A comparison of beta adrenergic blocking drugs in the treatment of hypertension

Morgan, T. O.; Anavekar, S. N.; Sabto, J.; Wj, Louis; Doyle, Austin E.

doi:10.1136/pgmj.50.583.253

Cited by 93 publications

(27 citation statements)

References 4 publications

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“…Although the consensus seems to be that 13-blockers and diuretic drugs, alone or in combination, are an effective form of therapy irrespective of which agents are used (BUhleret al, 1975;Davidson et al, 1976; Dustan et al, 1974;Hamer, 1976;Morgan et al, 1974;Stumpe & Kolloch, 1976), the question of prediction of response remains unsolved. There is no simple clinical analysis to predict a patient's response to either a 13-blocking drug or diuretic.…”

Section: Introductionmentioning

confidence: 99%

Diuretics, beta‐blockers or both as treatment for essential hypertension.

Stumpe¹,

Overlack²

1979

Brit J Clinical Pharma

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1 Patients with borderline (group I) and sustained hypertension (group II) were treated with 3-blocking drugs, diuretics and the combination of both. In the two groups of patients the antihypertensive effectiveness of both short-term intravenous or chronically oral propranolol was directly related to the extent to which the drug produced an absolute reduction in plasma renin activity (PRA). No such a correlation could be obtained with pindolol. In group I following ,B-blockade, day-night profiles of PRA were similar to those observed in group II before treatment. Thus, in this latter subgroup, low renin profiles might reflect reduced ,3-adrenergic activity. 2 When the chronically 13-blockaded patients were changed to chronic diuretic therapy it became evident that young hypertensive patients of group II showed a more pronounced BP response than the patients of group I. In those patients of group II in whom pressure was not controlled by the diuretic alone, combination with a 13-blocker led to pressure normalization. 3 The 13-blocking drug induced reduction in pressure was greater in the 25-35 yr olds, than in those older than 55. In contrast, the antihypertensive effect of the diuretic was more pronounced in the 55-70 yr olds than in those younger than 40. 4 It is concluded that sympathetic nervous system activity mainly determined PRA as well as antihypertensive effectiveness of both the P-blockers and the diuretics. As to outpatient management it is proposed that with the exception of young borderline hypertensives who seem to respond best to 13-blockers, initial antihypertensive drug therapy may consist of a diuretic agent. If the antihypertensive effect of the diuretic is insufficient, combination with a P-blocking drug could be used to achieve the best effect.

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Section: Introductionmentioning

confidence: 99%

Diuretics, beta‐blockers or both as treatment for essential hypertension.

Stumpe¹,

Overlack²

1979

Brit J Clinical Pharma

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“…These drugs are equally effective in reducing blood pressure in patients with essential hypertension (Morgan et al, 1974), regardless of differences in bioavailability, affinity for 01-and 32-adrenoceptors, lipid solubility, metabolism and intrinsic sympathomimetic activity (ISA) (Imhof, 1976). How-ever, all fi-adrenoceptor blocking drugs share the ability to block 1l-adrenoceptors and consequently the mechanisms whereby blood pressure is reduced, are thought to be linked to this property.…”

Section: Introductionmentioning

confidence: 99%

Haemodynamic effects of metoprolol and pindolol: a comparison in hypertensive patients.

Svensson¹,

Gudbrandsson²,

Sivertsson³

et al. 1982

Brit J Clinical Pharma

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1 In a double‐blind study, 36 patients with essential hypertension were randomly allocated to treatment with either metoprolol, 100–300 mg/day, or pindolol, 5–15 mg/day for 6 months. Haemodynamic investigations were made on three separate occasions. Blood flow in the calves and in the forearm was determined by venous occlusion plethysmography after 6 weeks of placebo, after 6 weeks and again after 6 months of active therapy. 2 Both drugs reduced blood pressure significantly, by 17.1/11.8 mm Hg with metoprolol and 21.9/10.9 mm Hg with pindolol after 6 weeks (P less than 0.005). No further changes were seen after 6 months. 3 Heart rate after 6 weeks was significantly reduced by metoprolol (10.7 +/‐ 2.4 beats/min, P less than 0.001) but not by pindolol (4.4 +/‐ 2.3 beats/min, NS). After 6 months a significant reduction was seen also in the pindolol group (5.2 +/‐ 2.1 beats/min, P less than 0.05). 4 The vascular resistance in the calves at rest was reduced by pindolol (P less than 0.05), whereas resistance tended to increase with metoprolol. 5 Resting vascular resistance in the forearm after 6 months was significantly reduced in the metoprolol group (P less than 0.001) as well as in the pindolol group (P less than 0.02). The increase in forearm vascular resistance seen during leg exercise was not influenced by either drug. 6 Vascular resistance at maximal vasodilatation was unchanged in the calves, but a significant reduction (‐17.4 +/‐ 5.7%, P less than 0.01) in the forearm vascular bed was seen after 6 months of pindolol. No change was observed with metoprolol. 7 It is concluded that pindolol reduces elevated blood pressure partly through peripheral vascular mechanism. Metoprolol, on the other hand, probably acts mainly via central cardiac mechanisms.

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“…Drugs such as propranolol and timolol which lack ISA do this to a larger extent than drugs like pindolol and oxprenolol which possess intrinsic sympathomimetic activity (Morgan et al, 1974;McNeil & Louis, 1979). In a comparative study in hypertensive patients, metoprolol and atenolol (two cardioselective drugs which lack ISA), were shown to have a 30% incidence of significant bradycardia, defined as the development of pulse rates of less than 55 beats/min and some patients developed heart rates less than 50 beats/min.…”

Section: Cardiac Side-effectsmentioning

confidence: 99%

“…Intrinsic sympathomimetic activity (ISA) ISA is a property which has, in the past, been somewhat neglected but interest has been rekindled by reports that drugs with this property are less likely to induce bronchospasm and have a lower incidence of side effects such as Raynaud's phenomena (Morgan et al, 1974;Marshall et al, 1976). There have also been reports that rebound cardiac arrhythmias may follow abrupt withdrawal of P-adrenoceptorblockers with weak or absent ISA (Miller et al, 1975;Ross et al, 1981).…”

Section: Introductionmentioning

confidence: 99%

“…However, even under resting conditions, heart muscle is under sympathetic stimulation and the complete absence of sympathetic activity may on occasion lead to bradycardia, cardiac failure and conduction defects (Svendsen etal., 1979). Similarly there are suggestions that the absence of sympathetic activity in the bronchi may increase the percentage of the population developing bronchospasm and to increase the likelihood of patients with asthma developing an exacerbation of symptoms (Morgan et al, 1974;Hughes et al, 1976).…”

Section: Introductionmentioning

confidence: 99%

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