Modulation of renal medullary ionic hypertonicity by prostaglandins: data from tissue admittance studies in the rat.

Dobrowolski, Leszek; Kompanowska-Jezierska, Elżbieta; Sadowski, Janusz

doi:10.1113/jphysiol.1995.sp020772

Cited by 4 publications

(3 citation statements)

References 18 publications

(31 reference statements)

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“…In this study PG blockade depressed MBF and increased the ionic component of medullary hypertonicity measured as tissue Y ( Fig. 2), in agreement with our previous findings ( Dobrowolski et al . 1995 , Sadowski et al .…”

Section: Discussionsupporting

confidence: 93%

“…A screw‐ controlled snare was placed around the aorta above the renal arteries and RPP was continuously recorded and maintained constant throughout experiments at about 108 mmHg. The details of animal preparation, surgical techniques and clearance procedures as well as analytical techniques for plasma and urine osmolality, sodium and tritiated inulin have been described earlier ( Dobrowolski et al . 1995 ).…”

Section: Methodsmentioning

confidence: 99%

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Exaggerated volume expansion natriuresis in rats preloaded with hypertonic saline: a paradoxical enhancement by inhibition of prostaglandin synthesis

Kompanowska-Jezierska

Walkowska

Sadowski

1999

Acta Physiologica Scandinavica

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In preliminary experiments rats preinfused with hypertonic saline showed exaggerated natriuresis after an additional small volume expansion (SVE). This was systematically studied in anaesthetized Wistar rats prepared for clearance studies of the left kidney and measurements of medullary blood flow (MBF, laser-Doppler technique) and tissue electrical admittance (Y ), an index of interstitial ion concentration. The rats were preinfused i.v. with 3 mL of 5% NaCl during 90 min. A subsequent injection of isotonic saline, 0.5% of body weight, increased sodium excretion (UNaV ) from 2.1 +/- 0.5 to 4.5 +/- 1.1 micromol min-1 and urine flow (V ) from 12.0 +/- 2.3 to 24.3 +/- 5.6 microL min-1 (P < 0.02). The same volume of whole blood increased UNaV from 5.0 +/- 1.4 to 8.7 +/- 1.7 micromol min-1 and V from 22.3 +/- 5.1 to 37.4 +/- 5.9 microL min-1 (P < 0.01). The glomerular filtration rate, MBF and Y did not change. In rats preinfused with 0.9% saline no natriuresis was observed after SVE. To examine if prostaglandins (PG) were involved in SVE natriuresis, indomethacin (Indo), 5 mg kg-1 or sodium meclophenamate (Meclo), 7.5 mg kg-1, were added to the injected 0.9% saline. Paradoxically, both PG synthesis inhibitors enhanced natriuresis to SVE. After Indo UNaV increased from 2.0 +/- 0.6 to 7.6 +/- 1.3 micromol min-1, significantly more than after SVE alone (P < 0.001). At higher baseline UNaV, the increase with Meclo from 4.5 +/- 1.2 to 13.5 +/- 1.8 micromol min-1 was significantly higher than after whole blood infusion (P < 0.001). MBF decreased and Y increased after both inhibitors. Further studies are required to explain the enhancement of natriuresis after blockade of PG synthesis.

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Section: Discussionsupporting

confidence: 93%

Section: Methodsmentioning

confidence: 99%

Exaggerated volume expansion natriuresis in rats preloaded with hypertonic saline: a paradoxical enhancement by inhibition of prostaglandin synthesis

Kompanowska-Jezierska

Walkowska

Sadowski

1999

Acta Physiologica Scandinavica

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“…Also the post-Indo increase in the electrical admittance of medullary tissue, an index of extracellular NaCl concentration, did not differ from that seen after systemic administration of inhibitors of PG cyclo-oxygenase [2,14,19]. As suggested earlier [2,3], the mechanism of the increase was most probably dual.…”

Section: Discussionmentioning

confidence: 51%

Renal Medullary Infusion of Indomethacin and Adenosine

Dobrowolski

Sadowski²

2004

Kidney Blood Press Res

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Perfusion of the renal medulla and osmotic hypertonicity of its interstitium are the two important features of this zone which can influence body fluid homeostasis, especially arterial blood pressure. Separate manipulation of the two variables is best obtained with the intramedullary infusion of active agents. In this study, a set-up combining the possibility of infusion into the medulla with measurement of local blood flow (MBF, laser-Doppler flux) and extracellular ion concentration (tissue electrical admittance, Y) was used to determine effects of intramedullary indomethacin (Indo) and adenosine (Ado) in anaesthetized rats. Intramedullary Indo, 1 mg kg^–1h^–1, significantly increased tissue Y, by 12 ± 3%, and significantly decreased MBF by 20 ± 3%.There was also an unexplained increase of sodium excretion (U_NaV) by 169 ± 24% and of urine flow (V) by 62 ± 6% (n = 10, both p < 0.03). Intramedullary Ado, 5 µg kg^–1 h^–1, did not alter Y, MBF or U_NaV, whereas V increased 45 ± 6% and urine osmolality decreased 25 ± 4% (both changes significant). Elevation of medullary interstitial Ado to a level that did not alter MBF or U_NaV induced a moderate defect of urine concentration that was not due to a decrease in ionic medullary hypertonicity.

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Altered renal medullary blood flow: A key factor or a parallel event in control of sodium excretion and blood pressure?

Sadowski

Bądzyńska

2020

Clin Exp Pharma Physio

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In the context of the ongoing debate on the mechanism of blood pressure (BP) regulation and pathophysiology of arterial hypertension (“renocentric” vs “neural” concepts), attention is focused on the putative regulatory role of changes in renal medullary blood flow (MBF). Experimental evidence is analysed with regard to the question whether an elevation of BP and renal perfusion pressure (RPP) is likely to increase MBF due to its impaired autoregulation. It is concluded that such increases have been clearly documented only in rats with extracellular fluid volume expansion. A possible translation of this finding to BP regulation in health and hypertension in humans may only be a matter of speculation. Within the “renocentric” theory, the key event leading to restoration of initial BP level is pressure natriuresis. Its relation to elevation of renal interstitial hydrostatic pressure and to the phenomenon of “wash‐out” of renal medullary solutes by increasing MBF is discussed. We also assessed the validity of data supporting the putative mechanism of short‐term restoration of elevated BP owing to the release of a vasodilator lipid (medullipin) by the medulla. The structure of the proposed medullary lipid is still undefined, and there is no sound evidence on its mediatory role in lowering elevated BP level. In conclusion, MBF change can hardly be regarded as a crucial event in the regulation of BP: it can be involved in the control of sodium excretion and BP only in some circumstances, although its contributory role cannot be excluded.

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Modulation of renal medullary ionic hypertonicity by prostaglandins: data from tissue admittance studies in the rat.

Cited by 4 publications

References 18 publications

Exaggerated volume expansion natriuresis in rats preloaded with hypertonic saline: a paradoxical enhancement by inhibition of prostaglandin synthesis

Exaggerated volume expansion natriuresis in rats preloaded with hypertonic saline: a paradoxical enhancement by inhibition of prostaglandin synthesis

Renal Medullary Infusion of Indomethacin and Adenosine

Altered renal medullary blood flow: A key factor or a parallel event in control of sodium excretion and blood pressure?

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