M. Bono et al., IMPAIRED REGULATION OF LYMPHOCYTE BETA(2) -ADRENOCEPTORS IN A SUBSET OF PATIENTS WITH ESSENTIAL-HYPERTENSION, Nefrologia, 13(6), 1993, pp. 545-550
The sympathetic nervous system has been implicated in the pathogenesis
of essential hypertension. However, plasma catecholamine levels have
been reported to be within the normal range in the majority of patient
s with essential hypertension, although an increased adrenergic respon
se in target tissues has not been ruled out. The aim of this study was
to evaluate the state of beta-adrenoceptors, which are the effecters
of the sympathetic nervous system in target tissues, in essential hype
rtension. We studied 52 non-treated hypertensive patients and 28 normo
tensive controls of similar age and sex. beta(2)-adrenoceptors were me
asured in intact lymphocytes, using the hydrophilic ligand [H-3]GCP-12
177. Hypertensive patients showed values of mean blood pressure (p < 0
.01), heart rate (p < 0.01) and body mass index (p < 0.05) higher than
normotensive controls, although there were no significant differences
in plasma catecholamine levels between both groups. A positive relati
onship was found between beta(2)-adrenergic receptors and mean blood p
ressure when both hypertensive patients and control subjetcs were cons
idered together (r = 0.40, p < 0.01). Hypertensive patients showed a m
ean beta-adrenoceptor density higher than normotensive controls (1,881
+/- 567 vs 1,344 +/- 207 receptors/lynphocyte, p < 0.01), but there w
as a considerable overlap. Hypertensive patients were subclassified in
to two groups: Group I: hypertensive patients with a normal beta-adren
oceptor density (< 7,100, n = 26), and Group II: hypertensive patients
with an increased receptor density (> 1,100, n = 26). There were no d
ifferences with respect to age, sex, body mass index, mean blood press
ure, heart rate, plasma catecholamine levels or receptor affinity betw
een the two groups of patients. In normotensive subjects there was an
inverse relationship between plasma epinephrine levels and beta-adreno
ceptor density (r = - 0.51, p < 0.01). A similar finding was observed
in the hypertensive patients from Group I (r = - 0.44, p < 0.05), wher
eas hypertensive patients from Group II showed no such correlation. Ou
r results suggest that there is an important subset of essential hyper
tensive patients who have an impaired beta(2)-adrenoceptor regulation,
which is demonstrated by an increased beta(2)-adrenoceptor density an
d by an alteration in the physiological regulation by its endogenous a
gonist.