Propranolol therapy in essential hypertension

Lydtin, H; Kusus, T; Daniel, Werner G.; Schierl, W; Ackenheil, Manfred; H, Kempter; Lohmöller, G; Niklas, M; Walter, Ingeborg

doi:10.1016/0002-8703(72)90397-3

Cited by 69 publications

(20 citation statements)

References 16 publications

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“…Propranolol has been used as an anti hypertensive drug (11), but the exact mecha nism of this drug is still unknown (12)(13)(14)(15). Propranolol (10 mg/kg/day) prevented an increase in the blood pressure and heart rate of SHR after 4 weeks and 6 weeks of treat ment.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamics and monoamine oxidase activity in spontaneously hypertensive rats (SHR)

et al. 1983

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Abstract-The relationship between the onset of hypertension and changes in monoamine oxidase (MAO) activity in the brains and hearts of spontaneously hypertensive rats (SHR) were studied. After 7-weeks-old, blood pressure of SHR increased rapidly and reached a level of 170 to 180 mmHg; but following 4 weeks of propranolol treatment (10 mg/kg/day), blood pressure decreased significantly compared to that of untreated SHR. Heart/body weights ratio of SHR was higher than that of normotensive Wistar Kyoto rats (WKY). MAO activities in the brain stem, the medulla oblongata and pons of the SHR were significantly higher than those in WKY at 7 weeks of age, and MAO activity in the brain stem of the propranolol-treated SHR was significantly lower than that in the untreated SHR. Propranolol inhibited MAO activity in brain tissue in vitro, and the 150 values of propranolol were identical (1 X10-4 M) in SHR and WKY. In both the WKY strain and the SHR, the Vmax values of heart MAO increased with age, and the Vmax values of SHR were twice those of WKY. Km values for tyramine of heart MAO in WKY and SHR were approx. 100 PM and 140 ,iM, respectively; however, these values were not age-dependent. It was concluded that an increase in MAO activity in SHR brain stem may trigger a reduction in noradrenaline content and that propranolol may be responsible for its restoration, thus reducing peripheral sympathetic activity; moreover, the increase in MAO activity in the hearts of SHR may be of genetic origin.

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Section: Discussionmentioning

confidence: 99%

Hemodynamics and monoamine oxidase activity in spontaneously hypertensive rats (SHR)

et al. 1983

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“…Reduction in cardiac output as the sole responsible mechanism of antihypertensive action of /3-adrenoceptor blockers 101 has been challenged. Evidence has been presented that chronic administration of ft-adrenoceptor blocking drugs reduces peripheral resistance.…”

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confidence: 99%

“…Evidence has been presented that chronic administration of ft-adrenoceptor blocking drugs reduces peripheral resistance. 101 The sympathetic nervous system controls the release of renin from juxtaglomerular cells in the kidney via /S-adrenoceptors. Consequently drugs blocking these receptors reduce plasma renin levels both in normotensive and hypertensive subjects.…”

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confidence: 99%

Recent developments in noradrenergic neurotransmission and its relevance to the mechanism of action of certain antihypertensive agents.

Langer¹,

Cavero²,

Massingham³

1980

Hypertension

165

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SUMMARY This report reviews a number of significant developments in the fields of noradrenergic transmission and adrenergic receptors which suggest that, hi addition to the classical postsynaptic adrenoceptors, there are also presynaptic adrenoceptors that help modulate tbe release of norepinephrine (NE) from peripheral as well as central noradrenergic nerve endings during nerve stimulation. In particular, stimulation of presynaptic a-adrenoceptors reduces this release of transmitter and tbe reverse is observed after blockade of these receptors. Clearcut pharmacological differences exist between the postsynaptic aradrenoceptors that mediate the responses of certain organs and the presynaptic aradrenoceptors that modulate the NE release during nerve stimulation. Therefore, subdassification of a-adrenoceptors into a, and a, subtypes is warranted but must be considered to be independent of the anatomical location of these receptors.Some noradrenergic nerve endings have also been shown to possess /3-adrenergic receptors, tbe stimulation of which increases the quantity of transmitter released by nerve impulses. Physiologically, these receptors could be activated by circulating epinepbrine (E) and be involved in essential hypertension. A third type of catecholamine receptor found at the noradrenergic nerve ending is the Inhibitory dopamine (DA) receptor, which might be of significance in the development of new antihypertensive agents. Application of these new concepts of noradrenergic neurotransraission and the subdassification of a-adrenoceptors to tbe treatment of hypertension is presented. Gonidtne, for example, appears to be a potent aradrenoceptor agonist; the central receptor involved in its antihypertensive action is pharmacologically an a,-type but located postsynaptically. Clonidine also induces activation of peripheral presynaptic aradrenoceptors, which might contribute to its cardiovascular action.The antihypertensive effects of a-methyldopa are related to tbe formation of a-methylnorepinephrine, a preferential a r adrenoceptor agonist, which can stimulate peripheral presynaptic aradrenoceptors leading to a decrease of NE release and a reduction in sympathetic tone.

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“…However, owing to its cardiodepressant effect, the use of pro pranolol has not gained wide acceptance for fear of precipitating cardiac failure particu larly in patients with impaired cardiocirculatory conditions [6][7][8], This often occurs to patients with dialysis-resistant hypertension. The depressant effect of propranolol on car diac output has been well documented in pa tients with mild to moderate hypertension [9,10] and circulatory hyperkinesis [ 11 ]. No study, however, has been published so far on the chronic hemodynamic effect of propranolol in patients with malignant hypertension or with dialysis-resistant hypertension who are, ac cording to some reports [4,5,12], those show ing a very marked response to propranolol treatment.…”

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confidence: 99%

Chronic Hemodynamic Effects of Propranolol Treatment in Dialysis-Refractory Hypertension

Maggiore

Zoccali

Monzani

et al. 1978

Nephron

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The hemodynamic mechanism of the hypotensive effect of propranolol was studied by quantitative radiocardiography in 8 patients with dialysis-resistant hypertension. Propranolol treatment brought about a decrease in mean arterial pressure and peripheral vascular resistances. The cardiac index was slightly reduced only in the early stage of the treatment. No significant difference was found between patients on treatments lasting longer than 3 months and patients with dialysis-controlled hypertension. The results show that propranolol can be used safely as the sole antihypertensive agent in patients with dialysis-resistant hypertension.

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Propranolol therapy in essential hypertension

Cited by 69 publications

References 16 publications

Hemodynamics and monoamine oxidase activity in spontaneously hypertensive rats (SHR)

Hemodynamics and monoamine oxidase activity in spontaneously hypertensive rats (SHR)

Recent developments in noradrenergic neurotransmission and its relevance to the mechanism of action of certain antihypertensive agents.

Chronic Hemodynamic Effects of Propranolol Treatment in Dialysis-Refractory Hypertension

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