Abstract

Renal denervation is reported to treat resistant essential hypertension. Many suggest that afferent renal nerves (ARN) are responsible for the full expression of hypertension. We hypothesized that osmosensitive ARN activate sites in the CNS that contribute to hypertension by evoking excessive sympathetic nerve activity. To determine the central projections, a dual lumen cannula was implanted through the left ureter into the renal pelvis of the rat. Several days later, renal pelvic afferents were bathed with different concentrations of NaCl (20, 308 and 500 mEq/L) using a push‐pull perfusion for 2 hrs while recording arterial pressure in conscious rats. Activation of CNS sites was identified using immunohistochemical detection of c‐Fos protein and compared to controls (no infusion or denervation). Many sites were dose‐dependently stimulated in response to intrarenal infusion of NaCl. These included the nucleus tractus solitarius, area postrema, parabrachial nucleus, paraventricular hypothalamus, and other areas. The results indicate that stimulation of osmosensitive ARN leads to activation of central autonomic sites involved in the regulation of sympathetic outflow. Thus, this work identifies likely sites mediating ARN‐induced sympathoexcitation contributing to the pathogenesis of hypertension.Grant Funding Source: Supported by USPHS HL25449 (ADL) and DA017371 (MMK).

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