Renal endothelin system and excretory function in Wistar–Kyoto and Long–Evans rats

Girchev, R; Bäcker, Angela; Markova, P.; Kramer, Herbert J.

doi:10.1111/j.1748-1716.2005.01501.x

Cited by 8 publications

(4 citation statements)

References 38 publications

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“…With respect to the altered renal ET system in rats with spontaneous hypertension, which we found in the present and previous studies, it may be inferred that these are due to strain differences and are independent of BP alterations as we showed recently in Long-Evans rats [30] . In fact, the use of WKY rats as controls for SHR was challenged by some authors (for review, see Lindpaintner et al [31] ), but in the past and at present WKY rats were used as controls by most investigators, e.g.…”

Section: Discussionsupporting

confidence: 63%

Interaction of Endothelin with Renal Nerves Modulates Kidney Function in Spontaneously Hypertensive Rats

Girchev

Bäcker

Markova

et al. 2006

Kidney Blood Press Res

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Background and Methods: We investigated kidney function, renal endothelin-1 concentration, prepro-endothelin-1 mRNA as well as endothelin receptor A and B mRNA expression and receptor properties in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) with intact renal nerves and 7 days after renal denervation. In addition, responses of renal function to the non-selective ET_A/ET_B receptor blocker bosentan (10 mg/kg i.v. bolus injection) were studied. Results: In SHR, renal papillary prepro-endothelin-1 mRNA expression, endothelin-1 tissue concentrations and endothelin receptor density were significantly lower than in normotensive rats. Renal denervation was associated with a decrease in papillary tissue prepro-endothelin-1 mRNA and in WKY rats also with a significant reduction in papillary endothelin-1 content without affecting ET receptor density. Bosentan did not alter renal blood flow or glomerular filtration rate but decreased urine flow rate in both intact normotensive and hypertensive rats, whereas it decreased urine sodium and potassium excretion only in intact WKY. Bosentan had no effects on renal function in renal denervated rats. Conclusion: Since renal papillary endothelin-1 appears to counteract the fluid and sodium retaining effects of renal nerve activity, an impaired renal endothelin-1 synthesis in SHR may contribute to excessive sodium retention and thus to the pathogenesis of hypertension in SHR.

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Section: Discussionsupporting

confidence: 63%

Interaction of Endothelin with Renal Nerves Modulates Kidney Function in Spontaneously Hypertensive Rats

Girchev

Bäcker

Markova

et al. 2006

Kidney Blood Press Res

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“…In conscious animals (rats and dogs), antagonism of either ET A or ET B receptors has slight effects on basal RBF and GFR [837,843,[849][850][851] . ETA receptor blockade produces renal vasodilation and enhances pressure-dependent renin release [849,852] .…”

Section: Endothelin Effects On Renal Hemodynamicsmentioning

confidence: 99%

The Renal Microcirculation

et al. 2008

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“…BQ-788 did not inhibit constriction (C and D). #Significant difference from sham for P Ͻ 0.05. synthesis that suggest plasma ET-1 levels are primarily regulated at the level of promoter activation (15,28) and that the kidney and heart are primary sites of ET-1 production (17,25). Several transcription factors have been identified that modulate ET-1 synthesis including hypoxia inducible factor (HIF) (11,41).…”

Section: ) Et B Receptor Mrna Expression Is Not Different In Tissuesmentioning

confidence: 99%

Endothelin type A receptor antagonist normalizes blood pressure in rats exposed to eucapnic intermittent hypoxia

Allahdadi

Cherng²,

Pai³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Allahdadi KJ, Cherng TW, Pai H, Silva AQ, Walker BR, Nelin LD, Kanagy NL. Endothelin type A receptor antagonist normalizes blood pressure in rats exposed to eucapnic intermittent hypoxia. Am J Physiol Heart Circ Physiol 295: H434-H440, 2008. First published May 30, 2008 doi:10.1152/ajpheart.91477.2007.-We have reported that eucapnic intermittent hypoxia (E-IH) causes systemic hypertension, elevates plasma endothelin 1 (ET-1) levels, and augments vascular reactivity to ET-1 and that a nonspecific ET-1 receptor antagonist acutely lowers blood pressure in E-IH-exposed rats. However, the effect of chronic ET-1 receptor inhibition has not been evaluated, and the ET receptor subtype mediating the vascular effects has not been established. We hypothesized that E-IH causes systemic hypertension through the increased ET-1 activation of vascular ET type A (ETA) receptors. We found that mean arterial pressure (MAP) increased after 14 days of 7 h/day E-IH exposure (109 Ϯ 2 to 137 Ϯ 4 mmHg; P Ͻ 0.005) but did not change in sham-exposed rats. The ETA receptor antagonist BQ-123 (10 to 1,000 nmol/kg iv) acutely decreased MAP dose dependently in conscious E-IH but not sham rats, and continuous infusion of BQ-123 (100 nmol ⅐ kg Ϫ1 ⅐ day Ϫ1 sc for 14 days) prevented E-IHinduced increases in MAP. ET-1-induced constriction was augmented in small mesenteric arteries from rats exposed 14 days to E-IH compared with those from sham rats. Constriction was blocked by the ETA receptor antagonist BQ-123 (10 M) but not by the ET type B (ET B) receptor antagonist BQ-788 (100 M). ETA receptor mRNA content was greater in renal medulla and coronary arteries from E-IH rats. ETB receptor mRNA was not different in any tissues examined, whereas ET-1 mRNA was increased in the heart and in the renal medulla. Thus augmented ET-1-dependent vasoconstriction via vascular ETA receptors appears to elevate blood pressure in E-IHexposed rats. sleep apnea; BQ-123; BQ-788; mitochondrial ribonucleic acid OBSTRUCTIVE SLEEP APNEA is characterized by repeated upper airway obstruction during sleep and affects between 5% and 20% of the population (32). This syndrome of sleep-disordered breathing leads to episodic hypoxia and sleep deprivation. Recent epidemiological studies reveal that sleep apnea and other forms of sleep-disordered breathing increase the risk for hypertension and associated metabolic disorders (24). However, the mechanisms whereby sleep apnea and the associated eucapnic intermittent hypoxia (E-IH) cause systemic hypertension remain incompletely understood. Recent studies show that patients with sleep apnea have increased circulating levels of endothelin (ET)-1 (29, 42), a potent vasoconstrictor and mitogenic peptide implicated in the development of many forms of arterial hypertension (1). Furthermore, the synthesis of ET-1 is increased by hypoxia, shear stress, oxidative stress, and catecholamines, which are elevated in E-IH-exposed rats and sleep apnea (42, 47). We have previously described that both blood pressure and plasma ET-1 levels are incre...

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Renal endothelin system and excretory function in Wistar–Kyoto and Long–Evans rats

Abstract: The present data show that the selective ET(A) or ET(B) receptor blockade differentially affects tubular water and salt handling, which becomes apparent in conditions of low renal papillary endothelin receptor number and tissue endothelin-1 concentration.

Cited by 8 publications

References 38 publications

Interaction of Endothelin with Renal Nerves Modulates Kidney Function in Spontaneously Hypertensive Rats

Interaction of Endothelin with Renal Nerves Modulates Kidney Function in Spontaneously Hypertensive Rats

The Renal Microcirculation

Endothelin type A receptor antagonist normalizes blood pressure in rats exposed to eucapnic intermittent hypoxia

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