Effect of blood pressure on medial medulla-induced muscle atonia.
Stimulation of the medial medullary reticular formation (MMRF) has long been reported to produce generalized inhibition of skeletal muscle activity. However, several studies have reported that in most cases MMRF stimulation produces only increases in muscle tone. In the present investigation we have found that blood pressure is a critical variable, determining whether MMRF stimulation will produce muscle excitation or inhibition. When mean arterial pressure (MAP) was greater than 80 mmHg but less than 148 mmHg, MMRF stimulation produced muscle antonia. Reductions of blood pressure by pharmacological or mechanical techniques induced a reversal of response to MMRF stimulation; stimulation that produced inhibition in base-line conditions produced excitation after MAP reduction. MAP reductions of as little as 10% could cause the reversal response. In contrast, the EMG reduction to MMRF stimulation was not changed or was augmented when MAP was raised. MMRF induced atonia, and its reversal by blood pressure reduction persisted after bilateral isolation of the carotid sinus combined with vagotomy, and in the 6-hydroxydopamine-treated cat. Spinal transection at the cervicothoracic junction did not block atonia or the reversal response. It is suggested that the reversal is mediated centrally.
D000313:Adrenal Medulla / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure; D001933:Brain Stem / Q000502:physiology; D002339:Carotid Arteries / Q000294:innervation; D002415:Cats; D003655:Decerebrate State; D003714:Denervation; D004576:Electromyography; D005260:Female; D006892:Hydroxydopamines; D008297:Male; D009132:Muscles / Q000502:physiology*; D016627:Oxidopamine; D013116:Spinal Cord / Q000502:physiology; D014628:Vagotomy
D006892:Hydroxydopamines; D016627:Oxidopamine