Supported by Grant AA07839 from the National Institute on Alcohol Abuse and Alcoholism.
Autonomic Modulation of Altered Diurnal Hemodynamic Profiles in Ethanol-Fed Hypertensive Rats
Article first published online: 3 MAY 2006
Alcoholism: Clinical and Experimental Research
Volume 29, Issue 4, pages 499–508, April 2005
How to Cite
El-Mas, M. M. and Abdel-Rahman, A. A. (2005), Autonomic Modulation of Altered Diurnal Hemodynamic Profiles in Ethanol-Fed Hypertensive Rats. Alcoholism: Clinical and Experimental Research, 29: 499–508. doi: 10.1097/01.ALC.0000159108.23375.B6
- Issue published online: 3 MAY 2006
- Article first published online: 3 MAY 2006
- Received for publication October 26, 2004; accepted January 1, 2005.
A recent report from the authors’ laboratory showed that circadian hemodynamic rhythms are altered in hypertension due partly to irregularities in cardiovascular autonomic control. This study investigated the long-term effects of chronic ethanol feeding (5% w/v, 12 weeks) on the circadian profiles of blood pressure (BP), heart rate (HR), and their variability in spontaneously hypertensive rats (SHRs) and age-matched Wistar-Kyoto (WKY) rats.
Radiotelemetry was used for hemodynamic monitoring. The time-domain measures of the variability of BP (standard deviation of mean arterial pressure SDMAP) and HR (standard deviation of R-R intervals SDRR and root mean square of successive differences in R-R intervals rMSSD) were taken as indices of cardiovascular autonomic activity.
Control WKY rats displayed normal circadian rhythms (i.e., higher dark-time compared with light-time values) of BP, HR, and their variability indices during weeks 6 through 12 of the study. These circadian rhythms were abolished (BP), inverted (HR, SDMAP), or enhanced (SDRR, rMSSD) in SHRs. Ethanol feeding produced sustained hypotension during both light and dark cycles that was 3-fold greater in SHRs than in WKY rats. SDMAP was not affected by ethanol in WKY rats and showed reductions, mostly during light times, in SHRs. Ethanol also caused significant increases in HR in SHRs only during dark periods, probably because of the inhibition of cardiac vagal activity as indicated by temporal reductions in rMSSD.
These results implicate autonomic factors in the altered diurnal hemodynamic profile by ethanol in SHRs and highlight the possibility of increased risk of cardiac events in hypertensive patients due to alcohol use.