Effects of Nitric Oxide Inhibition on the Renal Papillary Blood Flow Response to Saline-Induced Volume Expansion in the Rat

1994 ◽  
Vol 86 (4) ◽  
pp. 405-409 ◽  
Author(s):  
Noemí M. Atucha ◽  
Ana Ramírez ◽  
Tomás Quesada ◽  
Joaquán García-Estañ
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Methyl Ester ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Renal Medulla ◽  
Synthesis Inhibitor ◽  
Doppler Flowmetry ◽  
Extracellular Volume Expansion

1. Evidence indicates that nitric oxide (NO) exerts a paracrine influence in the renal medulla. Increases in papillary blood flow are thought to be an important determinant of the renal response to extracellular volume expansion. Therefore, in the present study, we have evaluated the role of NO in mediating papillary blood flow (laser-Doppler flowmetry) and excretory responses to volume expansion with isotonic saline (3% body weight, 15 min). 2. Infusion of the NO synthesis inhibitor Nω-nitro-l-arginine methyl ester (10 μg min−1 kg−1), significantly attentuated the renal diuretic and natriuretic responses to volume expansion as well as the renal hydrostatic interstitial pressure increase induced by this manoeuvre. The percentages of the water and sodium excreted in 1 h by the Nω-nitro-l-arginine methyl ester-pretreated animals were 36% and 40% of the load, whereas those of the control animals were 44% and 65%, respectively. 3. In similar experiments performed in the exposed papilla of Munich Wistar rats, the same dose of Nω-nitro-l-arginine methyl ester reduced basal papillary blood flow and blunted the elevation in papillary blood flow induced by volume expansion (6% versus 16% in the control animals). 4. These results indicate that the inhibition of NO synthesis blunts the renal excretory and papillary responses to volume expansion, suggesting that NO modulates these responses through changes in papillary blood flow and renal interstitial hydrostatic pressure.

Role of prostaglandins on the renal effects of angiotensin and interstitial pressure during volume expansion

1993 ◽  
Vol 265 (6) ◽  
pp. R1469-R1474 ◽  
Author(s):  
J. M. Pinilla ◽  
A. Alberola ◽  
J. D. Gonzalez ◽  
T. Quesada ◽  
F. J. Salazar
Keyword(s):  
Volume Expansion ◽  
Left Kidney ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Synthesis Inhibitor ◽  
Extracellular Volume Expansion ◽  
The Right

This study was undertaken to determine, in anesthetized dogs, the role of renal prostaglandins (PG) in mediating the natriuretic response to increased renal interstitial hydrostatic pressure (RIHP) during extracellular volume expansion (ECVE) with isotonic saline. It was also determined if the intrarenal angiotensin II (ANG II) effects during ECVE are potentiated by the inhibition of PG synthesis. ECVE induced similar elevations of RIHP, natriuresis, and fractional lithium excretion in dogs treated (n = 7) and not treated with a PG synthesis inhibitor (n = 5). In other experimental groups, the effects of the intrarenal maintenance of ANG II levels (n = 6) by infusing captopril and ANG II into the right renal artery were compared with those induced by the simultaneous infusion of captopril, ANG II, and a PG synthesis inhibitor (n = 6). In response to ECVE, renal blood flow and glomerular filtration rate were similar in both kidneys when ANG II levels were maintained constant and were significantly higher in the left kidney when ANG II levels were maintained constant and PG synthesis was inhibited in the right kidney. However, when compared with the left kidney, the ECVE-induced increments of natriuresis and RIHP in the right kidney were reduced by the same magnitude when intrarenal ANG II was maintained constant with (36 and 53%, respectively) and without (40 and 54%, respectively) the simultaneous PG synthesis inhibition. Our results indicate that during ECVE, renal PGs do not play an important role in mediating the RIHP-induced increments in natriuresis and decrements in proximal sodium reabsorption. (ABSTRACT TRUNCATED AT 250 WORDS)

Systemic inhibition of nitric oxide and prostaglandins in volume-induced natriuresis and hypertension

1998 ◽  
Vol 274 (1) ◽  
pp. R175-R180 ◽  
Author(s):  
James D. Krier ◽  
Juan Carlos Romero
Keyword(s):  
Nitric Oxide ◽  
Mean Arterial Pressure ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Significant Elevation ◽  
Synthesis Inhibition ◽  
Anesthetized Dogs ◽  
Change Map

