Biomedical subjects

B Ablad

Publications and source records attributed to B Ablad.

At least 37 records · Page 2Linked to original sources

PubMed1977

Reduced adrenal amine synthesis in spontaneously hypertensive rats after long-term treatment with propranolol.

Male spontaneously hypertensive rats were either fed a diet containing 3 mg/g of (+/-)-propranolol, giving a mean daily intake of 178 +/- 4.2 mg/kg, or a control diet from 7 weeks of age for 6 months. Three days after cessation of propranolol-treatment, the arterial blood pressure of the treated group was about 10% lower than that of the control group. Adrenal dopamine content and tyrosine hydroxylase activity were reduced to 76% and 71% of the control values, respectively. The results indicate that propranolol causes a reduced sympathetic discharge through its central action, although blockade of beta-adrenoceptor-mediated local regulatory mechanisms cannot be excluded.

Adrenal Glands↗

PubMed1977

Mode of action of beta blockers in angina pectoris.

The therapeutic effect of beta adrenoceptor blockers in angina pectoris can be ascribed to an inhibition of beta1 receptor mediated stimulation of heart rate and myocardial contractility, resulting in an improved oxygen supply-demand balance in the myocardium. When given in equipotent beta1 blocking doses, the nonselective blocker propranolol and the beta1 selective blocker metoprolol differ markedly as regards inhibition of adrenaline induced beta2 mediated vasodilatation. Only propranolol will inhibit this effect. After propranolol, adrenaline therefore elicits a haemodynamic effect pattern characterized by high peripheral vascular resistance, high arterial blood pressure, low cardiac output and increased cardiac size. In view of these findings it is suggested that a beta1 selective blocker may be a more efficient antianginal agent than a nonselective blocker in those patients in which the anginal attack is associated with a significant release of adrenaline. The clinical relevance of this hypothesis has not been tested.

Adrenergic beta-Antagonists↗

PubMed1976

Anti-hypertensive effect of metoprolol in spontaneously hypertensive rats.

1. Oral and intravenous administration of metoprolol to adult spontaneously hypertensive rats (SHR) with established hypertension lowered arterial blood pressure within 4 days of treatment. 2. Steady state plasma concentrations of metoprolol were similar to those of patients during anti-hypertensive treatment with this drug. 3. The neuroeffector function of portal veins of SHR treated orally for 14 days or intravenously for 4 days was not impaired when studied in vitro. This is in contrast to previous findings after long-term treatment. 4. It is concluded that the anti-hypertensive effect of metoprolol in SHR in many respects resembles that observed in patients. It is suggested that impairment of vasomotor nerve control may contribute to the anti-hypertensive effect of beta-adrenoreceptor antagonists.

Animals↗

PubMed1976

Some aspects of the pharmacology of beta-adrenorecptor blockers.

The pharmacodynamic properties of a beta-blocker are mainly determined by its affinity to beta1 and beta2-receptors respectively and by its intrinsic activity. It is suggested that there is no absolute organ separation of the two receptor sub-types. Instead both beta1 and beta2-receptors are involved in the mediation of the same effect. The frequency distribution ratio of beta1/beta2-receptors varied markedly among various effector responses. A non-selective and a beta1-selective blocker may have different haemodynamic effects when the levels of circulating adrenaline are high, because of their markedly different potency in inhibiting the beta2-mediated vasodilator effect of adrenaline. Data are presented which suggest the existence of a presynaptic beta1-receptor mediating a positive feedback mechanism on neuronal release of noradrenaline.

Adrenergic beta-Antagonists↗

PubMed1976

Haemodynamic effects of beta-adrenorecptor blockers in hypertension.

The haemodynamic effect pattern of beta-blockers in hypertension is discussed. The time curve of the antihypertensive effect differs from that of cardiac beta-blockade. The antihypertensive effect is characterized by a slower onset at the start of treatment and a more gradual disappearance when therapy is withdrawn. It appears that the crucial effect of beta-blockers in hypertension is a gradually developing reduction in total peripheral vascular resistance. The mechanism of this apparent vasodilator action is unknown. Various possible factors involved are mentioned. One is a reduced efficiency of transmitter release from the peripheral adrenergic neuron. Such an action may contribute to the antihypertensive effect, as judged by results of animal experiments described.

Adrenergic beta-Antagonists↗

PubMed1975