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At least 703 records · Page 39Linked to original sources

PubMed2000

Phosphorylation of caldesmon by p21-activated kinase. Implications for the Ca(2+) sensitivity of smooth muscle contraction.

We have previously shown that p21-activated kinase, PAK, induces Ca(2+)-independent contraction of Triton-skinned smooth muscle with concomitant increase in phosphorylation of caldesmon and desmin but not myosin-regulatory light chain (Van Eyk, J. E., Arrell, D. K., Foster, D. B., Strauss, J. D., Heinonen, T. Y., Furmaniak-Kazmierczak, E., Cote, G. P., and Mak, A. S. (1998) J. Biol. Chem. 273, 23433-23439). In this study, we provide biochemical evidence implicating a role for PAK in Ca(2+)-independent contraction of smooth muscle via phosphorylation of caldesmon. Mass spectroscopy data show that stoichiometric phosphorylation occurs at Ser(657) and Ser(687) abutting the calmodulin-binding sites A and B of chicken gizzard caldesmon, respectively. Phosphorylation of Ser(657) and Ser(687) has an important functional impact on caldesmon. PAK-phosphorylation reduces binding of caldesmon to calmodulin by about 10-fold whereas binding of calmodulin to caldesmon partially inhibits PAK phosphorylation. Phosphorylated caldesmon displays a modest reduction in affinity for actin-tropomyosin but is significantly less effective in inhibiting actin-activated S1 ATPase activity in the presence of tropomyosin. We conclude that PAK-phosphorylation of caldesmon at the calmodulin-binding sites modulates caldesmon inhibition of actin-myosin ATPase activity and may, in concert with the actions of Rho-kinase, contribute to the regulation of Ca(2+) sensitivity of smooth muscle contraction.

Actins↗

PubMed1995

Crossbridge dynamics in muscle contraction.

The study deals with the description of muscle contraction based on biochemical studies and describes four major approaches for coupling calcium kinetics with crossbridge (Xb) cycling. The analysis illuminates two controversial points: 1) the relationship between Xb attachment/detachment and Xb cycling, i.e., the transition between weak to strong conformations, and 2) the effect of calcium on Xb function: does it regulate Xb kinetics or Xb recruitment.

Animals↗

PubMed2003

Transabdominal ultrasound measurement of pelvic floor muscle activity when activated directly or via a transversus abdominis muscle contraction.

AIMS: The purpose of the present study was to compare the effectiveness of instruction to contract the pelvic floor muscles (PFM), the transversus abdominis (TrA), and the TrA + PFM visualized as displacement of the pelvic floor by ultrasound. MATERIALS AND METHODS: Twenty female physical therapists, mean age 41.1 years (range 26-56) participated in the study. A 3.5 MHz 35 mm curved linear array ultrasound transducer (Dornier Medtech) was placed in the mid-sagittal plane immediately suprapubically, angled at 15-30 degrees from the vertical depending on subcutaneous fat and anatomical variations, to image the pelvic floor. Six trials of three maneuvers in random order were performed: contraction of PFM, TrA, and TrA + PFM. RESULTS: In spite of correct contractions assessed by palpation and clinical observation, one subject demonstrated a downward movement of the pelvic floor during PFM contraction on ultrasound. Six subjects (30%) showed a downward movement during a TrA- contraction, and two during the combined TrA + PFM contraction. Instruction to contract PFM produced significantly greater mean displacement: 11.2 mm (95% CI 7.2-15.3) than TrA 4.3 mm (95% CI -0.2-8.8), P < 0.01, and combination: 8.5 mm (95% CI 5.2-12), P = 0.04. Hence, instruction of PFM contraction produced a 61.6% greater displacement of the pelvic floor in the correct direction than a TrA contraction. CONCLUSIONS: It is concluded that ultrasound is a more valid method than palpation and clinical observation to assess PFM function, and that instruction to contract the PFM produces a significantly more effective pelvic floor muscle contraction than instruction to perform a TrA contraction.

Abdomen↗

PubMed2002

Endothelin-1--induced enhancement of coronary smooth muscle contraction via MAPK-dependent and MAPK-independent [Ca(2+)](i) sensitization pathways.

