Panzenbeck M J, Harrison P C, Madwed J B, McFarland M L, Winquist R J, Frei P, Weldon S, Desai S N
Pharmacology Department, Boehringer Ingelheim Pharmaceuticals, Ridgefield, Connecticut 06877-0368.
Am J Physiol. 1994 Jun;266(6 Pt 2):H2430-5. doi: 10.1152/ajpheart.1994.266.6.H2430.
We tested the hypothesis that baroreflex attenuation during sodium depletion is due to increased prostaglandin (PG) levels. We studied baroreflex sensitivity before and after PG synthesis inhibition in conscious cynomolgus monkeys. Arterial pressure and pulse interval (PI) were measured during intravenous infusions of phenylephrine (1-20 micrograms.kg-1.min-1, n = 6) and nitroprusside (1-10 micrograms.kg-1.min-1, n = 7). Infusions were repeated 30 min after indomethacin (Indo, 6 mg/kg iv). The slope (in ms/mmHg) of the mean arterial blood pressure-PI plot was used as an index of baroreflex sensitivity. Plasma renin activity (PRA) was elevated (47.9 +/- 9.7 vs. 8.8 +/- 3.3 ng angiotensin I.ml-1.h-1) after sodium depletion (P < 0.05). Baroreflex sensitivity to hypotension and hypertension was significantly (P < 0.05) attenuated by sodium depletion (3.69 +/- 0.9 vs. 0.9 +/- 0.1 ms/mmHg and 7.38 +/- 0.6 vs. 5.04 +/- 0.9 ms/mmHg, respectively). Indo decreased PRA to 28.6 +/- 5.7 ng angiotensin I.ml-1.h-1 (P < 0.05) in sodium-depleted monkeys and decreased heart rate -21 +/- 3.7 from a baseline of 166 +/- 9.40 beats/min in normal monkeys and -22 +/- 2.9 from a baseline of 191 +/- 7.9 beats/min in low-sodium monkeys (P < 0.05). Indo did not significantly change baroreflex sensitivity in either group. Thus the baroreflex was attenuated in conscious nonhuman primates during sodium depletion; acute PG synthesis blockade did not improve baroreflex sensitivity. Indo decreased heart rate without changing arterial pressure; suggesting that PGs caused a downward resetting of the pressure-heart rate relationship.
钠耗竭期间压力感受器反射减弱是由于前列腺素（PG）水平升高所致。我们研究了在清醒食蟹猴中抑制PG合成前后的压力感受器反射敏感性。在静脉输注去氧肾上腺素（1 - 20微克·千克⁻¹·分钟⁻¹，n = 6）和硝普钠（1 - 10微克·千克⁻¹·分钟⁻¹，n = 7）期间测量动脉压和脉搏间期（PI）。在静脉注射吲哚美辛（Indo，6毫克/千克）30分钟后重复输注。平均动脉血压 - PI图的斜率（毫秒/毫米汞柱）用作压力感受器反射敏感性的指标。钠耗竭后血浆肾素活性（PRA）升高（47.9 ± 9.7对8.8 ± 3.3纳克血管紧张素I·毫升⁻¹·小时⁻¹）（P < 0.05）。钠耗竭显著（P < 0.05）减弱了对低血压和高血压的压力感受器反射敏感性（分别为3.69 ± 0.9对0.9 ± 0.1毫秒/毫米汞柱和7.38 ± 0.6对5.04 ± 0.9毫秒/毫米汞柱）。在钠耗竭的猴子中，Indo将PRA降低至28.6 ± 5.7纳克血管紧张素I·毫升⁻¹·小时⁻¹（P < 0.05），在正常猴子中使心率从基线的166 ± 9.40次/分钟降低 - 21 ± 3.7次/分钟，在低钠猴子中使心率从基线的191 ± 7.9次/分钟降低 - 22 ± 2.9次/分钟（P < 0.05）。Indo在两组中均未显著改变压力感受器反射敏感性。因此，在钠耗竭期间清醒的非人类灵长类动物的压力感受器反射减弱；急性PG合成阻断并未改善压力感受器反射敏感性。Indo降低了心率而未改变动脉压；这表明PG导致压力 - 心率关系向下重置。