Nitric oxide (NO) synthesis inhibition with N G-nitro-l-arginine methyl ester (l-NAME) (10 μg ⋅ kg−1 ⋅ min−1iv), cyclooxygenase inhibition with meclofenamate (Meclo; 5 mg/kg iv bolus), and combination of drugs (l-NAME+Meclo) were used to investigate the roles of NO and prostaglandins (PG) in the hemodynamic and natriuretic responses to isotonic saline volume expansion (VE; 5% body wt over 60 min) in anesthetized dogs. Before VE,l-NAME ( n = 6), Meclo ( n = 6), andl-NAME+Meclo ( n = 6) produced significant increments in mean arterial pressure (MAP) of 12 ± 2, 15 ± 3, and 17 ± 3 mmHg, respectively. VE did not change MAP in Meclo-treated dogs, but produced a significant elevation in the control dogs (14 ± 6 mmHg), inl-NAME-treated dogs (17 ± 6 mmHg), and in dogs pretreated withl-NAME+Meclo (12 ± 5 mmHg). VE alone induced marked natriuretic responses in the control (38 ± 9 to 562 ± 86 μmol/min),l-NAME (31 ± 9 to 664 ± 65 μmol/min), and Meclo groups (41 ± 10 to 699 ± 51 μmol/min). However, this natriuretic response was attenuated in dogs pretreated with l-NAME+Meclo (12 ± 4 to 185 ± 52 μmol/min). These results indicate that 1) blockade of both NO and PGs has significant diminishing effects on volume-induced natriuresis, 2) NO blockade alone impairs volume-induced natriuresis in a manner that requires further increases in MAP to restore the natriuresis, and 3) PG blockade alone does not curtail volume-induced natriuresis.

Interactions between angiotensin and nitric oxide in the renal response to volume expansion

1995 ◽  
Vol 269 (3) ◽  
pp. R504-R510 ◽  
Author(s):  
M. T. Llinas ◽  
J. D. Gonzalez ◽  
F. J. Salazar
Keyword(s):  
Nitric Oxide ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Synthesis Inhibition ◽  
Renal Response ◽  
Group 2 ◽  
Extracellular Volume Expansion

This study examined, in anesthetized dogs, the possible interactions between nitric oxide (NO) and angiotensin II (ANG II) in mediating the renal response to an extracellular volume expansion (ECVE). It was found that the intrarenal maintenance of ANG II levels (group 1) or the intrarenal NO synthesis inhibition (group 2) did not induce changes in renal hemodynamics but reduced (P < 0.05) the ECVE-induced increments in sodium excretion and fractional lithium excretion (FeLi). In the third group, ANG II synthesis was inhibited during NO synthesis blockade. It was found in this group that the NO synthesis inhibition reduced the ECVE-induced increment in sodium excretion (P < 0.05) but did not modify the ECVE-induced increment in FeLi. These results suggest that the increase of proximal sodium reabsorption induced by the No synthesis inhibition is mediated by endogenous ANG II levels. In the fourth group, it was observed that NO synthesis inhibition, during the intrarenal maintenance of ANG II levels, induced a decrease of renal blood flow (P < 0.05) and reduced the natriuretic response to ECVE to a lower level (P < 0.05) than that observed in groups 1 and 2. The results of this group suggest that endogenous NO modulates the vasoconstrictor and antinatriuretic effects of ANG II during an ECVE. In summary, the results of this study suggest that there is an important interaction between NO and ANG II in mediating the renal response to an ECVE.

Restoration of tubuloglomerular feedback in volume-expanded rats by angiotensin II

1990 ◽  
Vol 259 (4) ◽  
pp. F565-F572 ◽  
Author(s):  
J. Schnermann ◽  
J. P. Briggs
Keyword(s):  
Angiotensin Ii ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Tubuloglomerular Feedback ◽  
Plasma Angiotensin ◽  
Single Nephron ◽  
Saline Administration ◽  
Flow Pressure ◽  
Extracellular Volume Expansion

Experiments were performed in anesthetized rats to examine whether angiotensin II corrects the attenuation of tubuloglomerular feedback (TGF) responses produced by acute extracellular volume expansion. Volume expansion was achieved by an infusion of isotonic saline at a rate of 9 ml/h. When urine flow had stabilized, an increase in loop of Henle flow from 0 to 45 nl/min caused a fall in stop-flow pressure (PSF) by 3.7 +/- 0.3 mmHg and in single-nephron glomerular filtration rate (SNGFR) by 5.1 +/- 1.7 nl/min. During continued saline administration angiotensin II was infused at 16, 48, or 96 ng.kg-1.min-1 while renal arterial pressure was held constant by suprarenal aortic clamping. The mean responses of PSF increased to 5.9 +/- 0.6, 9.8 +/- 0.7, and 14.9 +/- 1.7 mmHg. Angiotensin II infused at 54 ng.kg-1.min-1 increased the SNGFR response to 15.1 +/- 2.1 nl/min, whereas kidney GFR and distal SNGFR fell. Subcapsular pressure was not significantly altered by angiotensin II infusion (16 ng.kg-1.min-1). Plasma angiotensin (y, pg/ml) as a function of angiotensin II infusion rate (x, ng.kg-1.min-1 for approximately 20 min) was found to fit the function y = 2.89 + 3.53x. An infusion of approximately 15 ng.kg-1.min-1 restored plasma angiotensin levels in the volume-expanded rats to hydropenic values. These data confirm that angiotensin II may play a role as a physiological regulator of TGF sensitivity.

