Correlation between radiocontrast-induced urinary urodilatin excretion and fractional excretion of sodium (FeNa) after cardiac angiography

The action of theophylline on the adenosine-induced decrease in renin release was studied in anesthetized dogs. Adenosine inhibited renin release, decreased GFR and fractional sodium excretion, and decreased the concentration of angiotensin II in the renal lymph. Theophylline (5 mumol/min intrarenally) had no significant effect on GFR or RBF yet produced a significant increase in the release of renin and the fractional excretion of sodium. The intrarenal infusion of adenosine (3 X 10(-7) mol/min) during theophylline infusion produced no effect on GFR or RBF, but fractional sodium excretion and renin release were significantly decreased. Adenosine was infused at a lower dose (3 X 10(-8) mol/min) during theophylline (5 X 10(-6) mol/min) infusion in a second group of dogs. With the exception of fractional sodium excretion, all effects of adenosine were effectively antagonized by theophylline. Theophylline at 5 X 10(-6) mol/min, which stimulates renin release and effectively antagonizes the renal effects of adenosine, had no detectable effect on cAMP measured in renal cortex. Furthermore, no change in cortical cAMP was observed until theophylline was increased 50-fold over the dose effective in antagonizing adenosine. These findings demonstrate that theophylline, at concentrations having no effect on cortical cAMP, antagonizes the effect of adenosine on renin release. The results are also consistent with the view that theophylline stimulates renin release by a mechanism other than its action on cAMP.

Download Full-text

Renal haemodynamic and tubular actions of urotensin II in the rat

Journal of Endocrinology ◽

10.1677/joe-08-0260 ◽

2008 ◽

Vol 198 (3) ◽

pp. 617-624 ◽

Cited By ~ 15

Author(s):

Alaa E S Abdel-Razik ◽

Ellen J Forty ◽

Richard J Balment ◽

Nick Ashton

Keyword(s):

Body Weight ◽

Renal Medulla ◽

Fractional Excretion ◽

Haemodynamic Effects ◽

Urotensin Ii ◽

Sprague Dawley ◽

Minimal Impact ◽

Sprague Dawley Rats ◽

Fractional Excretion Of Sodium ◽

Excretion Rates

Urotensin II (UTS) is a potent vasoactive peptide that was originally identified in teleost fish. Mammalian orthologues of UTS and its receptor (UTSR) have been described in several species, including humans and rats. We have shown previously that bolus injections of UTS caused a decrease in urine flow and sodium excretion rates in parallel with marked reductions in renal blood flow (RBF) and glomerular filtration rate (GFR). The aim of this study was to determine the effect of UTS infusion at a dose that has minimal impact upon renal haemodynamics in order to identify a potential direct tubular action of UTS. Infusion of rat UTS (rUTS) at 0.6 pmol/min per 100 g body weight in male Sprague–Dawley rats, which had no effect on RBF and caused a 30% reduction in GFR, resulted in a significant increase in the fractional excretion of sodium (vehicle 2.3±0.6 versus rUTS 0.6 pmol 4.5±0.6%, P<0.05) and potassium. At the higher dose of 6 pmol/min per 100 g body weight, haemodynamic effects dominated the response. rUTS induced a marked reduction in RBF and GFR (vehicle 1.03±0.06 versus rUTS 6 pmol 0.31±0.05 ml/min per 100 g body weight, P<0.05) resulting in an anti-diuresis and anti-natriuresis, but no change in fractional excretion of sodium or potassium. Uts2d and Uts2r mRNA expression were greater in the renal medulla compared with the cortex. Together, these data support an inhibitory action of Uts2d on renal tubule sodium and potassium reabsorption in the rat, in addition to its previously described renal haemodynamic effects.

