PRES- and orthostatic-induced heart-rate changes as markers of labile hypertension: magnitude and reliability measures

Abstract

Listen

Translate article

Split-half and test-retest reliabilities of heart-rate responses to a baroreceptor manipulation and an orthostatic maneuver were compared between subjects with either normal or elevated blood-pressure. Ten subjects showing elevated resting blood-pressure and 11 normotensive subjects participated in two experimental sessions, each including heart-rate recordings during baroreceptor manipulation and orthostatic challenge. Carotid baroreceptors were manipulated by applying the baroreceptor-specific phase-related external suction (PRES) technique. The orthostatic stimulation procedure (OSP) was a change of body position from lying to standing. Heart rate responses evoked by OSP failed to discriminate significantly between the groups either in the magnitude or the (test/retest) reliability measure. The PRES procedure also failed to discriminate with the conventional magnitude measure, but the reliability measures showed significant differences. Paradoxically, the high-blood-pressure group manifested the higher baroreceptor reliability. The present findings are consistent with the view that operant conditioning produces phasic blood-pressure increases. In this view, blood-pressure increases activate the arterial baroreceptors which, in turn, dampen pain and/or stress sensitivity. Individuals showing high consistency (reliability) in their cardiovascular responses are more likely to learn this form of conditioning, and hence to eventually increase their tonic blood-pressure. High reliability of cardiovascular responses may therefore constitute a risk for hypertension. Aside from such theoretical considerations, the findings indicate that less conventional dependent variables like reliability may be worth exploring in the search for the etiology of essential hypertension, and that, in this search, specificity (relative to baroreceptor function) is more important than the magnitude of the heart-rate changes that are produced.