Abstract

The effects of acute increases in peripheral osmolality on cardiac baroreflex sensitivity were tested in conscious, unrestrained rats by fitting values for arterial blood pressure and heart rate during acute pressor and depressor responses to a four-parameter, sigmoid logistic function curve. Cardiac baroreceptor reflex function curves were produced before and following 30 min intravenous (i.v.) infusion of 2.5 M NaCl, an equipressor concentration of phenylephrine, isotonic saline, or 2.5 M NaCl following central administration of an angiotensin-converting enzyme (ACE) inhibitor. Hypertonic saline infusion increased blood pressure, reduced heart rate and baroreflex sensitivity (gain and range), and shifted the baroreflex function curve to a higher operating blood pressure. These effects were prevented or attenuated by prior central administration of an ACE inhibitor. Isotonic volume expansion did not alter baroreflex responses. Finally, phenylephrine produced similar changes in blood pressure but did not alter cardiac baroreflex responses. These data demonstrate that acute increases in peripheral osmolality and/or sodium decrease cardiac baroreflex sensitivity through generation of central angiotensin II, independent of changes in extracellular fluid volume and blood pressure.

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