Long term treatment of moderate hypertension with the beta1-receptor blocking agent metoprolol

102

All beta‐adrenoceptor blocking drugs that have been described share the common property of being competitive inhibitors. They differ in their associated properties, the presence or absence of cardioselectivity, membrane stabilizing activity, and partial agonist activity. Recently some beta‐adrenoceptor blocking drugs have been reported which also possess alpha‐adrenoceptor blocking activity. The associated properties have been used as a basis for classifying beta‐adrenoceptor blocking drugs (Fitzgerald, 1969, 1972). The presence or absence of cardioselectivity is most useful for dividing beta‐adrenoceptor blocking drugs. The non‐selective drugs (Division I) can be further divided according to the presence or absence of intrinsic sympathomimetic activity (ISA) and membrane stabilizing activity (Fitzgerald's groups I‐IV). Group I possess both membrane activity and ISA, e.g. alprenolol, oxprenolol, group II just membrane action, e.g. propanolol, group III ISA but no membrane action, e.g. pindolol. Fitzgerald placed pindolol in group I but should be placed in group III as it possesses a high degree of beta‐adrenoceptor blocking potency in relation to its membrane activity (Prichard, 1974). Finally drugs in group IV have neither ISA nor membrane action, e.g. sotalol, timolol. The cardioselective drugs (Division II) can be similarly sub‐divided into groups I‐IV according to the presence or absence of ISA or membrane action (Fitzgerald grouped all these together as group V). Lastly there are new beta‐adrenergic receptor blocking drugs which in addition have alpha‐ adrenergic receptor blocking properties (Division III).

Section: Effect On the Central Nervous Systemsupporting

confidence: 53%

Section: Effect On the Central Nervous Systemmentioning

confidence: 85%

Section: Effect On the Central Nervous Systemmentioning

confidence: 99%

See 1 more Smart Citation

The second Lilly Prize Lecture, University of Newcastle, July 1977. beta‐Adrenergic receptor blockade in hypertension, past, present and future.

Prichard¹

1978

102

“…On the other hand, the majority of studies in hypertensive subjects suggests that maximal exercise capacity is not affected during ,-adrenoceptor blockade (Hansson et al, 1977;Reybrouck et al, 1977;Franz et al, 1979Franz et al, , 1982Franz et al, , 1985Lijnen et al, 1979;Leenen et al, 1980;Losment et al, 1986). It is likely that the reduction of maximal exercise cardiac output during ,-adrenoceptor blockade (Epstein et al, 1965;Ekblom et al, 1972) is involved in the reduction of maximal exercise capacity in normotensive subjects.…”

Section: Introductionmentioning

confidence: 99%

Exercise haemodynamics and maximal exercise capacity during beta‐ adrenoceptor blockade in normotensive and hypertensive subjects.

Baak

Koene

Verstappen

1988

1 The effects of atenolol administration on maximal exercise capacity and exercise haemodynamics have been compared in eight normotensive and eight mildly hypertensive subjects, matched for sex, age, body weight, and maximal oxygen uptake, and familiar with maximal exercise testing. 2 Supine and exercise blood pressure, and exercise total peripheral resistance were significantly higher, and exercise cardiac output was significantly lower in the hypertensive than in the normotensive subjects.3 Administration of atenolol (1 x 100 mg day-') for 3 days reduced supine and exercise systolic blood pressure, heart rate, and cardiac output, and increased exercise stroke volume. Supine and exercise diastolic blood pressure and exercise total peripheral resistance were unaffected by atenolol. The effects of atenolol did not differ in the normotensive and the hypertensive subjects. 4 Maximal work load, maximal oxygen uptake, and maximal heart rate were reduced to a similar extent in normotensive and hypertensive subjects during atenolol treatment. 5 It is concluded that there is no difference in the effects of short-term atenolol administration on exercise haemodynamics and maximal exercise capacity in normotensive and mildly hypertensive subjects.

“…Weil & Chidsey, 1968;Finnerty et al, 1970; Sederberg-Olsen & Ibsen, 1972;Hansson et al, 1977;Koshy et al, 1977;Ibsen et al, 1978;. Addition of diuretics restore the sensitivity to treatment resulting both in a reduction in blood pressure and volumes (Rpnnov-Jessen & Hansen, 1969;Finnerty etal., 1970;Dustan, Tarazi & Bravo, 1972;Geyskes et al, 1975;.…”

Section: Introductionmentioning

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.