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Renal chemoreceptors in the rat.

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There are afferent nerve fibers responsive to alterations of the kidney's chemical environment in the renal nerves of the rat. In anesthetized, artificially ventilated, male Sprague-Dawley rats, single unit recordings were prepared by dissection of the centrally cut nerves of the right kidney. The stimuli used included occlusion of the renal artery, systemic asphyxia, changes in renal arterial and venous pressures, changes in ureteral pressure, and cyanide infusion. We found a population of sensory nerve fibers whose endings are activated only during markedly impaired renal blood flow (produced by clamping the renal artery, severe hypotension below 40 mm Hg, and prolonged occlusion of the renal vein), and during systemic asphyxia. The same units are not responsive to increases and decreases in systemic arterial pressure (range: 40--190 mm Hg), to ureteral pressure (range: 0--50 mm Hg), or to changes in renal venous pressure. None of the 40 single units studied was spontaneously active; their pattern of activation during renal ischemia always was characterized by trains of impulses. These sensory units have functional properties distinctly different from those of known renal mechanoreceptors. They appear to be a homogeneous group of sensory elements, and we have termed them renal ("R") chemoreceptors. Evidence also is presented which is consistent with the concept that a chemical substance released by or accumulated within the kidney might be the agent activating these chemoreceptors during renal ischemia.
Ovid Technologies (Wolters Kluwer Health)
Title: Renal chemoreceptors in the rat.
Description:
There are afferent nerve fibers responsive to alterations of the kidney's chemical environment in the renal nerves of the rat.
In anesthetized, artificially ventilated, male Sprague-Dawley rats, single unit recordings were prepared by dissection of the centrally cut nerves of the right kidney.
The stimuli used included occlusion of the renal artery, systemic asphyxia, changes in renal arterial and venous pressures, changes in ureteral pressure, and cyanide infusion.
We found a population of sensory nerve fibers whose endings are activated only during markedly impaired renal blood flow (produced by clamping the renal artery, severe hypotension below 40 mm Hg, and prolonged occlusion of the renal vein), and during systemic asphyxia.
The same units are not responsive to increases and decreases in systemic arterial pressure (range: 40--190 mm Hg), to ureteral pressure (range: 0--50 mm Hg), or to changes in renal venous pressure.
None of the 40 single units studied was spontaneously active; their pattern of activation during renal ischemia always was characterized by trains of impulses.
These sensory units have functional properties distinctly different from those of known renal mechanoreceptors.
They appear to be a homogeneous group of sensory elements, and we have termed them renal ("R") chemoreceptors.
Evidence also is presented which is consistent with the concept that a chemical substance released by or accumulated within the kidney might be the agent activating these chemoreceptors during renal ischemia.

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