Arterial baroreceptor denervation impairs long-term regulation of arterial pressure during dietary salt loading.

摘要

Experiments were performed to examine the contribution of arterial baroreceptors to long-term regulation of mean arterial pressure (MAP) during changes in dietary salt intake. Normotensive Sprague-Dawley rats were subjected to either sinoaortic denervation (SAD; n = 8) or Sham surgery (n = 6) and instrumented 1 wk later with radiotelemetry transmitters for continuous minute-to-minute monitoring of MAP and heart rate (HR) over the 8-wk protocol. Rats consumed three levels of dietary NaCl: 0.4% NaCl (week 1), 4.0% NaCl (weeks 2-4), and 8.0% NaCl (weeks 5-7). Rats returned to a 0.4% NaCl diet during the eighth week of the experiment. During week 1 (0.4% NaCl), there were no differences between Sham and SAD groups for 24-h averages of MAP or HR. However, by the third week of 4.0% NaCl, 24-h MAP was elevated significantly from baseline in SAD (10 +/- 2 mmHg) but not Sham (1 +/- 1 mmHg) rats. By the end of the third week of 8.0% NaCl diet, 24-h MAP was elevated 15 +/- 2 mmHg above control in SAD rats compared with a 4 +/- 1 mmHg increase in Sham rats (P < 0.05). Hourly analysis of the final 72 h of each level of dietary salt revealed a marked effect of dietary NaCl on MAP in SAD rats, particularly during the dark cycle. MAP increased approximately 20 and 30 mmHg in SAD rats over the 12-h dark cycle for 4.0 and 8.0% NaCl diets, respectively. In contrast, increased dietary NaCl had no effect on MAP during any phase of the light or dark period in Sham rats. These data support the hypothesis that arterial baroreceptors play a critical role in long-term regulation of MAP under conditions of altered dietary salt intake. Finally, hourly analysis of MAP revealed that the majority of the hypertensive response to increased NaCl occurs during the dark cycle in SAD rats. Hence, previous investigations may have underestimated the magnitude of the hypertensive response to increased dietary NaCl in animals with baroreceptor dysfunction.