We have recently reported that sinoaortic denervation (SAD) causes salt-dependent hypertension in the rat (Hypertension 19:475,1992). The present study was performed to investigate the hemodynamic mechanisms of hypertension in this model. SAD rats (N=3) were instrumented with an aortic flow probe for measurement of cardiac output (CO). Two weeks later, these rats were implanted with a telemetry transmitter for measurement of arterial pressure (AP). One week later, computerized measurements of AP and CO (24 hours/day) were started and continued over the next 5 weeks. Dietary sodium chloride (NaCl) content (%) was altered as follows: week 1 (0.4%), weeks 2 & 3 (8.0%), and weeks 4 & 5 (0.4%). The control (0.4%) level for AP was 125 ± 2.6 mmHg.Within 5 days of 8% NaCl intake, AP had increased to a steady-state level of 139 ± 1.8 mmHg and remained elevated for the duration of high NaCl consumption. The CO level for control (0.4%) was 98.4 ±9.3 ml/min. During the high NaCl period, CO remained within 5% of control value. The total peripheral resistance (TPR; as calculated by AP/CO), however, increased 15% by day 5 of high NaCl intake, and remained elevated for the duration of the increased NaCl period. AP and TPR returned to control levels within 24 hours of return to 0.4% NaCl. We therefore conclude that salt-induced hypertension appears to be mediated by a change in TPR in SAD rats. (Supported by NIH Grant HL50371).
|Original language||English (US)|
|State||Published - Dec 1 1996|