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PubMed2005

Muscle contractions, AICAR, and insulin cause phosphorylation of an AMPK-related kinase.

We hypothesized that AMP-activated protein kinase-related kinase 5 (ARK5)/novel kinase family 1 (NUAK1), an AMP-activated protein kinase (AMPK)-related kinase that has been found to be stimulated by protein kinase B (Akt), would be expressed in rat skeletal muscle and activated by electrically elicited contractions, 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR), or insulin. We verified expression of ARK5 in muscle through RT-PCR and Western blot. Cross-reactivity of ARK5 immunoprecipitates with antibodies against phospho-AMPK was increased by approximately 30% by muscle contractions and approximately 60% by incubation of muscle with AICAR. AMPK was not detected in the ARK5 immunoprecipitates. Despite the apparent increase in phosphorylation of ARK5 at a site essential to its activation, neither contractions nor AICAR increased ARK5 activity. For muscles from animals injected with saline or insulin, we probed nonimmunoprecipitated samples in sequence for phosphotyrosine (P-Tyr), ARK5, and phosphorylated substrates of Akt (P-AS) and found that the ARK5 band could be precisely superimposed on phosphoprotein bands from the P-Tyr and P-AS blots. In the band corresponding to ARK5, insulin increased P-Tyr content by approximately 45% and cross-reactivity with the antibody against P-AS by approximately threefold. We also detected ARK5 in phosphotyrosine immunoprecipitates. Our data suggest that increased phosphorylation of ARK5 by muscle contractions or exposure to AICAR is insufficient to activate ARK5 in skeletal muscle, suggesting that some other modification (e.g., phosphorylation on tyrosine or by Akt) may be necessary to its activity in muscle.

Amino Acid Sequence↗
PubMed1993

Effect of upper airway muscle contraction on supraglottic resistance and stability.

The activation of upper airway (UAW) muscles is believed to increase UAW patency to air flow. To evaluate the mechanisms by which UAW muscles act to prevent UAW collapse, pressure-flow relationships of the isolated UAW as well as the negative pressure required to cause UAW collapse (Pcrit) were assessed before and during electrical stimulation of four UAW muscle pairs in anesthetized dogs. Stimulation of each of the muscles shifted the pressure-flow curve toward lower pressures for any given flow rate, indicating UAW dilatation. UAW resistance decreased from 7.9 +/- 0.6 to 0.4 +/- 0.1, 2.7 +/- 0.6, 2.3 +/- 0.8 and to 4.8 +/- 1.5 cmH2O.L-1.sec during genioglossus, geniohyoid, sternothyroid and sternohyoid stimulation respectively (P < 0.01 in all cases). However, only genioglossus stimulation significantly increased Pcrit (from -3.4 +/- 0.6 to -12.0 +/- 1.8 cmH2O, P < 0.001). Relaxation of the genioglossus thus appears to produce the main impediment to air flow through the UAW, and contraction of this muscle improves UAW patency both by dilating the supraglottic airway and by stiffening its walls.

Airway Resistance↗
PubMed2007

Possible CaMKK-dependent regulation of AMPK phosphorylation and glucose uptake at the onset of mild tetanic skeletal muscle contraction.

The Ca(2+)/calmodulin (CaM) competitive inhibitor KN-93 has previously been used to evaluate 5'-AMP-activated protein kinase (AMPK)-independent Ca(2+)-signaling to contraction-stimulated glucose uptake in muscle during intense electrical stimulation ex vivo. With the use of low-intensity tetanic contraction of mouse soleus and extensor digitorum longus (EDL) muscles ex vivo, this study demonstrates that KN-93 can potently inhibit AMPK phosphorylation and activity after 2 min but not 10 min of contraction while strongly inhibiting contraction-stimulated 2-deoxyglucose uptake at both the 2- and 10-min time points. These data suggest inhibition of Ca(2+)/CaM-dependent signaling events upstream of AMPK, the most likely candidate being the novel AMPK kinase CaM-dependent protein kinase kinase (CaMKK). CaMKK protein expression was detected in mouse skeletal muscle. Similar to KN-93, the CaMKK inhibitor STO-609 strongly reduced AMPK phosphorylation and activity at 2 min and less potently at 10 min. Pretreatment with STO-609 inhibited contraction-stimulated glucose uptake at 2 min in soleus, but not EDL, and in both muscles after 10 min. Neither KN-93 nor STO-609 inhibited 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside-stimulated glucose uptake, AMPK phosphorylation, or recombinant LKB1 activity, suggestive of an LKB1-independent effect. Finally, neither KN-93 nor STO-609 had effects on the reductions in glucose uptake seen in mice overexpressing a kinase-dead AMPK construct, indicating that the effects of KN-93 and STO-609 on glucose uptake require inhibition of AMPK activity. We propose that CaMKKs act in mouse skeletal muscle regulating AMPK phosphorylation and glucose uptake at the onset of mild tetanic contraction and that an intensity- and/or time-dependent switch occurs in the relative importance of AMPKKs during contraction.

AMP-Activated Protein Kinase Kinases↗
PubMed2004

17beta-Oestradiol enhances aortic endothelium function and smooth muscle contraction in male spontaneously hypertensive rats.

17beta-Oestradiol (E(2); oestrogen) is known to increase endothelium-dependent vasodilatation and NO (nitric oxide) production. It is also known to decrease the response of VSMCs (vascular smooth muscle cells) to vasoconstrictors in vitro. E(2) induces a decrease in age-related BP (blood pressure) development in MSHR (male spontaneously hypertensive rats). Whether this decrease is due to an effect on the endothelium or smooth muscle is unknown. To determine this effect, we examined the role of E(2) on vascular endothelium and smooth muscle separately. We treated MSHR with E(2) (2 mg x kg(-1) of body weight x week(-1)) for 5-7 weeks and then examined the vasoconstrictor response in the intact and denuded rings (with or without endothelium respectively). SBP (systolic BP) was measured weekly. Aortic cGMP and cAMP contents, aortic vasoconstrictor response, endothelium suppression of the vasoconstrictor response and basal NO release from aortic rings were all measured at the end of the study. We found that the age-related development of SBP in MSHR was decreased in E(2)-treated rats. The vascular response of denuded rings to a vasoconstrictor (phenylephrine and KCl) was increased in E(2)-treated rats; however, this phenomenon was masked in intact rings. The enhanced endothelial function appears to override the E(2)-increased smooth muscle vasoconstrictor response. Endothelium suppression, NO release and aortic cGMP content were all significantly higher in E(2)-treated rats than in controls. Thus our results suggest that E(2) improves endothelium function; furthermore, the accompanied NO/cGMP increase and the endothelium suppression may be associated with an E(2)-induced BP-lowering effect in MSHR.

Aging↗
PubMed1978

The influence of middle-ear muscle contraction on auditory threshold for selected pure tones.

The influence of middle-ear muscle (MEM) contraction on auditory threshold has been measured for pure tones of 0.25, 0.5, and 1.5 kHz. The reflex-activating signal was a 3-kHz pure tone. Signal paradigms were chosen to reduce or eliminate the effects of binaural loudness summation, contralateral direct masking, and contralateral remote and backward masking effects, and to maximize the influence of MEM contraction. Results indicate that under no condition was behavioral threshold affected by the MEM contraction induced using a pure-tone stimulus of 3 kHz, 105 dB SPL.

Adult↗