Central control of cardiac baroreflex responses during peripheral hyperosmolality

Acute increases in peripheral osmolality evoke a presser response and baror eflex-mediated bradycardia. These experiments were designed to determine if the fall in heart rate during peripheral sodium loading is I) equivalent t o bradycardia accompanying phenylephrine (PE) infusion, 2) mediated by the parasympathetic (PSNS) or sympathetic (SNS) nervous system, and 3) controll ed 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 gr oups. However, heart rate fell more in animals infused with PE. Furthermore , pretreatment with methylatropine to block the PSNS had no effect on brady cardia, whereas blocking SNS influences on cardiac function significantly a ttenuated the fall in heart rate during peripheral hyperosmolality. Finally , kainic acid administration in the MnPO before testing increased bradycard ia observed during hypertonic saline loading. Taken together, these data su ggest that acute peripheral hyperosmolality acts at the MnPO to reduce card iac SNS withdrawal during the presser response that reduces the associated baroreflex bradycardia.