scholarly journals Studies on the mechanism of natriuresis accompanying increased renal blood flow and its role in the renal response to extracellular volume expansion.

1965 ◽  
Vol 44 (11) ◽  
pp. 1857-1865 ◽  
Author(s):  
L E Earley ◽  
R M Friedler
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Renal Response ◽  
Extracellular Volume Expansion

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.

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.

Role of Oxytocin in the Natriuresis of Extracellular Volume Expansion

1969 ◽  
Vol 130 (4) ◽  
pp. 1276-1279 ◽  
Author(s):  
S. G. Massry ◽  
H. Vorherr ◽  
C. R. Kleeman
Keyword(s):  
Volume Expansion ◽  
Extracellular Volume ◽  
Extracellular Volume Expansion

Extracellular Volume Expansion Caused by Protein Malnutrition in Peritoneal Dialysis Patients with Appropriate Salt and Water Removal

2008 ◽  
Vol 28 (4) ◽  
pp. 407-412 ◽  
Author(s):  
M.-José Fernández-Reyes ◽  
M.-Auxiliadora Bajo ◽  
Gloria del Peso ◽  
Dabaiba Regidor ◽  
Covadonga Hevia ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Protein Malnutrition ◽  
Water Removal ◽  
Dialysis Patients ◽  
Extracellular Volume Expansion

Effects of volume expansion on renal nerve activity, renal blood flow, and sodium and water excretion in conscious dogs

1985 ◽  
Vol 249 (5) ◽  
pp. F680-F687 ◽  
Author(s):  
H. Morita ◽  
S. F. Vatner
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Renal Vascular Resistance ◽  
Conscious Dogs ◽  
Renal Nerve ◽  
Water Excretion ◽  
Renal Nerve Activity ◽  
Renal Vascular

Effects of acute volume expansion with isotonic isoncotic 3% dextran in saline were examined on renal nerve activity (RNA), renal blood flow, vascular resistance, and sodium and water excretion in conscious dogs. In intact dogs, acute volume expansion increased mean arterial pressure 15 +/- 3 mmHg, left atrial pressure 5.5 +/- 0.6 mmHg, and decreased RNA 88 +/- 2%, whereas renal blood flow did not change and renal vascular resistance increased slightly. When renal perfusion pressure was maintained at control levels, volume expansion decreased RNA 87 +/- 2% and renal vascular resistance 15 +/- 4%. During the 80-min period after volume expansion, urine flow rate increased 0.66 +/- 0.13 ml/min and sodium excretion rose 3.89 +/- 0.54 mueq X min-1 X kg-1, whereas RNA remained depressed. Arterial baroreceptor denervation (ABD) did not diminish responses of RNA, renal blood flow, renal vascular resistance, or sodium and water excretion to volume expansion. After ABD plus bilateral cervical vagotomy, volume expansion did not decrease RNA, and diuretic and natriuretic responses were significantly attenuated (P less than 0.025). However, responses of renal blood flow to volume expansion were not altered significantly. In conscious dogs with renal denervation, responses of renal blood flow to volume expansion were not impaired, whereas diuretic and natriuretic responses were attenuated (P less than 0.025). Thus, in intact conscious dogs, vagally mediated reflex decreases in RNA induced by acute volume expansion exerted a significant effect on sodium and water excretion but little control of renal blood flow and renal vascular resistance.

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