Endothelin-1 (ET-1) has been implicated in coronary vasospasm by enhancing coronary vasoconstriction to vasoactive eicosanoids, and a role for protein kinase C (PKC) activation has been suggested. However, the cellular mechanisms downstream from PKC activation are unclear. We investigated whether physiological concentrations of ET-1 enhance coronary smooth muscle contraction by activating a PKC-mediated signaling pathway involving tyrosine phosphorylation and activation of mitogen-activated protein kinase (MAPK). Cell contraction was measured in smooth muscle cells isolated from porcine coronary artery, [Ca(2+)](i) was measured in fura-2 loaded cells, and tissue fractions were examined for reactivity with anti-phosphotyrosine (P-Tyr) and anti-MAPK antibodies using immunoprecipitation and immunoblot analysis. In Hanks' solution (1 mmol/L Ca(2+)), ET-1 (10 pmol/L) did not increase basal [Ca(2+)](i) (81 +/- 2 nmol/L) but caused cell contraction (10%) that was inhibited by calphostin C (10(-6) mol/L), inhibitor of PKC, tyrphostin (10(-6) mol/L), inhibitor of tyrosine kinase, and PD098059 (10(-6) mol/L), inhibitor of MAPK kinase. The vasoactive eicosanoid prostaglandin F(2alpha) (PGF(2alpha); 10(-7) mol/L) caused increases in cell contraction (11%) and [Ca(2+)](i) (122 +/- 9 nmol/L) that were inhibited by the Ca(2+) channel blocker verapamil (10(-6) mol/L) but not by calphostin C, tyrphostin, or PD098059. Pretreatment with ET-1 for 10 minutes enhanced cell contraction to PGF(2alpha) (33%) with no additional increase in [Ca(2+)](i) (124 +/- 10 nmol/L). Activation of PKC by phorbol 12-myristate 13-acetate (PMA; 10(-7) mol/L) caused cell contraction and enhanced PGF(2alpha) contraction (32%) with no additional increase in [Ca(2+)](i) (126 +/- 9 nmol/L). The ET-1-- and PMA-induced enhancement of PGF(2alpha) contraction was abolished by verapamil or calphostin C but not by tyrphostin or PD098059. ET-1 and PMA caused significant increases in tyrosine phosphorylation of MAPK that were inhibited by calphostin C, tyrphostin, and PD098059. PGF(2alpha) did not cause any additional increases in tyrosine phosphorylation of MAPK in tissues untreated or pretreated with ET-1 or PMA. Thus, physiological concentrations of ET-1 activate a Ca(2+)-independent PKC-mediated signaling pathway that involves tyrosine phosphorylation and activation of MAPK. The enhancement of PGF(2alpha)-induced coronary smooth muscle contraction by ET-1 involves additional activation of a Ca(2+)-sensitive PKC-mediated pathway but not tyrosine phosphorylation or activation of MAPK. The MAPK-dependent and MAPK-independent signaling pathways represent possible cellular mechanisms by which ET-1 could enhance coronary vasoconstriction to vasoactive eicosanoids in coronary vasospasm.

Animals↗

PubMed1994

Needle EMG registration of striated urethral wall and pelvic floor muscle activity patterns during cough, Valsalva, abdominal, hip adductor, and gluteal muscle contractions in nulliparous healthy females.

The aim of the present study was to describe co-activity patterns of the striated urethral wall muscle and the pelvic floor muscles (PFM) during contraction of outer pelvic muscles. Six healthy nulliparous physical education students, mean age 19.5 years (19-21) participated in the study. Concentric needle EMG and a Dantec amplifier were used for registrations. EMG activity was continuously recorded with the participants lying in a supine position. EMG was recorded during relaxation, contraction of the PFM, valsalva maneuver, coughing, hip adductor contraction, gluteal muscle contraction, backward tilting of the pelvis, and sit-ups. The procedure was performed with the needle in the striated muscle of the anterior wall of the urethra and then repeated with the needle set lateral to the urethra in the PFM. The results showed that the striated urethral wall muscle was contracted synergistically during PFM, hip adductor, and gluteal muscle contraction, but not during abdominal contraction. Both hip adduction, gluteal muscle, and abdominal muscle contraction gave synergistic contraction of the PFM. Thus the urethral wall striated muscle and the PFM react differently during abdominal contraction.

Adult↗

PubMed1993

A new perspective on muscle contraction.

