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At least 1,117 records · Page 62Linked to original sources
PubMed1975

Mechanical and biochemical cycles in muscle contraction.

The current biochemical approach to understanding the mechanism by which chemical energy is converted into mechanical energy in muscle is by investigating the kinetics of the reaction of ATP with the isolated contractile proteins in solution with stopped and quenched flow techniques. The results are interpreted in terms of a cycle of hydrolysis of ATP. The current mechanical approach lies through the kinetics of force production or length change in preparations with the contractile proteins intact, by following step changes in length or tension. The results are usually interpreted in terms of mechanical cycles of activity of cross-bridges, in which a cross-bridge progresses through a series of states with different mechanical properties. If the biochemist's and the mechanist's cycles are one and the same, a problem arises over the correspondence between states in the two cycles. One approach to answering this question is through the determination of the effect of pH and of such substances as ATP, ADP and inorganic orthophosphate on the mechanical response. We hope that these will act at known points in the biochemist's cycle and their influence upon the mechanical cycle should enable their location here to be ascertained. The paper deals with the effects of phosphate, ATP and magnesium ions on the mechanical response of insect flight muscle.

Actins↗
PubMed1979

Activation of AMP aminohydrolase during skeletal-muscle contraction.

AMP aminohydrolase activity is enhanced by 60% after 5 s tetanic stimulation of phosphorylase kinase-deficient mouse muscle and after 60 s tetanus in normal mice. During the recovery from tetanus the activity in the contralateral leg is similarly enhanced. The activation is stable to 1000-fold dilution and has a half-life of approx. 1 h.

AMP Deaminase↗
PubMed1997

Laryngeal reflex apnea is blunted during and after hindlimb muscle contraction in sheep.

This study was carried out on seven chloralose-anesthetized sheep and was designed to investigate the role of muscular afferent fiber stimulation on the duration of reflex apnea triggered by laryngeal stimulation (LS). In six animals, injection of distilled water onto the laryngeal mucosa provoked a 15.7 +/- 1.0 s (mean +/- SE) apnea associated with a rise in systemic blood pressure (+7 +/- 0.8 Torr). Electrically induced contractions (EIC) of the hindlimb muscles doubled the metabolic rate and ventilation and reduced the duration of the apnea produced by LS to 7.4 +/- 1.0 s (P < 0.01). Apnea duration was still reduced during the first minute after the cessation of EIC (7.2 +/- 1.1 s, P < 0.01) but returned to control after a 5-min recovery period (16.7 +/- 1.6 s). The apnea triggered by LS was also reduced during EIC when the venous return was impeded by occluding the inferior vena cava (5.2 +/- 1.1 s, P < 0.01), despite a profound hypocapnia (20.7 +/- 0.3 Torr). The duration of apnea was not significantly affected (14.2 +/- 1.4 s) by breathing a 6% CO2-14% O2 in N2 gas mixture that roughly mimicked the alveolar gas composition when the apnea turned off. These results suggest that chemical drive has a negligible role in the fast reinitiation of breathing after LS during muscular stimulation. Stimulation of muscle afferent fibers does, however, appear to be a potent source of ventilatory reflexes capable of counteracting the inhibition of breathing resulting from laryngeal stimulation. Conversely, it is postulated that any reduction in somatic afferent traffic during this type of reflex apnea, including that resulting from the LS-induced systemic vasoconstriction, may delay the termination of apnea.

Animals↗
PubMed2001

Thermodynamic features of myosin filament suspensions: implications for the modeling of muscle contraction.

The analysis of myosin filament suspensions shows that these solutions are characterized by highly nonideal behavior. From these data a model is constructed that allows us to predict that 1) when subjected to an increasing protein osmotic pressure, myosin filaments experience an elastic deformation, which is not linearly related to the acting force; and 2) at constant protein osmotic pressure, when the cross-bridges of the myosin filaments are subjected to an external, nonosmotic force parallel to the filament axis, they are deformed and the water activity coefficient is altered. As a consequence, in muscle, passive and active shortening of the sarcomere is expected to promote the change of the water-water and of the water-protein interactions. We thus propose to depict muscle contraction as a chemo-osmoelastic transduction, where the analysis of the energy partition during the power stroke requires consideration of the osmotic factor in addition to the chemoelastic ones.

