In different mammals, including humans, arterial pressure shows large phasic increases during rapid-eye-movement sleep (REMS). These arterial pressure surges are related to the activation of central autonomic commands (CAC) to the heart and blood vessels. Aim of this study was to determine the influence of essential hypertension on arterial pressure surges during REMS and on the concomitant regulation of heart period (HP). Six Spontaneously Hypertensive Rats (SHR) e six normotensive Wistar-Kyoto (WKY) rats were implanted under halothane/N2O anesthesia with electrodes for electroencephalographic and electromyographic recordings and with an arterial catheter for pressure measurement. HP and mean arterial pressure (MAP) beat-to-beat values were computed from blood pressure recordings. Data sequences comprising a MAP surge greater than 15 mmHg were collected during REMS. Sequences were normalized, synchronized at the beginning of the arterial pressure surge, and averaged within rats and groups. Data were analyzed by t-test and reported as mean ± SEM. The density (n/min) of arterial pressure surges in REMS resulted higher in SHR (0.26±0.03) than in WKY rats (0.18±0.02; p<0.05), suggesting that a higher frequency of activations of phasic CAC on blood vessels is present in hypertension. A decrease in HP accompanied arterial pressure surges in both groups, but was smaller in SHR (-19±1 ms) than in WKY rats (-262 ms, p<0.05). This may be due to a lower cardiac reactivity to phasic CAC in SHR with respect to normotensive rats, or to a smaller amplitude of CAC in hypertensive animals. According with the latter hypothesis, the MAP increase at the peak of arterial pressure surges was 291 mmHg in both strains, despite the enhanced vascular reactivity to neural commands of SHR (Kuo, Am. J. Physiol., 2000, 278:201-207). These results stress the role of REMS as a condition of choice for revealing regulatory disturbances in cardiovascular diseases.
Zoccoli G., Asti V., Berteotti C., Ferrari V., Franzini C., Lenzi P., et al. (2006). Effects of essential hypertension on phasic increases in arterial pressare during REM sleep..
Effects of essential hypertension on phasic increases in arterial pressare during REM sleep.
ZOCCOLI, GIOVANNA;ASTI, VALENTINA;BERTEOTTI, CHIARA;FERRARI, VERA;FRANZINI, CARLO;LENZI, PIERLUIGI;SILVANI, ALESSANDRO
2006
Abstract
In different mammals, including humans, arterial pressure shows large phasic increases during rapid-eye-movement sleep (REMS). These arterial pressure surges are related to the activation of central autonomic commands (CAC) to the heart and blood vessels. Aim of this study was to determine the influence of essential hypertension on arterial pressure surges during REMS and on the concomitant regulation of heart period (HP). Six Spontaneously Hypertensive Rats (SHR) e six normotensive Wistar-Kyoto (WKY) rats were implanted under halothane/N2O anesthesia with electrodes for electroencephalographic and electromyographic recordings and with an arterial catheter for pressure measurement. HP and mean arterial pressure (MAP) beat-to-beat values were computed from blood pressure recordings. Data sequences comprising a MAP surge greater than 15 mmHg were collected during REMS. Sequences were normalized, synchronized at the beginning of the arterial pressure surge, and averaged within rats and groups. Data were analyzed by t-test and reported as mean ± SEM. The density (n/min) of arterial pressure surges in REMS resulted higher in SHR (0.26±0.03) than in WKY rats (0.18±0.02; p<0.05), suggesting that a higher frequency of activations of phasic CAC on blood vessels is present in hypertension. A decrease in HP accompanied arterial pressure surges in both groups, but was smaller in SHR (-19±1 ms) than in WKY rats (-262 ms, p<0.05). This may be due to a lower cardiac reactivity to phasic CAC in SHR with respect to normotensive rats, or to a smaller amplitude of CAC in hypertensive animals. According with the latter hypothesis, the MAP increase at the peak of arterial pressure surges was 291 mmHg in both strains, despite the enhanced vascular reactivity to neural commands of SHR (Kuo, Am. J. Physiol., 2000, 278:201-207). These results stress the role of REMS as a condition of choice for revealing regulatory disturbances in cardiovascular diseases.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
