Prostacyclin synthesis in relation to sympathoadrenal activation. Effects of beta-blockade.
Results from several studies suggest that beta-adrenoceptor blockade causes increased biosynthesis of the vasodilator prostanoid prostacyclin in the arterial wall. This effect may contribute to the clinical effects of beta-blockers in hypertension and coronary heart disease. Studies in hypertensive patients and in animals indicate that the arterial pressure reduction after beta-blockade is related to the associated increase of prostacyclin biosynthesis, regarding both magnitude and time of onset of effect. Some observations suggest that the effects of beta-blockers in myocardial ischemia may in part be due to an improvement of coronary blood flow caused by increased prostacyclin biosynthesis.
Department of Cardiovascular Pharmacology, Astra Hässle AB, Mölndal, Sweden.
K
K
Pettersson
G
G
Hansson
J A
JA
Björkman
B
B
Ablad
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D011464:Epoprostenol / Q000096:biosynthesis*; D006801:Humans; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000502:physiology
D000319:Adrenergic beta-Antagonists; D000959:Antihypertensive Agents; D011464:Epoprostenol