Abstract
Exposure to cold environments is linked to cold-induced hypertension due to activated sympathetic nerve activity (SNA) and arterial baroreceptor reflex dysfunction. However, direct measurement of SNA during cold-induced hypertension and changes in baroreflex control of SNA remain unexplored. Chronically instrumented rats were exposed to cold temperatures (10 °C) over 4 days after a control period (24 °C), and renal and lumbar sympathetic nerve activities were simultaneously measured during cold-induced hypertension. Baroreflex curves for renal SNA (RSNA) and lumbar SNA and heart rate were generated by altering arterial pressure via a bolus intravenous infusion of vasoactive drugs. RSNA increased immediately after cold exposure, increased progressively throughout the 4-day period, and remained high after the cold exposure ended. Cold exposure shifted the RSNA baroreflex curve to the right and upward, gradually increasing the upper plateau (maximum capacity of sympathetic drive). The upper plateau remained elevated even after the cold exposure ended. Conversely, cold exposure increased lumbar SNA, heart rate, and arterial pressure, which subsequently returned to control levels after the cold exposure ended. These data indicate that cold exposure increases the maximum capacity to drive renal SNA in a regionally different and time-dependent manner through cumulative effects. Four days of cold exposure resulted in reversible effects increasing arterial pressure via lumbar SNA and heart rate, alongside time-dependent cumulative effects on RSNA. This study provides direct evidence of a self-activating pathway for RSNA that is activated by cold exposure, thus initiating cold-induced hypertension.
Published Version
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