Effect of antihypertensive treatment on the increased β-adrenoceptor density in patients with essential hypertension

Abstract

The effect of different antihypertensive drugs on the increased surface beta 2-adrenoceptor density in essential hypertension was evaluated to elucidate whether the possible effect of the treatment on these receptors was secondary to blood pressure decreases or a specific effect of the drugs. Thirty-nine untreated essential hypertensive patients and 28 normotensive control subjects were studied in basal conditions. Hypertensive patients were randomly assigned to three treatment groups: bisoprolol (10 mg/day, n = 15), enalapril (20 mg/day, n = 12), and verapamil SR (240 mg/day, n = 12), and were studied before and after 1 month of treatment. Plasma catecholamines were determined by a radioenzymatic assay. Surface beta 2-adrenoceptors were measured in intact lymphocytes by radioligand binding assay using the hydrophilic ligand [3H]-CGP12177. beta 2-adrenoceptor density was increased in hypertensive patients (P < .01). After treatment, mean blood pressure decreased similarly in the three groups, while plasma catecholamines showed no significant changes in any group. beta 2-adrenoceptor number decreased only in bisoprolol-treated patients (P < .05). Mean blood pressure decreases correlated with beta 2-adrenoceptor decrements only in bisoprolol-treated patients (r = 0.65, P < .05). beta 2-adrenoceptor density correlated with plasma epinephrine levels in the control group (r = -0.50, P < .01), but not in hypertensive patients before treatment. This correlation was also observed in hypertensive patients treated with bisoprolol (r = -0.52, P < .05), but not in those treated with verapamil or enalapril. Our results suggest that bisoprolol treatment reduces the increased surface beta 2-adrenoceptor density and restores its regulation by epinephrine in essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Polymorphisms of the β2‐adrenergic receptor gene (ADRB2) in relation to cardiovascular risk factors in men

“…The Arg16Gly genotype had 7.3 mmHg higher systolic blood pressure than the Arg16Arg genotype, independently of WHR. It has been implied that the β 2 ‐adrenergic receptor function may play a pathogenic role in essential hypertension, and an increased surface β 2 ‐adrenergic receptor density in lymphocytes has been reported in hypertensive subjects [23]. Moreover, the upregulation of the β 2 ‐adrenergic receptor density after intravenous administration of clonidine seems to be slower in hypertensives [24].…”

Ethnicity, gender, and age effects on adrenoceptors and physiological responses to emotional stress

“…The current study also examined the unique and joint effect of ethnicity, gender, and age on β 2 ‐adrenergic receptors on peripheral blood mononuclear cells. It has been suggested that individual differences in the β‐adrenergic receptor may account, in part, for the disparity in the prevalence of hypertension between Blacks and Whites (Bono et al, 1995; Brodde, Stuka, & Demuth, 1985; Brushi, Orlandini, & Pavarini, 1984; Calls et al, 2000; Feldman, Limbird, Nadeau, Roberston, & Wood, 1984). Although not entirely consistent, previous studies of healthy persons and those with diagnosed hypertension have reported independent effects of ethnicity, gender, and age with β 2 ‐adrenergic receptor number ( B max ), dissociation constant ( K d ), and cyclic adenosine monophosphate (AMP) production in response to agonist stimulation (Cases et al, 1991; Halper et al, 1984; Kafka et al, 1979; Mader & Davis, 1989; Michel, Brodde, & Insel, 1990; Mills, Dimsdale, Ziegler, & Nelesen, 1995; Muller, Weller, & Krone, 1994; Trimarco et al, 1983), as well as ethnic‐ (e.g., Sherwood & Hinderliter, 1993; Stein, Lang, Singh, He, & Wood, 2000; Watkins, Dimsdale, & Ziegler, 1995) and age‐related (Bertel, Buhler, Kiowski, & Lutold, 1980) differences in beta‐adrenergic responsiveness to agonist stimulation.…”

The Impact of β 2 Adrenergic Receptor Polymorphisms on the Outcomes in Cardiovascular Diseases

“…37 In a subsequent study Iaccarino et al 41 investigated the effects of β 2 AR variants on the left ventricular mass index (LVMi) regression when BP is reduced with β 1 -blockers (Atenolol), which are unable to completely block β 2 AR, 69,70 rather than with angiotensin-converting enzyme (ACE) inhibitors (Enalapril), which in hypertension reduce the whole sympathetic discharge. [71][72][73] This study showed that Glu27 patients presented a higher reduction in LVMi than Gln27 patients independently from treatment. 41 Moreover, the patients harboring Glu27 β 2 AR showed a larger regression of LVMi when treated with enalapril rather than atenolol.…”