Urinary excretion of vasoactive factors are correlated to sodium excretion

Jackson, Robert W.; Treiber, Frank A.; Harshfield, Gregory A.; Waller, Jennifer L.; Pollock, Jennifer S.; Pollock, David M.

doi:10.1016/s0895-7061(01)02169-0

Cited by 24 publications

(23 citation statements)

References 15 publications

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“…In a larger study investigating the relationship between vasoactive factors and sodium excretion, a significantly decreased basal level of urinary NOx in AAs as compared with EAs was reported, although diet was not controlled among the groups. 109 Although this group did not study vasodilation in response to a stimulus, they did find a significant correlation between sodium excretion and urinary levels of NOx in AAs but not in EAs. 109 These authors concluded that the NO natriuretic axis is more active in regulating blood pressure via sodium excretion/NO production in AAs than in EAs.…”

Section: Racial Differences In Nitric Oxide Production/bioavailabilitymentioning

confidence: 89%

“…109 Although this group did not study vasodilation in response to a stimulus, they did find a significant correlation between sodium excretion and urinary levels of NOx in AAs but not in EAs. 109 These authors concluded that the NO natriuretic axis is more active in regulating blood pressure via sodium excretion/NO production in AAs than in EAs. Another interesting study compared premenopausal AA and EA overweight women responses to weight loss in terms of oxidative stress (6-nitrotyrosine plasma levels and myelperoxidase levels) and NO bioavailability (NOx plasma levels).…”

Section: Racial Differences In Nitric Oxide Production/bioavailabilitymentioning

confidence: 89%

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Racial Differences in Nitric Oxide—Dependent Vasorelaxation

Mata‐Greenwood

Chen

2008

Reprod. Sci.

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Along with the growing heterogeneity of the American population, ethnic/racial disparity is becoming a clear health issue in the United States. The awareness of ethnic/racial disparities has been growing because of considerable data gathered from recent clinical and epidemiological studies. These studies have highlighted the importance of addressing these differences in the diagnosis and treatment of various diseases potentially according to race. It is becoming particularly clear that there is a 2-to 3-fold racial difference in certain cardiovascular diseases (eg, preeclampsia) associated with dysfunctional nitric oxide-mediated vasodilation. In this review, the authors summarize the current literature on racial disparities in nitric oxide-mediated vasodilation in relation to cardiovascular health with an emphasis on vascular nitric oxide bioavailability as a balance between production via endothelial nitric oxide synthase and degradation through reactive oxygen species. The major hypotheses postulated on the biological basis of these differences are also highlighted. KeywordsRace; nitric oxide; endothelial nitric oxide synthase Nitric oxide (NO) was discovered in 1988 as the vascular endothelial cell-derived factor that causes relaxation of the underlying vascular smooth muscle. 1-3 NO dilates all types of blood vessels by stimulating soluble guanylate cyclase that produces cyclic guanosine monophosphate in smooth muscle cells. 3 In addition to its vasodilatory properties, NO exerts some anti-inflammatory effects in the blood vessel wall by inhibiting leukocyte adhesion to the endothelium. 4 NO also inhibits platelet adhesion and activation, thereby acting as an antithrombotic factor. 5 NO inhibits smooth muscle cell proliferation and migration and regulates the expression of certain proteins involved in vessel wall remodeling, thereby contributing to the control of vascular compliance. 6 Other functions of NO not related to the cardiovascular system include regulation of neuronal proliferation/differentiation, 7 sexual function, 8 insulin release, 9 and immune responses in inflammation. 10 NO participates in a broad spectrum of physiologic and pathophysiologic processes, 11 such as neurodegeneration and memory function, 12,13 pulmonary vascular remodeling and apoptosis, 14 atherosclerosis, 15 and exercise-induced cardioprotection. 16 Impairment of NO bioavailability leads to endothelial dysfunction and is a pivotal event in the pathogenesis of many cardiovascular diseases such as hypertension, heart failure, and coronary artery disease. 17-19 NO-dependent endothelial dysfunction has also been associated with a range of other disorders such as pulmonary hypertension, 20 asthma, 14,20 erectile dysfunction, 8 preeclampsia, 21 and insulin resistance and diabetes mellitus. 9The ethnic/racial impact on health has been receiving considerable attention in recent years. The phenomenon of ethnic health disparities in cardiovascular and many other diseases is becoming clear, and awareness of the importance in ad...

