Antihypertensive Mechanisms of Beta-Adrenoceptor Blockade: A Review

Baak, Marleen A. van; Boudier, H A Struyker; Smits, J. F. M.

doi:10.3109/10641968509074754

Cited by 17 publications

(8 citation statements)

References 213 publications

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“…This is exemplified by the hemody namic actions of many [f-adrenoceptor blockers in hyper tensive patients or animals. These agents cause an early fall in cardiac output, whereas a simultaneous decrease in blood pressure is prevented by a rise in total peripheral resistance [2]. The rise in peripheral resistance seems to be due to a generalized constriction of arterioles [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Role of Baroreflex Activation in the Regional Hemodynamic Effects of the Beta-Blockers Tertatolol and Propranolol in Conscious Spontaneously Hypertensive Rats

Struyker-Boudier¹,

Essen²,

Nievelstein³

et al. 1986

Am J Nephrol

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The effects of the β-adrenoceptor-blocking drugs tertatolol and propranolol on regional hemodynamics were compared in intact and sinoaortic denervated (SAD) conscious spontaneously hypertensive rats (SHR). Miniaturized Doppler flow probes were used for the continuous determination of changes in flows and resistances in the renal, mesenteric, and hindquarter vascular beds. In intact animals 5 mg/kg propranolol i.v. caused an initial increase and a later gradual fall in mean arterial blood pressure (MAP) and an early rise in all three resistances. In SAD rats the reduction in MAP occurred more readily and no increases in RR and MR were observed. RR even decreased significantly. 0.5 mg/kg tertatolol i.v. caused a similar change in MAP as did propranolol. In contrast, tertatolol increased resistance only in the hindquarter vascular bed, both in intact and SAD animals. These data show an important role of sinoaortic baroreflex activation in the early peripheral vasoconstriction caused by propranolol in conscious SHR. Moreover, the data suggest that tertatolol inhibits the sympathetic nervous system-mediated reflex vasoconstriction.

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Section: Introductionmentioning

confidence: 99%

Role of Baroreflex Activation in the Regional Hemodynamic Effects of the Beta-Blockers Tertatolol and Propranolol in Conscious Spontaneously Hypertensive Rats

Struyker-Boudier¹,

Essen²,

Nievelstein³

et al. 1986

Am J Nephrol

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“…Stimulation of presynaptic dopamine (DAi) receptors by the increased (even though still relatively low) level of DA could lead to inhi bition of neuronal activity (NE release) in general [15], In the heart, the result would be decreased pi-adrenoceptor activity and bra dycardia [16], However, there is a significant difference between the acute hemodynamic profile of DBH inhibition observed in these studies and P-adrenoceptor blockade following pro pranolol administration. The rapid rise in total peripheral resistance, a hemodynamic pattern following Pi-adrenoceptor blockade [17] , is absent following DBH inhibition by SK&F 102698. Our results confirm the ob servations of Smits and Struyker-Boudier [18] , in that HR and CO decreased within an hour propranolol was given.…”

Section: Discussionmentioning

confidence: 99%

Effect of Dopamine β-Hydroxylase Inhibition on Systemic Hemodynamics in Conscious, Spontaneously Hypertensive Rats

Gellai¹,

DeWolf²,

Ruffolo³

1990

Pharmacology

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The acute and chronic effects of a potent and selective dopamine β-hydroxylase inhibitor, SK&F 102698 [l-(3,5-difluorobenzyl)imidazole-2-thiol], on systemic hemodynamic variables were assessed in chronically instrumented spontaneously hypertensive and normotensive Wistar rats. The changes observed in the hypertensive rats were compared with those obtained by vehicle in a different group of rats. Following intragastric administration of SK&F 102698 (75 mg/kg), blood pressure and cardiac output decreased gradually in both strains of rats, while total peripheral vascular resistance remained unchanged. The antihypertensive effect of repeated daily administration of SK&F 102698 in the hypertensive rats was sustained for the duration of treatment. During the acute phase, the decrease in cardiac output was due to bradycardia. In addition, as a result of hemodynamic changes, SK&F 102698 significantly reduced the minute work output of the heart. The results indicate that SK&F 102698 lowers blood pressure primarily by decreasing cardiac output.

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“…Significance of the differences from control period: *P <0.05, **P <0.01, ***P <0.001. (van Baak et al, 1985). This means that arterial pressure is maintained by perpheral vasoconstriction, probably neurally mediated and most likely due to increased sympathetic outflow in some other vascular areas.…”

Section: Discussionmentioning

confidence: 99%

“…Previous investigations on the effect of various Padrenoceptor antagonists on sympathetic activity have produced conflicting results (see Korner., 1982, van Baak et al, 1985. It should be noted, however, that the animals used for those studies were either normotensive or hypertensive and either anaesthetized or conscious, and the reported effects were monitored for only 2 h after administration ofthe P-adrenoceptor blockers being tested.…”

Section: Discussionmentioning

confidence: 99%

“…Different modes of action have been suggested to explain the antihypertensive effects of P-adrenoceptor antagonists, including inhibition of sympathetic outflow to peripheral blood vessels (see Wallin et al, 1984;van Baak et al, 1985). Depending on the experimental method and set-up and the dose of the Padrenoceptor antagonist, both inhibitory and excitatory responses have been obtained.…”

Section: Introductionmentioning

confidence: 99%

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Increase of renal sympathetic nerve activity by metoprolol or propranolol in conscious spontaneously hypertensive rats

Majcherczyk¹,

Mikulski²,

Sjölander³

et al. 1987

British J Pharmacology

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Mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were recorded in conscious spontaneously hypertensive rats (SHR). Infusion of metoprolol (4 μmol kg−1 h−1) or propranolol (1.5 μmol kg−1 h−1) reduced HR and significantly increased RSNA. Administration of metoprolol caused a sustained decrease of MAP starting in the third hour of infusion. In contrast, administration of propranolol induced a biphasic response in MAP. It is suggested that the increase of RSNA after both β‐adrenoceptor blocking drugs is due to a decrease in arterial baroreceptor activity.

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Antihypertensive Mechanisms of Beta-Adrenoceptor Blockade: A Review

Cited by 17 publications

References 213 publications

Role of Baroreflex Activation in the Regional Hemodynamic Effects of the Beta-Blockers Tertatolol and Propranolol in Conscious Spontaneously Hypertensive Rats

Role of Baroreflex Activation in the Regional Hemodynamic Effects of the Beta-Blockers Tertatolol and Propranolol in Conscious Spontaneously Hypertensive Rats

Effect of Dopamine β-Hydroxylase Inhibition on Systemic Hemodynamics in Conscious, Spontaneously Hypertensive Rats

Increase of renal sympathetic nerve activity by metoprolol or propranolol in conscious spontaneously hypertensive rats

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Antihypertensive Mechanisms of Beta-Adrenoceptor Blockade: A Review

Cited by 17 publications

References 213 publications

Role of Baroreflex Activation in the Regional Hemodynamic Effects of the Beta-Blockers Tertatolol and Propranolol in Conscious Spontaneously Hypertensive Rats

Role of Baroreflex Activation in the Regional Hemodynamic Effects of the Beta-Blockers Tertatolol and Propranolol in Conscious Spontaneously Hypertensive Rats

Effect of Dopamine &beta;-Hydroxylase Inhibition on Systemic Hemodynamics in Conscious, Spontaneously Hypertensive Rats

Increase of renal sympathetic nerve activity by metoprolol or propranolol in conscious spontaneously hypertensive rats

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Effect of Dopamine β-Hydroxylase Inhibition on Systemic Hemodynamics in Conscious, Spontaneously Hypertensive Rats