ABSTRACT
This study was designed to determine whether resetting of the carotid sinus baroreceptors in chronic renal hypertension is due to altered distensibility of the wall, or changes in the properties of the receptor elements, or both. Dogs were made hypertensive by 50% constriction of the left renal artery with a Goldblatt clamp and by right nephrectomy one week later. Five to nine weeks after nephrectomy, when mean blood pressure had risen by 35-46 mm Hg, the isolated carotid sinus wall deformation, measured from still photographs, and gross baroreceptor nerve action potentials (N) were recorded in response to step intrasinus pressure forcings (P), ranging from zero to 300 mm Hg, in increments of 25 mm Hg. Measured wall deformation was converted to strain-energy density (SED), a scalar value, as the best indicator of the mechanical state of the sinus wall. Plots of N vs. P data followed an S-shaped pattern, but were shifted toward the P-axis, as compared to controls. Plots of SED vs. P, though linear over most of the pressure range, were shifted toward the SED-axis, as compared to controls. A plot of N vs. SED, derived from the composite plots of N vs. P and SED vs. P, followed an S-shaped pattern and also was shifted toward the SED-axis. We conclude that the nonlinearity in the N vs. P curve is due largely to the inability of the receptor elements to respond to increasing wall strain and to resetting of the baroreceptors due to changes in the receptor properties rather than in the wall elements.