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Section: Racial Differences In Nitric Oxide Production/bioavailabilitymentioning

confidence: 89%

Section: Racial Differences In Nitric Oxide Production/bioavailabilitymentioning

confidence: 89%

Racial Differences in Nitric Oxide—Dependent Vasorelaxation

Mata‐Greenwood

Chen

2008

Reprod. Sci.

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“…Several lines of evidence demonstrate that urinary excretion of endothelin specifically reflects renal endothelin production. Renal endothelin production is increased in experimental animals given a high salt diet (17) and changes in sodium excretion are tightly correlated to urinary excretion of ET-1 in humans (118). Patients with hypertension, in particular those with salt-sensitive hypertension, were found to excrete less ET-1 in their urine than normotensive subjects, indicating reduced renal ET-1 production in the hypertensive subjects (119).…”

Section: Essential Hypertensionmentioning

confidence: 99%

Contrasting Actions of Endothelin ET_Aand ET_BReceptors in Cardiovascular Disease

Schneider

Boesen

Pollock

2007

Annu. Rev. Pharmacol. Toxicol.

262

247

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First identified as a powerful vasoconstrictor, endothelin has an extremely diverse set of actions that influence homeostatic mechanisms throughout the body. Two receptor subtypes, ET A and ET B , which usually have opposing actions, mediate the actions of endothelin. ET A receptors function to promote vasoconstriction, growth, and inflammation while ET B receptors produce vasodilation, increases in sodium excretion, and inhibit growth and inflammation. Potent and selective receptor antagonists have been developed and have shown promising results in the treatment of cardiovascular diseases such as pulmonary arterial hypertension, acute and chronic heart failure, hypertension, renal failure and atherosclerosis. However, results are often contradictory and complicated because of the tissue-specific vasoconstrictor actions of ET B receptors and the fact that endothelin is an autocrine and paracrine factor whose activity is difficult to measure in vivo. Considerable questions remain regarding whether ET A selective or non-selective ET A /ET B receptor antagonists would be useful in a range of clinical settings. Keywordsreceptor localization; pulmonary hypertension; heart failure; chronic kidney disease Shortly after it was discovered that the vascular endothelium releases a peptide capable of profound vasoconstriction, a considerable amount of attention was paid to the potential actions of endothelin in the pathogenesis of cardiovascular disease. We have since learned a great deal about how this paracrine factor influences function in an extremely wide range of areas including neurotransmission, cell growth and epithelial transport, just to name a few. This myriad of activities has allowed the endothelin system to garner a tremendous amount of attention from the pharmaceutical industry with the development of numerous receptor specific and non-specific antagonists as well as efforts to identify drugs that inhibit endothelin synthesis. This work has led to new therapeutic approaches to pulmonary arterial hypertension and most likely other diseases in the not too distant future. In addition to this enormous drug discovery effort, it has also become clear that endothelin plays an important physiological role in maintaining blood pressure homeostasis, for example, by facilitating the excretion of a high salt diet. Because of the almost bewildering range of actions of the endothelin peptides, we limit this review to focus on the receptor-specific cardiovascular actions of endothelin. ENDOTHELIN PEPTIDESEndothelin-1, a 21-amino-acid long peptide first isolated from the supernatant of cultured endothelial cells, is perhaps the most potent vasoconstrictor substance known (1). The human Address for Correspondence: David M. Pollock, Ph.D., Vascular Biology Center, Medical College of Georgia, 1459 Laney Walker Blvd., Augusta, GA 30912-2500, +1-706-721-8517 office, +1-706-721-9799 fax, dpollock@mcg.edu. NIH Public Access Author ManuscriptAnnu Rev Pharmacol Toxicol. Author manuscript; available in PMC 2010 February 22. P...

