Central control of cardiac baroreflex responses during peripheral hyperosmolality

Acute increases in peripheral osmolality evoke a presser response and baroreflex-mediated bradycardia. These experiments were designed to determine if the fall in heart rate during peripheral sodium loading is I) equivalent to bradycardia accompanying phenylephrine (PE) infusion, 2) mediated by the parasympathetic (PSNS) or sympathetic (SNS) nervous system, and 3) controlled by the median preoptic nucleus (MnPO). Male rats received an intravenous infusion of isotonic saline, hypertonic saline (2.5 M NaCl), or PE for 30 min. Blood pressure increased equivalently in the hypertonic NaCl and PE groups. However, heart rate fell more in animals infused with PE. Furthermore, pretreatment with methylatropine to block the PSNS had no effect on bradycardia, whereas blocking SNS influences on cardiac function significantly attenuated the fall in heart rate during peripheral hyperosmolality. Finally, kainic acid administration in the MnPO before testing increased bradycardia observed during hypertonic saline loading. Taken together, these data suggest that acute peripheral hyperosmolality acts at the MnPO to reduce cardiac SNS withdrawal during the presser response that reduces the associated baroreflex bradycardia.