Hypotensive action of propranolol

Waal, H. J.

doi:10.1002/cpt196675588

Cited by 87 publications

(23 citation statements)

References 16 publications

(18 reference statements)

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“…Prichard & Gillam (1966a) have postulated that blockade of the sympathetic supply to the heart is the primary cause of its hypotensive action. Waal (1966), however, noted that the hypotension was related neither to the fall in the heart rate nor to the dose-level of drug required to produce an antiarrhythmic effect. She also drew attention to the " striking similarity" between the hypotensive action of quinidine and propranolol.…”

Section: Discussionmentioning

confidence: 95%

“…its principal applications have been in the relief of anginal pain and control of arrhythmias, the drug has also been reported to lower blood pressure in hypertensive subjects, although estimates of its efficacy in this respect vary (Prichard & Gillam, 1964, 1966aRichards, 1966;Waal, 1966;Paterson & Dollery, 1966). It has been postulated that propranolol exerts its antihypertensive effect through either a specific blockade of al-receptors (Prichard & Gillam, 1964) or a non-specific (local anaesthetic, quinidine-like) action (Waal, 1966).…”

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confidence: 99%

“…It has been postulated that propranolol exerts its antihypertensive effect through either a specific blockade of al-receptors (Prichard & Gillam, 1964) or a non-specific (local anaesthetic, quinidine-like) action (Waal, 1966). In this paper an attempt has been made to reproduce the antihypertensive action of propranolol in hypertensive animals and to offer some explanation of its mode of action.…”

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confidence: 99%

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A comparison of some cardiovascular properties of propranolol, MJ 1999 and quinidine in relation to their effects in hypertensive animals

Farmer¹,

Levy²

1968

British J Pharmacology

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1. A comparison of some cardiovascular effects of propranolol, MJ 1999 and quinidine has been made in rats and dogs. 2. After intravenous, subcutaneous or oral administration to rats and dogs, propranolol was found to be 2-4 times more potent than MJ 1999 in blocking the chronotropic and vasodepressor responses to intravenously administered isoprenaline. 3. Propranolol and quinidine affected the e.c.g. of rats and dogs in a similar manner.4. At dose-levels causing effective blockade of al-receptors propranolol and MJ 1999 had no hypotensive effect after short-or long-term administration to conscious hypertensive rats and dogs. 5. At very high dose-levels propranolol and quinidine, but not MJ 1999, lowered blood pressure in the hypertensive rat. This effect of propranolol is probably related to one or more of the properties that propranolol and quinidine have in common rather than to a blockade of ,8-receptors. 6. The possible relevance of these results to the use of propranolol as a hypotensive agent in man is discussed.Propranolol is the first a-receptor antagonist to enjoy wide clinical use. While its principal applications have been in the relief of anginal pain and control of arrhythmias, the drug has also been reported to lower blood pressure in hypertensive subjects, although estimates of its efficacy in this respect vary (Prichard & Gillam, 1964, 1966aRichards, 1966;Waal, 1966; Paterson & Dollery, 1966). It has been postulated that propranolol exerts its antihypertensive effect through either a specific blockade of al-receptors (Prichard & Gillam, 1964) or a non-specific (local anaesthetic, quinidine-like) action (Waal, 1966). In this paper an attempt has been made to reproduce the antihypertensive action of propranolol in hypertensive animals and to offer some explanation of its mode of action. Accordingly, the cardiovascular effects of propranolol in normotensive and hypertensive rats and dogs have been determined and compared with those obtained with quinidine and MJ 1999 [4-(2. isopropylamino-l-hydroxyethyl) methanesulphonanilide hydrochloride], a P-receptor

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Section: Discussionmentioning

confidence: 95%

mentioning

confidence: 99%

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confidence: 99%

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A comparison of some cardiovascular properties of propranolol, MJ 1999 and quinidine in relation to their effects in hypertensive animals

Farmer¹,

Levy²

1968

British J Pharmacology

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“…The increase in arterial pressure during exercise is reduced by the intravenous injection of propranolol through a reduction in cardiac output (Epstein et al, 1965;Shinebourne et al, 1968). The oral administration of propranolol for several weeks leads to a gradual and significant reduction in arterial pressure in hypertensive patients (Prichard & Gillam, 1964;Patterson & Dollery, 1966;Waal, 1966;Frohlich, Tarazi, Dustan & Page, 1968). The mechanism of this hypotensive action is not clear but it does not seem to be due to the acute effects of blockade of adrenergic f8-receptors, showed that the changes in heart rate and cardiac output produced by propranolol were similar after acute intravenous injection and prolonged oral administration, but a reduction in arterial pressure occurred only after oral administration.…”

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confidence: 99%

Inhibition of the carotid sinus reflex by the chronic administration of propranolol

Dunlop¹,

Shanks²

1969

British J Pharmacology

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PIlar,uac'uh'ic'. Di)ivisioii, Imipcrial Chlemiical Inidustrie.s Limitedl, A lderlev Park, MaCcle,.fiw/1dl1. The changes in heart rate and arterial pressure produced by the intravenous injection of isoprenaline (05 [rg/kg), noradrenaline (10 jg/kg), phenylethylamine (0.5 mg/kg), amphetamine (0 5 mg/kg) and by bilateral occlusion of the carotid arteries and by stimulation of the central ends of both vagus nerves have been recorded in groups of dogs anaesthetized with pentobarbitone.2. The acute intravenous injection of propranolol (1 mg/kg) reduced the increases in heart rate produced by the six procedures, the increases in arterial pressure in response to the last five procedures and the decrease in pressure produced by isoprenaline. 3. This decrease produced by propranolol in the pressor responses resulted from a reduction in the increases in cardiac output elicited by the five procedures and has been attributed to blockade of cardiac adrenergic ,0-receptors. 4. Three groups of dogs were pretreated for 6 weeks by the oral administration of either placebo, propranolol 50 mg/kg daily or propranolol 10 mg/kg twice daily. The responses to the six test procedures were obtained 17 24 hr after the last dose of propranolol, when only minimal blockade of adrenergic /99-receptors was present. In the propranolol-treated groups, the pressor response to carotid occlusion but not to the other test procedures was significantly reduced. 5. The pressor response to carotid occlusion was not reduced in a fourth group ot dogs given a single dose of propranolol (50 mg/kg) 24 hr before the test procedures. 6. The mechanism of this selective reduction in the pressor response to occlusion of the carotid arteries is not clear. It is suggested that it may contribute to the hypotensive action of propranolol in man during prolonged oral administration.Several reports have shown that the intravenous injection of propranolol (5 15 mg) under resting conditions in patients with normal or raised arterial pressure

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“…There have been some investigators who have found a less favourable response of blood pressure to propranolol (Humphreys & Devlin, 1968;Paterson & Dollery, 1966;Richards, 1966;Richardson, Freund, Gear, Mauck & Preston, 1968;Waal, 1966). In all these instances the maximuni dose used was less than the average dose of about 400-500 mg a day used by Prichard & Gillam (1969), who in addition (unlike the investigators mentioned above) used a diuretic in more than half of their patients.…”

Section: Introductionmentioning

confidence: 96%

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

Prichard¹

1978

Brit J Clinical Pharma

102

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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).

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Hypotensive action of propranolol

Cited by 87 publications

References 16 publications

A comparison of some cardiovascular properties of propranolol, MJ 1999 and quinidine in relation to their effects in hypertensive animals

A comparison of some cardiovascular properties of propranolol, MJ 1999 and quinidine in relation to their effects in hypertensive animals

Inhibition of the carotid sinus reflex by the chronic administration of propranolol

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

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