Contrasting effects of acute beta blockade with propranolol on plasma catecholamines and renin in essential hypertension: a possible basis for the delayed antihypertensive response
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Plasma renin activity
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Cerebroventricular Propranolol Elevates Cerebrospinal Fluid Norepinephrine and Lowers Blood Pressure
Ventriculocisternal administration of dl - and d -propranolol produced dose-dependent increases in cerebrospinal fluid norepinephrine and reductions in blood pressure. A highly significant correlation was found between the increase in norepinephrine and the hypotensive effect. The propranolol-induced hypotension was prevented by intracisternal phentolamine. These data indicate that the hypotensive effect of centrally administered propranolol results from a drug-induced release of norepinephrine, which stimulates central alpha receptors to lower arterial pressure.
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Norepinephrine extraction was found to be decreased in the lungs of immobilised rats. Administration of epinephrine to intact rats up to the same level in the blood plasma as after stress, induced an increase in the norepinephrine extraction by the lungs. The data obtained suggest that norepinephrine inactivation due to immobilisation stress is unrelated to the plasma epinephrine level. The role of the lungs in the maintenance of increased plasma of norepinephrine by means of decreasing its metabolic inactivation, is discussed.
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1. In patients with mild or moderate essential hypertension, oral propranolol, given in incremental doses, produced a moderate but significant lowering of blood pressure which was correlated with the concentration of propranolol in plasma. 2. Propranolol also reduced plasma renin activity (PRA) in the supine posture, on standing and after intravenous frusemide. However, 'supine' and 'frusemide' PRA values were markedly reduced at a plasma concentration of propranolol that had little effect on blood pressure. 3. On administration of propranolol there was little correlation between blood pressure decrease and PRA suppression, and even less between pretreatment PRA values and hypotensive response. 4. It is concluded that in patients with mild and moderate hypertension and low or normal plasma renin activity, suppression of PRA is not an important determinant of the hypotensive response to propranolol.
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The plasma half-life of propranolol after intramuscular injection is 100 min in the New Zealand female rabbit. After the administration of a single dose of propranolol. there is a lowering of plasma renin activity (PRA) and an inverse correlation between PRA and plasma propranolol. It appears that the effect of propranolol on PRA is related to the plasma level of the drug which directly relates to the time of the last administration of the drug.
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1. Stepwise increases of oral doses of propranolol produced both a significant lowering of blood pressure and suppression of plasma renin activity in sixteen patients with mild or moderate normal-renin essential hypertension. 2. The hypotensive and the renin-suppressive actions of propranolol were differently related to plasma propranolol concentrations. At the lowest propranolol concentrations (15–40 nmol/l), there was almost no decrease in blood pressure whereas plasma renin activity and responsiveness to renin-releasing stimuli (standing, intravenous frusemide) were already strongly depressed (greater than 50%). Therefore in a large number of normal-renin hypertensive patients under small doses of propranolol, the renin-suppressive action of the drug can be dissociated from the hypotensive effect. Dissociation of the two effects, though in the opposite way, was also observed in three of four low-renin hypertensive patients, whose blood pressure was decreased by propranolol without further reduction of the already suppressed plasma renin activity. 3. It is concluded that in patients with mild and moderate hypertension and low or normal plasma renin activity, the hypotensive effect of propranolol cannot be attributed to suppression of renin activity. These conclusions do not necessarily apply to high-renin hypertensive patients.
Plasma renin activity
Essential hypertension
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Coronary artery occlusion
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