Download Full-text

Enhanced renal sensitivity of the spontaneously hypertensive rat to urotensin II

AJP Renal Physiology ◽

10.1152/ajprenal.90374.2008 ◽

2008 ◽

Vol 295 (4) ◽

pp. F1239-F1247 ◽

Cited By ~ 10

Author(s):

Alaa E. S. Abdel-Razik ◽

Richard J. Balment ◽

Nick Ashton

Keyword(s):

Renal Function ◽

Spontaneously Hypertensive Rat ◽

Renal Medulla ◽

Fractional Excretion ◽

Urotensin Ii ◽

Spontaneously Hypertensive ◽

Wky Rats ◽

Hypertensive Rat ◽

Fractional Excretion Of Sodium ◽

Wistar Kyoto

Urotensin II (UII) has been implicated widely in cardiovascular disease. The mechanism(s) through which it contributes to elevated blood pressure is unknown, but its emerging role as a regulator of mammalian renal function suggests that the kidney might be involved. The aim of this study was to determine the effect of UII on renal function in the spontaneously hypertensive rat (SHR). UII infusion (6 pmol·min−1·100 g body wt−1) in anesthetized SHR and control Wistar-Kyoto (WKY) rats produced marked reductions in glomerular filtration rate (ΔGFR WKY, n = 7, −0.3 ± 0.1 vs. SHR, n = 7, −0.6 ± 0.1 ml·min−1·100 g body wt−1, P = 0.03), urine flow, and sodium excretion rates, which were greater in SHR by comparison with WKY rats. WKY rats also showed an increase in fractional excretion of sodium (ΔFENa; +0.6 ± 0.1%, P = 0.02) in contrast to SHR in which no such change was observed (ΔFENa −0.6 ± 0.2%). Blockade of the UII receptor (UT), and thus endogenous UII activity, with urantide evoked an increase in GFR which was greater in SHR (+0.3 ± 0.1) compared with WKY rats (+0.1 ± 0.1 ml·min−1·100 g body wt−1, P = 0.04) and was accompanied by a diuresis and natriuresis. UII and UT mRNA expression were greater in the renal medulla than the cortex of both strains; however, expression levels were up to threefold higher in SHR tissue. SHR are more sensitive than WKY to UII, which acts primarily to lower GFR thus favoring salt retention in this model of hypertension.

Download Full-text

Inhibition of nitric oxide synthesis attenuates pressure-induced natriuretic responses in anesthetized dogs

AJP Renal Physiology ◽

10.1152/ajprenal.1993.264.1.f79 ◽

1993 ◽

Vol 264 (1) ◽

pp. F79-F87 ◽

Cited By ~ 60

Author(s):

D. S. Majid ◽

A. Williams ◽

L. G. Navar

Keyword(s):

Nitric Oxide ◽

Blood Flow ◽

Sodium Excretion ◽

Renin Angiotensin System ◽

Fractional Excretion ◽

Urine Flow ◽

Synthesis Inhibition ◽

Fractional Excretion Of Sodium ◽

Anesthetized Dogs ◽

Pressure Natriuresis

Inhibition of nitric oxide (NO) synthesis by intrarenal administration of nitro-L-arginine (NLA) leads to decreases in urinary sodium excretion (UNaV) in association with the increases in renal vascular resistance (RVR). In the present study, we examined the ability of the kidney to alter its sodium excretion in response to acute changes in renal arterial pressure (RAP) in anesthetized dogs before and during intrarenal infusion of NLA (50 micrograms.kg-1.min-1). NO synthesis inhibition in 11 dogs increased RVR by 32 +/- 4% and decreased renal blood flow (RBF) by 25 +/- 3%, outer cortical blood flow by 25 +/- 6%, urine flow by 37 +/- 14%, UNaV by 71 +/- 5%, and fractional excretion of sodium (FENa) by 71 +/- 4%. Glomerular filtration rate was not significantly changed during NLA infusion. As previously reported, there was suppression of the RBF autoregulation plateau during NO synthesis inhibition. In addition, there was a marked attenuation of urine flow and UNaV responses to reductions in RAP (150 to 75 mmHg), with significant reductions in the slopes of the relationships between RAP vs. UNaV and RAP vs. FENa during NLA infusion. Similar responses were observed in nine other dogs treated with the angiotensin receptor antagonist losartan, indicating that an augmented activity of the renin-angiotensin system is not responsible for attenuation of the slope of the pressure-natriuresis relationship during NLA infusion. These data suggest that NO may participate in the mediation of the pressure-natriuresis response.

