Labetalol, a cross-over double blind controlled trial

1 Labetalol has been compared with propranolol in a double‐blind, double‐dummy study of 24 patients with mild or moderate essential hypertension. 2 Two patients were unable to tolerate propranolol and five labetalol, because of symptom side effects; this difference was not significant (P greater than 0.1). 3 On a self‐administered questionnaire, labetalol was associated with a greater number of side effects per patient than propranolol, but no individual side effect was significantly more common with either drug. 4 There was no difference in the number of spontaneously reported side effects between the two drugs. 5 Both drugs impaired pulmonary function, but propranolol caused a greater reduction than labetalol after 8 weeks of treatment. 6 We conclude that labetalol and propranolol are similarly effective and acceptable to the patient.

Section: Discussionsupporting

confidence: 69%

“…relatively few side-effects (Frick & Porsti, 1976;Sanders, Routledge, Rao, Gales, Davies & Rawlins, 1978;Pugsley, Nassim, Armstrong & Beilin, 1979). We have compared the side-effects of labetalol and propranolol in 24 patients with mild or moderate hypertension which had previously failed to respond to a thiazide diuretic alone.…”

Section: Introductionmentioning

confidence: 99%

Comparison of labetalol and propranolol in hypertension.

Nicholls¹,

Husaini²,

Bulpitt³

et al. 1980

“…It has seldom necessitated withdrawal of the drug (Brogden et al, 1978;Weidmann et al, 1978;Sanders et al, 1978;Pugsley et al, 1979;Dawson et al. 1979; Kane et al, 1979).…”

Section: Discussionmentioning

confidence: 99%

Blood pressure, body fluid volumes and glomerular filtration rate during treatment with labetalol in essential hypertension.

Rasmussen¹,

Nielsen²

1981

1 In a single blind study seventeen patients with mild or moderate essential hypertension and normal renal function were treated with labetalol alone in increasing doses from 300 via 600 to 1200 mg daily. 2 Average supine BP (systolic/diastolic) was reduced by 24/19 mm Hg. Seven patients attained a diastolic BP less than or equal to Hg. A significant postural fall in systolic BP was recorded, but no symptomatic orthostatic hypotension occurred. 3 In twelve patients measurements of plasma volume (125I‐albumin), extracellular volume (82Br‐space) and glomerular filtration rate (51Cr‐EDTA clearance) on placebo and subsequently labetalol showed no systemic changes. 4 Side effects were few causing two withdrawals because of impotence and arthralgia. 5 It is concluded that monotherapy with labetalol results in clinically relevant, persistent and dose dependent reduction in BP in patients with mild or moderate essential hypertension, apparently without concomitant expansion of body fluid volumes or influence on glomerular filtration rate.

“…Labetalol is a combined ac-and ,B-adrenoceptor antagonist, and an effective antihypertensive drug (Prichard, Thompson, Boakes, & Joekes, 1975;Sanders, Routledge, Rao, Gales, Davies & Rawlins, 1978). Considerable variation in plasma labetalol concentrations is likely to occur between individuals after oral administration because of extensive firstpass metabolism of the drug (Richards, Maconochie, Bland, Hopkins, Woodings & Martin, 1977) and to investigate this further, the pharmacokinetics and effects of labetolol were studied both between and within individual hypertensive patients.…”

Section: Introductionmentioning

confidence: 99%

Pharmacokinetics, beta‐adrenoceptor blockade and anti‐hypertensive action of labetalol during chronic oral treatment

Sanders¹,

Davies²,

Rawlins³

1980

1 fl-adrenoceptor blockade, plasma labetalol concentrations and anti-hypertensive actions were investigated at 2 hourly intervals during the interdose period of chronic oral therapy in six hypertensive patients.2 f,-adrenoceptor blockade varied during the inter-dose period and was maximal 2 and 4 h after the oral dose (P < 0.05). 3 Systolic pressure rose during the interdose period (P < 0.05). A significant correlation was found between the degree of fl-adrenoceptor blockade and the change in systolic pressure at 2 h after the oral dose.4 Efficacy of labetalol as a P-adrenoceptor antagonist and anti-hypertensive drug was assessed 2 h after an oral dose during chronic eight hourly dosage in sixteen hypertensive patients. Pharmacokinetics of labetalol were studied in the same patients. 5 Peak plasma labetalol concentration occurred 2 h after the oral dose and subsequently the plasma concentration declined monoexponentially.6 The steady state concentration (Css) of labetalol was correlated significantly with the daily oral dose in mg kg , the mid point labetalol concentration (Cmax + Cmin) and the isoprenaline dose ratio-I 2 at 2 h after the oral dose.7 No correlation was found between the antihypertensive effect and the Css ng ml-1 labetalol or between the isoprenaline dose ratio-I and the Css labetalol ng ml-.