Role of myocardial contractility and autonomic control in the hypotensive response to a limited access ethanol paradigm in SHRs.
BACKGROUND
Previous experimental studies that evaluated the chronic hemodynamic effect of ethanol employed the continuous exposure protocol of ethanol, which does not mimic the pattern of alcohol consumption in humans. This study dealt with the long-term hemodynamic and cardiovascular autonomic effects of ethanol, in a limited-access regimen in telemetered spontaneously hypertensive rats (SHRs).


METHODS
Changes in blood pressure (BP), heart rate (HR), myocardial contractility (dP/dt(max)), and spectral cardiovascular autonomic profiles during the ethanol exposure period (2.5 or 5% w/v, 8 h/d, 8:30 am till 4:30 pm) were followed for 12 weeks.


RESULTS
Compared with control pair-fed SHRs, body weight and urine output, osmolality, and potassium levels were decreased in SHRs receiving 5% but not 2.5% ethanol. Blood pressure showed progressive falls during ethanol-feeding periods with a maximum effect observed at week 5. The peak hypotensive effect was maintained thereafter in SHRs receiving 5% ethanol in contrast to steady rises in BP in the 2.5% ethanol group to near-control levels by the conclusion of the study. Heart rate was slightly but significantly increased by ethanol 5% whereas dP/dt(max) showed persistent reductions. Power spectral analysis showed that ethanol attenuated the baroreflex gain of HR as suggested by the reductions in index alpha, the spectral index of spontaneous baroreflex sensitivity (BRS).


CONCLUSIONS
It is concluded that limited access ethanol drinking in SHRs elicited hypotension that was concentration dependent and mediated, at least partly, through reductions in myocardial contractility. Baroreflex sensitivity attenuation by ethanol appeared to have limited the tachycardic response to ethanol and perhaps its capacity to offset the evoked hypotension.