One of the most promising hypotheses regarding the etiology of isolated clinic hypertension is that the observed cuff reaction among isolated clinic hypertensive patients represents a conditioned emotional response to blood pressure determinations (Pickering et al., 1990). In short, isolated clinic hypertensives exhibit a conditioned hypertensive response to the cues present during blood pressure determination such as the presence of a physician or the sight of the occluding cuff.
This would explain why blood pressure recordings decrease with repeated blood pressure determinations for a portion of patients with isolated clinic hypertension, reflecting a deconditioning or extinction effect.
Some support for this hypothesis can be derived from a study by Rostrup et al. (1990) in which the casual blood pressures of a group of men increased from the first to the second clinic visit, but only when the men were led to believe their first recording was high. In addition, Mancia and colleagues (Mancia et al., 1983; Mancia et al., 1987) obtained continuous measures of blood pressure and heart rate using an intra-arterial recorder during multiple cuff blood pressure determinations by a physician in both hypertensive and normotensive patients.
Their data showed immediate rises in both systolic ( + 27 mm Hg) and diastolic blood pressure ( + 15 mm Hg) as the physician approached the patient. Although the magnitude of this reaction declined with repeated measurements during the first visit, the full intensity of the reaction was observed again when the physician returned for a second visit.
These findings parallel the magnitude and pattern of cardiovascular reactions typically observed in studies on phobic patients who are exposed to feared stimuli, lending some support to the conditioning hypothesis of isolated clinic hypertension.
The conditioning hypothesis proposed by Pickering and colleagues (1990) presumes that the conditioned response is related to an emotional reaction, perhaps involving the threat of negative evaluation, fear of interacting with authoritative medical personnel, or potentially learning that one has been diagnosed with a chronic medical condition.
Congruent with this interpretation, it has long been suspected that isolated clinic hypertensive patients are more anxious than their hypertensive counterparts. However, existing studies have failed to support this hypothesis (Gerardi et al., 1985; Larkin et al., 1998b; Siegel, Blumenthal, and Divine, 1990). It must be noted though that only a few investigations have been conducted evaluating the relation between self-reported anxiety and isolated clinic hypertension.
Those that have been conducted have typically used general measures of anxiety, rather than more specific measures of social and evaluative anxiety or fears of death and illness that may more accurately fit isolated clinic hypertensive patients. In a related area, it has also been hypothesized that isolated clinic hypertensives are more physiologically responsive to environmental challenges (including blood pressure determinations) than actual hypertensives or normal blood pressure controls. A few studies have examined this hypothesis, and findings have been largely negative, with Gerardi et al. (1985) finding partial support, but other studies failing to find reactivity differences between isolated clinic hypertensive and non-isolated clinic hypertensive patients during laboratory challenges (Cardillo et al., 1993; Larkin et al., 1998b; Lerman et al., 1989; Siegel et al., 1990; White et al., 1989).
Although these findings appear to argue against the role of a conditioned emotional response in the etiology of isolated clinic hypertension, it is possible that hypertensive cuff reactions observed among isolated clinic hypertensive patients involve interoceptive conditioning, in which the conditioned blood pressure response is not emotionally mediated. We know, for example, that many autonomic functions (for example, salivation and eye blinks) can become conditioned to any number of external stimuli, and there is no reason to exclude blood pressure conditioning as another possibility. Therefore, the failure to demonstrate that isolated clinic hypertensive patients are either more anxious in clinical settings or more prone to reacting to stressful stimuli with blood pressure increases than patients with established hypertension is not sufficient for totally disregarding the conditioning hypothesis.