Task-dependence of Jaw Elevator and Depressor Co-activation

Elevator muscle activity per unit bite-force has been shown to be higher in chewing than in isometric biting. We tested the hypothesis that surplus elevator activity is evoked in response to a possible co-activation of jaw-opener muscles during the masticatory power stroke. In 32 subjects, digastric and bilateral masseter and temporalis activities were recorded during unilateral chewing of test foods, isometric biting on a force transducer, and during balancing of the jaw against maximum effort of depressor muscles. During elevator peak effort in chewing, the digastric activity was 113% higher than during peak effort in isometric biting. Comparison of balancing and chewing trials revealed that a 6% increase of elevator activity would suffice to compensate for this increased depressor action. Elevator activity in chewing, however, was up to 130% higher than in clenching. We conclude that depressor counteraction could have only a minor influence on the generation of surplus muscle activity in chewing.

Pharmacological profile of depressor response elicited by sarthran in rat ventrolateral medulla

Injection of sarthran, an angiotensin receptor antagonist, bilaterally into the rostral ventrolateral medulla (RVLM) of α-chloralose-anesthetized rats decreases arterial pressure (AP) to the same extent as total autonomic blockade. This response is not reproduced by selective AT1antagonists. To examine the pharmacological profile of the response elicited by [Sar1, Thr8]ANG II (sarthran), the ability of angiotensin analogs to inhibit the effect of sarthran injected into the RVLM was tested. Coinjection of angiotensin II (ANG II) prevented the sarthran-evoked decrease in AP, but this action of ANG II was markedly attenuated by pretreatment of the RVLM with the aminopeptidase inhibitor amastatin. Coinjection of ANG(3–8) or a selective agonist of AT4receptors prevented the effect of sarthran injected into the RVLM. ANG(1–7) was also able to prevent the effect of sarthran. None of the angiotensin fragments tested substantially altered blood pressure when injected alone into the RVLM. These results suggest that the depressor action of sarthran injected into the RVLM is not dependent on ANG II receptors, though the nature of the site or sites of action of sarthran within the RVLM remains uncertain.