Abstract
To determine whether impaired reflex control of heart rate was evident in rats of the inbred Dahl hypertension-sensitive (SS/Jr) strains. Phenylephrine and sodium nitroprusside were administered through jugular catheters in graded doses to elicit a range of pressor and depressor responses, for which corresponding reflex decreases and increases in heart rate were recorded. To assess the relative contributions of sympathetic and parasympathetic branches of autonomic control to baroreflex functioning, atropine methyl nitrate and atenolol were administered to establish vagal blockade, and cardiac sympathetic blockade, respectively. Assuming a sigmoidal relationship between mean arterial pressure and heart rate changes, our results indicated that SS/Jr rats exhibited elevated blood pressure set-points for baroreceptor activation and roughly similar baroreflex sensitivity compared with SR/Jr rats. In contrast, using linear regression analyses, our results indicated that SS/Jr rats had significant reductions in baroreceptor sensitivity when arterial pressure was increased by phenylephrine. Baroreceptor sensitivity was similar between rats of the two strains when arterial pressure was reduced by administration of nitroprusside. Atropine and atenolol had similar effects on baroreflex control of heart rate in both strains. However, pressor responses to phenylephrine were significantly greater in SS/Jr rats, an effect which had previously been reported in Dahl salt-sensitive (DS) rats and attributed to deficits in autonomic reflex control of vascular resistance. The present results indicate that the method of analysis for determination of baroreceptor sensitivity can influence the conclusions drawn in studies of hypertensive and normotensive strains of rat. Although deficits in baroreflex control of heart rate have consistently been reported in DS rats, the present results did not confirm those findings in inbred Dahl rats when mean arterial pressure and heart rate change data were analyzed by fitting a logistic equation to sigmoid data. In contrast, using linear regression analysis, those same data did reveal a defect in baroreceptor sensitivity of SS/Jr rats after acute increases in arterial pressure. Caution should be exercised in the selection of a method for analysis of baroreceptor data and the interpretation of the findings.
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