Atenolol v placebo in mild hypertension: renal metabolic and stress antipressor effects.

Abstract

1 The effects of 8 week treatment periods of atenolol and placebo on effective renal plasma flow (ERPF), glomerular filtration rate (GFR), plasma renin activity (PRA), oral glucose, fasting lipids and Achilles tendon reflex were compared in a double-blind crossover trial in ten subjects with mild hypertension. 2 Atenolol reduced resting blood pressure and pulse rate but did not prevent the rise in blood pressure and pulse rate in response to three kinds of stress. 3 Mean glomerular filtration rate and effective renal plasma flow were below the normal range during placebo (1.31 ml/s and 7.40 ml/s respectively) but were not significantly different on atenolol (1.23 ml/s and 7.18 ml/s). Serum urea was significantly (P < 0.01) higher on atenolol (6.7 mmol/l) than on placebo (5.6 mmol/l) but serum creatinine did not change. PRA was lower on atenolol (0.42 nmol 1-1 h-') than on placebo (1.01 nmol 1-' h'-). 4 The mean values of fasting cholesterol, triglycerides, ankle jerk contraction time, spirometry, weight, serum potassium, sodium and chloride were similar on atenolol and placebo. 5 Fasting blood sugar was a little higher (P < 0.05) on atenolol and the 1 and 2 h post-glucose serum insulin levels were a little lower (P < 0.01). 6 The cardioselectivity of atenolol does not impair its anti-hypertensive effect and may be associated with less effect on renal function. The metabolic effects of atenolol seem to differ from those of metoprolol.

Responses to mental stress and physical provocations before and during long term treatment of hypertensive patients with beta‐adrenoceptor blockers or hydrochlorothiazide.

“…Adaptation is not a major problem with CWT, as is sometimes the case with other mental stress tests, since heart rate responses to CWT have been found to be similar on three occasions during a 3 month period in placebo-treated post-infarction patients (Olsson et al, 1986 (Folkow, 1982;Eliasson et al, 1983). Our findings of unchanged blood pressure responsiveness to stress during 3-adrenoceptor blockade, despite attenuated heart rate responsiveness and clearly reduced blood pressure levels, are in agreement with previous findings with oral treatment with non-selective 1-adrenoceptor antagonists (Nyberg et al, 1977;Houben et al, 1983;Floras et al, 1985) or 1l-selective antagonists (Nyberg et al, 1977;Heidbreder etal., 1978;Waal-Manning & Bolli, 1980;Houben et al, 1983;Francois et al, 1984;Floras et al, 1985) for varying periods of time. Only two studies have reported decreases in blood pressure reactivity to mental stress during 3-adrenoceptor blockade (Guazzi et al, 1976;Dunn et al, 1978), but the possibility of adaptation to the stress procedure was not investigated in these studies.…”