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“…Electrolyte concentrations were determined by ion-selective electrodes (Synchron EL-ISE; Beckman Instruments, Brea, CA). Urinary cGMP concentration was measured by a scintillation proximity method, as described previously (14). ELISA kits were utilized to quantify urinary microalbumin concentration (Nephrat; Exocell, Philadelphia, PA) and plasma insulin concentration (ALPCO Diagnostics, Windham, NH).…”

Section: Analysesmentioning

confidence: 99%

Posttranslational regulation of NO synthase activity in the renal medulla of diabetic rats

Lee¹,

Sasser²,

Hobbs³

et al. 2005

American Journal of Physiology-Renal Physiology

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1177 NOS3 was evident only in the thick ascending limb, with no apparent differences between groups. In summary, glucose-dependent osmotic diuresis alone did not alter NOS activity or expression in the renal medulla. Diabetic hyperglycemia increased medullary NOS3 activity without a concomitant increase in NOS3 protein levels; however, NOS3 phosphorylation was reduced at Thr 495 and Ser 633 . Thus changes in the phosphorylation of NOS at known regulatory sites might represent the primary mechanism underlying increased renal medullary NOS activity in diabetic hyperglycemia. streptozotocin; phosphorylation; phlorizin; nitric oxide synthase; NOS3; NOS1 AN IMPORTANT PHYSIOLOGICAL regulator of renal function, nitric oxide (NO) is synthesized as a by-product of the conversion of L-arginine to L-citrulline. The greatest capacity for renal NO synthesis resides in the medulla (23, 34), which expresses all three isoforms of NO synthase (NOS) (18). A paracrine NO system has been postulated to reside within the renal medulla, relying on cross-talk between epithelial and microvascular cells to match vasa recta blood flow to tubular metabolic transport activity (6). Accordingly, a decrease in NO production achieved by medullary interstitial infusion of NOS inhibitors leads to a reduction in medullary blood flow and salt retention, whereas infusion of NOS substrate increases medullary blood flow (15, 28). A previous report (3) from our laboratory revealed that NO production is modulated by shear stress in an inner medullary collecting duct cell line (IMCD-3), suggesting that tubular fluid flow may play a role in regulating sodium and water excretion by virtue of shear stress-mediated control of NO production. Moreover, Ortiz et al. (27) recently reported that flow stimulates translocation and phosphorylation of NOS3 and an associated increase in NO production by isolated thick ascending limb segments. However, it is unclear whether chronic increases in urine flow per se provoke an increase in NO synthesis and/or NOS expression in the renal medulla. One approach to examining this postulate is to determine whether pathophysiological states associated with increased urine flow are associated with increased NOS activity in the renal medulla. For example, urine flow is significantly increased in type 1 diabetes mellitus (T1D) because of a glucose-dependent osmotic diuresis. Thus, if shear stress represents an important determinant of NO production in the thick ascending limb and/or collecting duct, one would predict that renal medullary NOS activity would be increased in T1D.Most of the literature concerning the renal complications of T1D focuses on alterations in glomerular structure/function or impaired regulation of arteriolar tone/reactivity. However, recent studies have revealed that the early stage of T1D is accompanied by altered expression of multiple renal medullary transport proteins: e.g., the bumetanide-sensitive NaϪ cotransporter; epithelial Na ϩ channel subunits-␣, -␤, and -␥; aquaporins 2 and 3; urea transporter-A1 ...

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Urinary excretion of vasoactive factors are correlated to sodium excretion

Cited by 24 publications

References 15 publications

Racial Differences in Nitric Oxide—Dependent Vasorelaxation

Racial Differences in Nitric Oxide—Dependent Vasorelaxation

Contrasting Actions of Endothelin ET_Aand ET_BReceptors in Cardiovascular Disease

Posttranslational regulation of NO synthase activity in the renal medulla of diabetic rats

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Urinary excretion of vasoactive factors are correlated to sodium excretion

Cited by 24 publications

References 15 publications

Racial Differences in Nitric Oxide—Dependent Vasorelaxation

Racial Differences in Nitric Oxide—Dependent Vasorelaxation

Contrasting Actions of Endothelin ETAand ETBReceptors in Cardiovascular Disease

Posttranslational regulation of NO synthase activity in the renal medulla of diabetic rats

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Contrasting Actions of Endothelin ET_Aand ET_BReceptors in Cardiovascular Disease