-mediated dilation (FMD)) and HO-1 gene expression were characterized in 10 BS/GS patients and in 10 normotensive subjects. EPCs defined by cell surface antigens CD34+kinase-insert domain receptor (KDR+), CD133+KDR+ and CD133+CD34+KDR+ cells were quantitiated via direct three-color flow-cytometry analysis, HO-1 gene expression by reverse transcription-PCR and FMD by B-mode echo scan of the right brachial artery. Correlation analysis was carried out regarding FMD and EPCs, FMD and HO-1 and EPCs and HO-1. In BS/GS, CD34+KDR+ cell numbers did not differ from controls while CD133+KDR+ and CD133+CD34+ KDR+ cell numbers were higher. HO-1 gene expression, as well as FMD, was higher in BS/GS compared with controls. Both CD133+KDR+ and CD133+CD34+KDR+ strongly correlated with both FMD and HO-1. FMD and HO-1 were also strongly correlated. These results document in a human system that EPC numbers and specific populations are related to important clinical and biochemical factors involved in cardiovascular (CV) status and reaffirm the utility of BS/GS patients as a useful system to investigate EPC's role(s) in the pathophysiology of cardiovascular remodeling in humans.

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Section: Discussionsupporting

confidence: 86%

Section: Introductionmentioning

confidence: 97%

Endothelial progenitor cells relationships with clinical and biochemical factors in a human model of blunted angiotensin II signaling

et al. 2011

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“…We showed, in fact, in Bartter's and Gitelman's patients [15] an anomaly in the intracellular Ca 2+ and IP 3 signaling system [16,17], a reduced protein kinase C activity [17,18] and upregulation of the nitric oxide system [19,20]. We have also studied aspects of these diseases connected with electrolyte abnormalities [21] and, more recently, with magnesium handling and chondrocalcinosis [22].…”

mentioning

confidence: 99%

Hypomagnesemia and Chondrocalcinosis in Bartter’s and Gitelman’s Syndrome: Review of the Pathogenetic Mechanisms

2000

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“…Deficiency of NO is known to contribute to the pathogenesis of hypertension [19,20]. In a previous report [4], increased levels of NO might be viewed as a possible determinant of vascular hyporeactivity. The cellular source of the increased urinary nitrite excretion observed in children with Bartter syndrome cannot be deduced from this study.…”

Section: Discussionmentioning

confidence: 90%

“…These events are not caused by hypokalemia, because they are still present even after the patients are made normokalemic [2], nor by prostaglandin overproduction, because they do not disappear after treatment with inhibitors of prostaglandin synthesis [3]. Recent evidence in adult Bartter syndrome suggests that increased nitric oxide (NO) synthesis may account for the reduced vascular response of the disease [4]. However, to our knowledge, no studies have investigated renal NO and adrenomedullin, another vasodilator peptide, production in children with Bartter syndrome. NO is synthesized from L-arginine by the enzyme nitric oxide synthase (NOS).…”

Section: Introductionmentioning

confidence: 99%

Adrenomedullin and nitrite levels in children with Bartter syndrome

Balat

Çekmen

Yürekli

et al. 2000

Pediatric Nephrology

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Children with Bartter syndrome have lower than normal vascular reactivity with normotension in spite of biochemical and hormonal abnormalities which are typical of hypertension. Nitric oxide (NO) is a potent endogenous vasodilator, and plays an important role in the control of vascular tone. Adrenomedullin (AM) is a novel hypotensive peptide originally isolated from human pheochromocytoma. The possible role of NO and AM in maintaining this reduced vascular reactivity was examined by studying plasma and urinary nitrite, a stable metabolite of NO, and AM levels in ten children with Bartter syndrome, ten healthy controls, and five children with hypokalemia of causes other than Bartter syndrome (pseudo-Bartter). Urinary excretion of nitrite (mumol/mg urinary creatinine) was 8.9 +/- 1.2 in children with Bartter syndrome, 4.7 +/- 0.9 in healthy controls, and 2.9 +/- 0.8 in pseudo-Bartter (P < 0.05). Plasma nitrite levels (mumol/l) were 101.9 +/- 23.4, 59.9 +/- 14.7, and 65.0 +/- 29.7, respectively (P < 0.05), in the three groups. Urinary excretion of AM (pmol/mg urinary creatinine) was 187 +/- 40, 65 +/- 10, and 160 +/- 50, respectively (P < 0.05), in the three groups. Plasma AM levels were 47.4 +/- 1.8, 39.9 +/- 5.9, and 42.4 +/- 3.9, respectively (P > 0.05), in the three groups. The same parameters were repeated in the two groups of controls and in the Bartter patients in the 6th month of therapy. Urinary nitrite and AM levels were still higher in the Bartter patients than in the other groups. We conclude that in Bartter syndrome the increased NO production may be responsible for the reduced vascular response of the disease. Initially, increased levels of AM in Bartter syndrome and pseudo-Bartter may be a compensatory response to acute hypokalemia; however, continuation of a high level of urinary excretion of AM in children with Bartter syndrome may suggest also the possible role of AM in the reduced vascular response of the disease.

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Increased urinary NO2−/NO3− and cyclic guanosine monophosphate levels in patients with bartter's syndrome: Relationship to vascular reactivity

Cited by 49 publications

References 23 publications

Endothelial progenitor cells relationships with clinical and biochemical factors in a human model of blunted angiotensin II signaling

Endothelial progenitor cells relationships with clinical and biochemical factors in a human model of blunted angiotensin II signaling

Hypomagnesemia and Chondrocalcinosis in Bartter’s and Gitelman’s Syndrome: Review of the Pathogenetic Mechanisms

Adrenomedullin and nitrite levels in children with Bartter syndrome

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