Download Full-text

Deletion of proton-sensing receptor GPR4 associates with lower blood pressure and lower binding of angiotensin II receptor in SFO

AJP Renal Physiology ◽

10.1152/ajprenal.00410.2016 ◽

2016 ◽

Vol 311 (6) ◽

pp. F1260-F1266 ◽

Cited By ~ 6

Author(s):

Xuming Sun ◽

Ellen Tommasi ◽

Doris Molina ◽

Renu Sah ◽

K. Bridget Brosnihan ◽

...

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Fractional Excretion ◽

Urine Osmolality ◽

Brain Regions ◽

Lower Blood Pressure ◽

Angiotensin Ii Receptor ◽

Lower Blood ◽

Fractional Excretion Of Sodium ◽

The Impact

Diets rich in grains and meat and low in fruits and vegetables (acid-producing diets) associate with incident hypertension, whereas vegetarian diets associate with lower blood pressure (BP). However, the pathways that sense and mediate the effects of acid-producing diets on BP are unknown. Here, we examined the impact of the deletion of an acid sensor GPR4 on BP. GPR4 is a proton-sensing G protein-coupled receptor and an acid sensor in brain, kidney, and blood vessels. We found that GPR4 mRNA was higher in subfornical organ (SFO) than other brain regions. GPR4 protein was abundant in SFO and present in capillaries throughout the brain. Since SFO partakes in BP regulation through the renin-angiotensin system (RAS), we measured BP in GPR4−/− and GPR4+/+ mice and found that GPR4 deletion associated with lower systolic BP: 87 ± 1 mmHg in GPR4−/− ( n = 35) vs. 99 ± 2 mmHg ( n = 29) in GPR4+/+; P < 0.0001, irrespective of age and sex. Angiotensin II receptors detected by 125I-Sarthran binding were lower in GPR4−/− than GPR4+/+ mice in SFO and in paraventricular nucleus of hypothalamus. Circulating angiotensin peptides were comparable in GPR4−/− and GPR4+/+ mice, as were water intake and excretion, serum and urine osmolality, and fractional excretion of sodium, potassium, or chloride. A mild metabolic acidosis present in GPR4−/− mice did not associate with elevated BP, implying that deficiency of GPR4 may preclude the effect of chronic acidosis on BP. Collectively, these results posit the acid sensor GPR4 as a novel component of central BP control through interactions with the RAS.

Download Full-text

Diagnostic value of urinary N-acetyl-β-d-glucosaminidase, its isoenzymes and the fractional excretion of sodium following renal transplantation

Clinica Chimica Acta ◽

10.1016/0009-8981(83)90312-1 ◽

1983 ◽

Vol 130 (3) ◽

pp. 369-376 ◽

Cited By ~ 19

Author(s):

Paul H. Whiting ◽

Jeffrey Petersen ◽

David A. Power ◽

Ronald D.M. Stewart ◽

Graeme R.D. Catto ◽

...

Keyword(s):

Renal Transplantation ◽

Fractional Excretion ◽

Diagnostic Value ◽

Fractional Excretion Of Sodium

Download Full-text

Comparison of the effects of parathyroid hormone (PTH) and recombinant PTH-related protein on bicarbonate excretion by the isolated perfused rat kidney

Journal of Endocrinology ◽

10.1677/joe.0.1260403 ◽

1990 ◽

Vol 126 (3) ◽

pp. 403-408 ◽

Cited By ~ 27

Author(s):

A. G. Ellis ◽

W. R. Adam ◽

T. J. Martin

Keyword(s):

