Role of ANG II in mediating somatosensory-induced renal nerve-dependent antinatriuresis in the rat

Abstract

This study examined the renal nerve-dependent renal hemodynamic and tubular responses to somatosensory stimulation in the anesthetized rat by use of subcutaneously applied capsaicin when the action of ANG II was blocked peripherally or selectively within the brain. Activation of skin somatosensory receptors caused a transient reversible 10–15% increase in blood pressure, and while renal perfusion pressure was regulated at control levels, there was a transient fall in urine flow and sodium excretion even though both renal blood flow and glomerular filtration rate were unchanged. These reflexly induced excretory responses were abolished when the renal nerves were sectioned. Administration of the ANG II AT1-receptor antagonist, losartan, either intravenously at 3 or 10 mg/kg or locally into the lateral cerebroventricles at 15 μg plus 7.5 μg/h, had no effect on capsaicin-induced vasopressor responses but blocked the reductions in urine flow and sodium excretion. These findings are consistent with ANG II being involved in at least two stages in the reflex, one centrally and one at the periphery.

Role of Brain Angiotensin II on Somatosensory-Induced Antinatriuresis in Hypertensive Rats

“…We have previously reported 6 that in this situation the capsaicin acts to depolarize the subcutaneous nociceptors, 16 giving rise to a somatosensory input, thus causing a reflex increase in renal sympathetic nerve activity and a renal nerve-mediated antidiuresis and antinatriuresis. 10 The present study supports this view in that the somatorenal reflex was intact in the Wistar rats. It was also clear that this somatosensory-mediated reflex neural control of urinary flow and sodium excretion was dependent on Ang II in the brain, as following blockade of its receptors with intracerebroventricular losartan, the excretory responses were prevented.…”

“…In our previous studies, we had shown that Ang II in the brain was necessary to allow a somatosensory-induced renal nerve-dependent antidiuresis and antinatriuresis to take place. 10,11 Indeed, this would be consistent with the observations of Sasaki and Dampney 14 and Hirooka and Dampney, 15 who showed that Ang II elicited an excitatory action at the rostral ventrolateral medulla, an important nucleus involved in determining sympathetic outflow, and appeared to have a facilitatory role in allowing somatosensory stimulation to elicit an increase in sympathetic outflow to the periphery. However, it was also evident that this somatosensory-mediated reflex neural control of sodium excretion was blunted in the SHRSP, 9,12 but whether this was due to a deficit within the brain or at the neuroeffector sites within the kidney was not clear.…”

“…It was also clear that this somatosensory-mediated reflex neural control of urinary flow and sodium excretion was dependent on Ang II in the brain, as following blockade of its receptors with intracerebroventricular losartan, the excretory responses were prevented. 10 Indeed, these observations support our previous study, which reported that if endogenous production of brain Ang II was blocked by captopril, exogenous Ang II administration into the brain could restore the excretory responses to subcutaneous capsaicin administration. 11 The situation in the SHRSP given saline intracerebroventricularly was very different, in that although the subcutaneous capsaicin produced a prompt and short-lived increase in blood pressure, there were small insignificant changes in urinary flow and sodium excretion.…”

“…[5][6][7] In our own studies, we showed that activation of the somatosensory system in the rat by electrical stimulation of the brachial nerves 8 or by administration of capsaicin to stimulate sensory receptors of the skin 9 reflexly increased renal sympathetic nerve activity and caused a renal nerve-dependent antinatriuresis and antidiuresis. The ability of the somatosensory system to cause a neurally mediated antinatriuresis was found to be blocked after the administration of losartan into the lateral cerebral ventricles of the brain 10 but was restored when angiotensin II (Ang II) was infused into the central nervous system. 11 This suggested that Ang II was a necessary component within the central neural pathways transmitting sensory information from the soma and eliciting an autonomic response.…”

The actions of Shiga toxin-2 administration into the brain on renal sympathetic nerve activity

“…Male Wistar rats (300-350 g) were placed into a stereotaxic frame and drugs were administered into the right lateral cerebroventricle [14]. For this purpose, a guide cannula, made up of stainless steel tubing (0.82 mm diameter) was placed at the site 1.0 mm posterior to the bregma, 2.5 mm lateral to midline and 2.55 mm ventral to the surface of the dura.…”