Animals↗
PubMed1997

Immunocytochemical localization of the alpha-1B adrenergic receptor and the contribution of this and the other subtypes to vascular smooth muscle contraction: analysis with selective ligands and antisense oligonucleotides.

The contribution of the alpha-1B adrenergic receptor (AR) to vascular smooth muscle contraction has been assessed using a combination of immunological, molecular biological and pharmacological approaches. A subtype-selective antibody detected alpha-1B immunoreactivity in the medial layer of the aorta, caudal, femoral, iliac, mesenteric resistance, renal and superior mesenteric arteries. Receptor protection assays and antisense oligonucleotides were used to assess the contribution of the alpha-1B AR to contraction. The alpha-1B AR was implicated in mediating the phenylephrine-induced contraction of the mesenteric resistance artery. The alpha-1D AR was implicated in mediating the contraction of the aorta, femoral, iliac and superior mesenteric arteries. Similarly, the alpha-1A AR was implicated in mediating contraction of the caudal and renal arteries. In vivo application of antisense oligonucleotides targeted to the translational start site of the alpha-1B AR had no effect on the phenylephrine-induced contraction of the femoral or renal arteries. In contrast, antisense oligonucleotides directed against the alpha-1D AR significantly inhibited the phenylephrine response in the femoral artery but had no effect on the renal artery. Application of alpha-1A AR antisense oligonucleotides inhibited the contraction of the renal artery without effect on the femoral artery. These data show that (1) alpha-1B AR immunoreactivity is widely distributed in the same peripheral arteries in which previous studies detected its mRNA, and (2) despite this distribution, receptor protection and antisense oligonucleotide studies indicate that the alpha-1B AR mediates the contraction of only the mesenteric resistance artery.

Animals↗
PubMed1979

[Oral propagation of the circular muscle contraction induced by local distension of the isolated guinea pig ileum (author's transl)].

The local distension of the intestinal wall was carried out by inflating a thin rubber balloon which had been fixed in the lumen and the contractions of the circular muscle were recorded at the points of 5 mm (PO1) and 20 mm (PO2) oral to the fixed balloon. The contractions elicited by local distension was blocked by tetrodotoxin and atropine, or removing longitudinal muscle, with the myenteric plexus adhering to it, from the intestine at the distending region. When 2 to 3 mm length of longitudinal muscle was stripped off around the intestine between PO1 and PO2, the contraction initiated at PO1 never reached to PO2. That is, the oral contraction did not propagate beyond the myenteric plexus-free region of the segment. When drugs were applied exclusively to the region around PO2, tetrodotoxin and hexamethonium, but not atropine, abolished the contraction at PO2, while the contraction at PO1 was clearly observed. It is likely that the contraction observed at the point of PO2 was evoked by non-cholinergic nervous mechanisms.

Animals↗
PubMed1993

Mechanism of rat uterine smooth muscle contraction induced by endothelin-1.

1. Endothelin (ET)-1 has been demonstrated to cause contraction of uterine smooth muscle. We investigated the role of ET receptor subtypes (ETA and ETB receptors) in ET-1-induced contraction of rat uterine smooth muscle by using the ETA receptor antagonist BQ-123 and the ETB receptor agonist BQ-3020. 2. ET-1 caused a contraction with superimposed oscillations of the rat isolated uterus suspended in Krebs-Ringer solution; both the amplitude of contraction as well as the oscillation frequency increased in a dose-dependent manner (10(-11)-10(-7)M). 3. BQ-123 (10(-6)M) markedly shifted the dose-response curve of ET-1 for both contractile effects and oscillation frequency to the right. 4. BQ-3020 (10(-11)-3 x 10(-7) M) did not cause uterine contraction; neither did it affect the dose-response curve of ET-1 for either the contractile effect or the increase in oscillation frequency. Thus, stimulation of ETB receptors is not involved in these responses. 5. The present findings suggest that ET-1-induced contractile responses and the increase in oscillation frequency in rat uterine smooth muscle is mediated through ETA receptors, and that ETB receptors play no role in these responses.

Amino Acid Sequence↗