Effect of saline expansion on peritubule capillary pressures and reabsorption

1981 ◽  
Vol 240 (2) ◽  
pp. F106-F110 ◽  
Author(s):  
C. E. Ott
Keyword(s):  
Hydrostatic Pressure ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Isotonic Saline ◽  
Oncotic Pressure ◽  
Capillary Uptake ◽  
Before And After ◽  
Dog Kidney ◽  
Capillary Pressures ◽  
Extracellular Volume Expansion

The effect of extracellular volume expansion on transcapillary Starling forces, capillary uptake, and the reabsorption coefficient in the peritubule microcirculation of the dog kidney was examined. Micropuncture techniques were used to obtain measurement before and after 4% body wt expansion with isotonic saline. Extracellular volume expansion significantly changed all Starling pressures and capillary uptake. Efferent arteriolar oncotic pressure, interstitial oncotic pressure, and capillary uptake decreased (33.1 +/- 3.3 to 22.1 +/- 4.1 mmHg; 5.2 +/- 0.4 to 4.0 +/- 0.3 mmHg; and 44.9 +/- 9.2 to 28.7 +/- 8.6 nl/min, respectively), whereas capillary hydrostatic pressure and interstitial hydrostatic pressure increased (11.3 +/- 1.2 to 13.7 +/- 1.4 and 5.9 +/- 1.0 to 10.4 +/- 1.2 mmHg, respectively). The calculated reabsorption coefficient was 2.40 during hydropenia and 2.36 nl . min-1 . mmHg-1 following volume expansion. The results show that extracellular volume expansion significantly depresses capillary uptake in the dog and suggest that the decreased uptake can be accounted for totally by changes in transcapillary pressures and a constant reabsorption coefficient.

Vascular and renal effects of dopamine during extracellular volume expansion: Role of nitric oxide pathway

Life Sciences ◽  
2006 ◽  
Vol 78 (14) ◽  
pp. 1543-1549 ◽  
Author(s):  
María A. Costa ◽  
Rosana Elesgaray ◽  
Analía Loria ◽  
Ana María Balaszczuk ◽  
Cristina Arranz
Keyword(s):  
Nitric Oxide ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Renal Effects ◽  
Extracellular Volume Expansion ◽  
Nitric Oxide Pathway

Role of nitric oxide pathway in hypotensive and renal effects of furosemide during extracellular volume expansion

2004 ◽  
Vol 22 (8) ◽  
pp. 1561-1569 ◽  
Author(s):  
Mar??a A Costa ◽  
Anal??a Loria ◽  
Rosana Elesgaray ◽  
Ana Mar??a Balaszczuk ◽  
Cristina Arranz
Keyword(s):  
Nitric Oxide ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Renal Effects ◽  
Extracellular Volume Expansion ◽  
Nitric Oxide Pathway

Role of prostaglandins and nitric oxide in mediating renal response to volume expansion

1995 ◽  
Vol 268 (6) ◽  
pp. R1442-R1448 ◽  
Author(s):  
F. J. Salazar ◽  
M. T. Llinas ◽  
J. D. Gonzalez ◽  
T. Quesada ◽  
J. M. Pinilla
Keyword(s):  
Nitric Oxide ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Fractional Excretion ◽  
Renal Hemodynamics ◽  
Synthesis Inhibitor ◽  
Synthesis Inhibition ◽  
Renal Response ◽  
The Right

The objective of the present study was to examine, in anesthetized dogs, the possible interaction between prostaglandins (PG) and nitric oxide (NO) in mediating the renal response to an extracellular volume expansion (ECVE). The renal response to ECVE was examined during 1) intrarenal infusion of a PG synthesis inhibitor, 2) intrarenal administration of a NO synthesis inhibitor, and 3) simultaneous inhibition of PG and NO synthesis in the right kidney. Compared with the control group, the ECVE-induced increments in sodium excretion and fractional excretion of lithium were not affected by the PG synthesis inhibition. The NO synthesis inhibition did not induce changes in renal hemodynamics but reduced (P < 0.05) the ECVE-induced increments in sodium excretion and fractional excretion of lithium. When PG and NO synthesis were simultaneously inhibited in the right kidney during ECVE, there were no significant differences between the renal hemodynamics of both kidneys. However, compared with the left kidney, the ECVE-induced changes in sodium excretion and fractional excretion of lithium were reduced in the right kidney. The reduction of the natriuretic response to ECVE was greater (P < 0.05) than in the dogs where only NO synthesis was inhibited. Our results suggest a major interaction between NO and PG in mediating the renal hemodynamic and excretory responses to an increase in extracellular volume.

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