Abstract

We recently provided highly suggestive preliminary evidence that the renal interstitium contracts reactively in vivo. We demonstrated that renal medullary direct interstitial volume expansion (rmDIVE = 100 μl bolus infusion of 0.9% saline (SS)/30 s) brought about a biphasic renal interstitial hydrostatic pressure (RIHP) response which was abolished when dibutyryl-cAMP was concomitant and interstitially infused. To assess more deeply the feasibility of the concept that the renal interstitium contracts in vivo, two experimental series (S1, S2) were performed in hydropenic rats subjected to acute left renal-denervation, hormonal clamping, and control of renal arterial pressure. In S1, RIHP and renal outer medullary blood flow (RoMBF) were continuously measured before and after a sudden micro-bolus (5μl) injection, into the renal medullary interstitium, of SS containing α-trinositol (α-TNS, anti-inflammatory drug) to either two doses 2 or 4 mM (SS + 2 α-TNS and SS + 4 α-TNS groups). No overall differences between groups in either ΔRIHP or %ΔRoMBF time courses were found; however, in the SS + 2 α-TNS group the data were less scattered and the ΔRIHP time course tended to peak faster and then persisted there, so that, this α-TNS dose was selected for S2. In S2, RIHP and RoMBF were similarly measured in rats randomly assigned to three groups: the CTR group (sham time-control), SS group (SS alone), and SS + α-TNS group. The micro-bolus injection of SS alone (SS group) was unable to increase ΔRIHP. The group with no micro-bolus injection (CTR group) experienced a decrease in ΔRIHP. The micro-bolus injection of SS + 2 α-TNS was accompanied by a differential increase in ΔRIHP (vs. CTR and SS groups). These responses were not associated with differential changes among groups in %ΔRoMBF or hemodilution parameters. These results provide additional evidence that the renal interstitium contracts in vivo.

Highlights

  • In hydropenic rats subjected to left renal denervation, hormonal clamping, and renal arterial pressure control, the renal medullary Direct Interstitial Volume Expansion induced by a 0.9% saline bolus infusion (100 μL / 30 s) into the left renal medullary interstitium brought about a biphasic renal interstitial hydrostatic pressure (RIHP) response

  • The most significant new findings from this study performed on hydropenic rats, are as follows: (a) The sudden micro-bolus (5 μl) injection of solely SS into the renal medullary interstitium is unable to increase the ΔRIHP; (b) The non-injection of a micro-bolus of SS into the renal medullary interstitium is accompanied by a decrease in ΔRIHP; and, (c) A sudden micro-bolus (5 μl) injection of SS + 2 mM α-Trinositol (α-TNS) into the renal medullary interstitium is accompanied by a differential increase in ΔRIHP that is ⁓ 200% higher than that found for the CTR group and ⁓ 100% higher than that found for the SS group

  • In the group in which there was not sudden micro-bolus injection into such a space (CTR group) ΔRIHP notably and significantly decreased by ⁓ 1 mmHg over time. These findings indicates that: (a) under the experimental conditions described here and by the time at which the sudden injection started, a SS micro-bolus of at least 5 μl was either unable to modify the ΔRIHP or was sufficient to maintain it without change; and (b) an interstitial volume deficit of just 5 μl (~2.5% of the renal interstitial volume) causes a decrease in ΔRIHP, which suggests that the renal medullary interstitium may function as a detector of interstitial volume

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Summary

Objectives

Because above paradigm was preliminary supported by the fact that db-cAMP abolished a reactive RIHP response induced by rmDIVE, we aimed to submit this paradigm to much more exacting test in order to support the feasibility of the concept

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