Why the study?
Does ANG II blockade prevent somatosensory-induced renal nerve-dependent antinatriuresis in anesthetized rats?
Does ANG II blockade prevent somatosensory-induced renal nerve-dependent antinatriuresis in anesthetized rats?
ANG II is involved both centrally and peripherally in mediating somatosensory-induced renal nerve-dependent antinatriuresis in rats.
ANG II mediates somatosensory antinatriuresis centrally and peripherally in rats; leaves open translation to human renal nerve function.
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 microg plus 7.5 microg/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.
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Huang et al. (1998) studied this question.
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