All beta-adrenoreceptor blocking drugs seem to be fairly rapidly and completely absorbed from the gastro-intestinal tract. The rate of absorption, however, appears to be lower in elderly patients and possibly also in patients with renal failure than in younger patients. The extent of bioavailability varies considerably between different beta-blockers. Some of these drugs(e.g. alprenolol and propranolol) have a low extent of bioavailability due to a high first-pass elimination effect, while pindolol and practolol for example are in influenced very little by this effect. However, as some beta-blockers from active metabolites, the bioavailability calculated as the ratio between the area under the plasma concentration time curve of unchanged drug after oral and intravenous administration does not give an accurate estimation of the fraction of the biologically active dose reaching the systemic circulation. The beta-blockers so far studied are rapidly distributed in the body. The t1/2 of distribution ranges between 5 to 30 minutes. The apparent volume of distribution varies 3- to 4-fold between the compounds but in all cases the apparent volume of distribution exceeds the physiological body space. In patients with impaired liver function an increase of the volume of distrubution of propranolol has been found. The beta-blockers are relatively rapidly eliminated from the body and most of them have an elimination half-life between 2 to 4 hours. For atenolol, practolol and sotalol higher values have been reported. The most lipophilic beta-blockers are almost completely metabolised in the liver, wheras those of lower lipophilicity are mainly excreted via the kidneys. Impraired liver and kidney function have been found to significantly influence the rate of elimination of those beta-blockers eliminated via the insufficient organ of elimination. Numerous investigators have shown that the beta-blocking effect is linearly related to the logarithm of the plasma concentration. In spite of this relationship, it is difficult from mean data to predict the individual plasma concentration which is necessary for a certain degree of beta-blockade. This might be due to variations in the quantitative formation of active metablolites, individual differences in the plasma protein binding and rather flat plasma level-response curves. Also with respect to the therapeutic effect, the plasma levels vary considerably between individuals. This limits the value of determination of plasma concentrations in order to adjust the therapeutic dose. Our recommendation is that these facilities should be utilised in selected patient groups, eg. those who have a poor therapeutic response to a beta-blocker although the dose is high, and those patient with impaired renal or liver function. The duration of beta-blockade is dose-dependent since the pharmacological effect declines with a constant rate (zero-order kinetics) within relatively wide dosage intervals...

Clinical pharmacokinetics of beta-adrenoreceptor blocking drugs.

https://www.amjmed.com/article/0002-9343(73)90136-8/pdf

Neurogenic Factors in Human Hypertension: Mechanism or Myth?

The β-adrenergic receptor blocking drugs (β-blockers) are proving to be extremely useful in antihypertensive therapy. The reasons for their antihypertensive effect are not entirely clear, but a reduction in cardiac output and in renin release by the kidney seem to be the most probable explanations.

Beta-adrenergic receptor blocking drugs in hypertension.

With heightened awareness of the need for better treatment of millions of hypertensive patients, physicians have markedly increased their use of antihypertensive drugs in the past few years. Empiri...

Propranolol in the treatment of hypertension.

https://www.amjmed.com/article/0002-9343(76)90904-9/pdf

The essential action of propranolol in hypertension

Propranolol therapy in essential hypertension.

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Propranolol therapy in essential hypertension.