Aspects of inhibition of myometrial hyperactivity in primary dysmenorrhea.
Uterine hypercontractility is considered to be an important factor in primary dysmenorrhea. A survey is given on possible mechanisms controlling the cytoplasmic concentration of free calcium and thereby contractile activity in the myometrial smooth muscle cell. Probably acting by different modes of action, inhibitors of prostaglandin synthesis, calcium antagonists and beta 2 stimulators have all been shown to reduce myometrial activity and relieve dysmenorrheic pain. The possibility of achieving further uterine relaxation after initial treatment with prostaglandin inhibitors by adding a calcium antagonist such as nifedipine is discussed. It is also suggested that when utilizing a reliable pressure recording technique in the evaluation of dysmenorrheic patients, the pronounced myometrial relaxation obtained by such combined therapy may be of diagnostic value.
D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D016861:Cyclooxygenase Inhibitors; D004412:Dysmenorrhea / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007473:Ion Channels / Q000502:physiology; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000503:physiopathology; D009215:Myometrium / Q000503:physiopathology*; D009543:Nifedipine / Q000494:pharmacology; D014599:Uterus / Q000187:drug effects / Q000503:physiopathology*
D000318:Adrenergic beta-Agonists; D002121:Calcium Channel Blockers; D016861:Cyclooxygenase Inhibitors; D007473:Ion Channels; D009543:Nifedipine; D002118:Calcium