CARDIOVASCULAR EFFECTS OF EATING, ATENOLOL AND THEIR INTERACTION - BETA(1)-ADRENERGIC MODULATION DOES NOT PLAY A PREDOMINANT ROLE IN THE GENESIS OF POSTPRANDIAL EFFECTS
C. Demey et al., CARDIOVASCULAR EFFECTS OF EATING, ATENOLOL AND THEIR INTERACTION - BETA(1)-ADRENERGIC MODULATION DOES NOT PLAY A PREDOMINANT ROLE IN THE GENESIS OF POSTPRANDIAL EFFECTS, British journal of clinical pharmacology, 36(5), 1993, pp. 427-435
1 Eight healthy subjects were investigated on four occasions at least
1 week apart when they either ate a standard 3100 kJ cold meal or fast
ed. One hour earlier, either 50 mg atenolol or placebo was administere
d . 2 Eating was followed by prominent changes of systolic cardiovascu
lar function: a rise of heart rate (+7, 95% CI: 4 to 9 beats min-1), s
ystolic BP (+5, CI: 1 to 8 mmHg), a drop of diastolic BP (-6, Cl:-9 to
-3 mmHg), shortening of the pre-ejection period PEP (-11, CI: -13 to
-9 ms) and electromechanical systole QS2c (-13, CI: -17 to -8 ms), a r
ise of the estimated cardiac output CO (+1.3, CI: 1.0 to 1.6 1 min-1)
and a reduction of the calculated total peripheral resistance TPR (-30
6, CI: -389 to -222 dyn s cm-5). 3 Eating was also followed by an incr
ease of the non-renal clearance of sorbitol (as a measure of hepatic b
lood flow) and this change was larger than proportional to the increas
e of CO. The plasma renin activity rose after the meal but the venous
plasma noradrenaline and adrenaline concentrations were not affected.
4 The postprandial effects peaked over the first 1-2 h after the meal
but remained well detectable up to 4 h after eating. 5 The administrat
ion of 50 mg atenolol before the meal reduced the postprandial effects
to the same extent as the atenolol effects in the fasting state. This
lack of interaction (or mere arithmetic additivity) indicates that th
e efferent beta1-adrenergic tone does not play a predominant role in t
he modulation of postprandial cardiovascular changes.