Parathyroid Hormone ◽

Rat Kidney ◽

Urine Volume ◽

Clinical Manifestations ◽

Fractional Excretion ◽

Bicarbonate Concentration ◽

Isolated Perfused Rat Kidney ◽

Amino Terminal ◽

Fractional Excretion Of Sodium ◽

Perfused Rat Kidney

ABSTRACT The isolated perfused rat kidney was used to study the effects of amino-terminal fragments of human parathyroid hormone, hPTH(1–34), bovine parathyroid hormone, bPTH(1–84) and of PTH-related proteins, PTHrP(1–34), PTHrP(1–84), PTHrP(1–108) and PTHrP(1–141) on urinary bicarbonate excretion. PTHrP(1–34) (7 nmol/l), bPTH(1–84) (5·5 nmol/l) and hPTH(1–34) (7 nmol/l) had similar effects in increasing bicarbonate excretion with respect to the control. At lower concentrations (0·7 nmol/l) all PTHrP components, but not hPTH(1–34) or bPTH(1–84) increased bicarbonate excretion significantly. Infusions of PTHrP(1–108) and PTHrP(1–141) at 0·7 nmol/l, while associated with a rise in urinary bicarbonate concentration and excretion during the early stages of perfusion, produced a sharp decline in bicarbonate concentration and excretion in the latter part of perfusion. The different peptides produced no significant differences in glomerular filtration rate, fractional excretion of sodium or urine volume. The absence of substantial differences between the effects of hPTH(1–34) and PTHrP(1–34) are as noted in previous studies. The differences between PTHrP(1–108)/PTHrP(1–141) and PTHrP(1–34) demonstrated here are consistent with (1) the clinical manifestations of acidosis in hyperparathyroidism and alkalosis in humoral hypercalcaemia of malignancy, and (2) an independent action of a component of PTHrP beyond amino acids 1–34. Journal of Endocrinology (1990) 126, 403–408

Download Full-text

Glomerular and tubular function during AT1 receptor blockade in pigs with neonatal induced partial ureteropelvic obstruction

AJP Renal Physiology ◽

10.1152/ajprenal.00407.2006 ◽

2007 ◽

Vol 292 (3) ◽

pp. F921-F929 ◽

Cited By ~ 8

Author(s):

Anni Eskild-Jensen ◽

Klaus Thomsen ◽

Christine Rungø ◽

Luis S. Ferreira ◽

Lene Fogt Paulsen ◽

...

Keyword(s):

Collecting Duct ◽

Fractional Excretion ◽

At1 Receptor ◽

Receptor Blockade ◽

Glomerular Function ◽

Contralateral Kidney ◽

Diagnostic Potential ◽

Fractional Excretion Of Sodium ◽

Renal Sodium Handling ◽

Immunohistochemical Analyses

Previously, we showed that neonatal induced chronic partial unilateral ureteral obstruction (PUUO) of the multipapillary pig kidney decreased glomerular filtration rate (GFR) of the obstructed kidney. We hypothesized that ANG II and nitric oxide (NO) are important for the changes in renal function and in the present study we examined the effects of chronic AT1 receptor blockade using CV-11974 (0.12 mg/h candesartan from age 23 to 30 days) on kidney function development after PUUO was induced in 2-day-old piglets. Moreover, the effect of superimposed acute NO inhibition using NG-nitro-l-arginine methyl ester (l-NAME; 15 mg/kg) was examined to identify if this has diagnostic potential. PUUO significantly increased GFR in the nonobstructed contralateral kidney independent of candesartan. In candesartan-treated piglets, the l-NAME-induced GFR reduction seen in normal and nonobstructed kidneys was absent in the partial obstructed kidneys. Urine output and fractional excretion of water were increased from the partial obstructed kidneys. Consistent with this immunohistochemical analyses showed a reduced aquaporin-2 labeling in the collecting duct principal cells. Moreover, renal sodium handling was compromised by PUUO evidenced by an increased fractional excretion of sodium which was enhanced by candesartan treatment. In conclusion, our findings suggest that the counterbalance between AT1 receptor-mediated vasoconstriction and NO-mediated vasodilatation which maintain GFR in normal young porcine kidneys is changed by neonatal induced chronic PUUO. This may have diagnostic potential in children with suspected congenital obstruction. Our results also demonstrate compromised tubular functions in response to chronic PUUO despite preservation of glomerular function.

Download Full-text