Recent experimental findings suggest that the myosin cross-bridge theory may no longer be adequate to account for certain basic facts concerning muscle contraction. A newly-proposed mechanism based on length changes in actin filaments might be the basis for a simpler explanation for how the free energy of ATP hydrolysis can be transduced into work by muscle fibers.

Actins↗

PubMed1998

Rostral ventrolateral medullary opioid receptor activation modulates pressor response to muscle contraction.

The effects of an opioid agonist, [D-Ala2]methionine enkephalinamide (DAME), administered into the rostral ventrolateral medulla (rVLM) or caudal ventrolateral medulla (cVLM) on cardiovascular responses to isometric muscle contraction were determined in anesthetized rats. A 30-s contraction evoked by tibial nerve stimulation increased mean arterial pressure (MAP) and heart rate (HR) by 34 +/- 6 mmHg and 40 +/- 7 beats/min, respectively, with a developed tension of 322 +/- 30 g, after bilateral insertion of microdialysis probes into the rVLM. Thirty-minute dialysis of DAME (10 and 100 microM) attenuated the contraction-evoked cardiovascular changes dose dependently (10 microM: MAP = 25 +/- 4 mmHg, HR = 27 +/- 3 beats/min, tension = 333 +/- 25 g; 100 microM: MAP = 14 +/- 4 mmHg, HR = 16 +/- 5 beats/min, tension = 330 +/- 34 g). Preadministration of an opioid antagonist, naloxone (100 microM), augmented contraction-evoked MAP and HR responses and blocked effects of 100 microM DAME. Microdialysis of DAME into the cVLM produced no changes in the pressor response to contraction. At end of each experiment, tibial nerve stimulation after neuromuscular blockade evoked no MAP or HR change. Results demonstrate that opioid receptor activation within the rVLM modulates cardiovascular responses to isometric muscle contraction.

Animals↗

PubMed1991

In situ NADH laser fluorimetry during muscle contraction in humans.

The aim of the present study was to use nicotinamide adenine dinucleotide phosphate, reduced (NADH) fluorimetry, to investigate in situ NADH changes during muscle contraction in humans on an isokinetic dynamometer. Thirteen healthy male subjects each performed one maximal voluntary contraction (MVC) with the knee extensor muscle. The NADH muscle fluorescence was monitored by a double beam laser fluorimeter which uses an optical fibre, percutaneously inserted through a needle into the vastus lateral muscle, to guide the light. The NADH fluorescence was continuously measured at a wavelength of 337 nm. To estimate the haemodynamic artefact, blood backscattering was simultaneously determined at a wavelength of 586 nm. The fluorescence signal was recorded before, during and after contractions at 50% of MVC. The fibre was kept out of contact with the muscle during contractions at 100% of MVC and was only put into contact with it at the end of the contraction. At the onset of contractions at 50% of MVC, NADH fluorescence increased rapidly for 3 s and remained stable thereafter until exhaustion. After a muscle measurement had been made, the optical fibre was put successively into solutions of increasing NADH concentration to ascertain the relationship between the muscle fluorescence signal and the muscle NADH level. This procedure yielded estimated mean values for muscle NADH of 0.172 mmol.kg-1, SEM 0.028 and of 0.184 mmol.kg-1, SEM 0.027 after contractions at 50% and 100% of MVC, respectively, from a resting value of 0.087 mmol.kg-1, SEM 0.015. These results indicated that in situ laser fluorimetry could be used to evaluate NADH changes in humans during muscle contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2000

Altered regulation of cardiac muscle contraction by troponin T mutations that cause familial hypertrophic cardiomyopathy.

To study the effect of troponin (Tn) T mutations that cause familial hypertrophic cardiomyopathy (FHC) on cardiac muscle contraction, wild-type, and the following recombinant human cardiac TnT mutants were cloned and expressed: I79N, R92Q, F110I, E163K, R278C, and intron 16(G(1) --> A) (In16). These TnT FHC mutants were reconstituted into skinned cardiac muscle preparations and characterized for their effect on maximal steady state force activation, inhibition, and the Ca(2+) sensitivity of force development. Troponin complexes containing these mutants were tested for their ability to regulate actin-tropomyosin(Tm)-activated myosin-ATPase activity. TnT(R278C) and TnT(F110I) reconstituted preparations demonstrated dramatically increased Ca(2+) sensitivity of force development, while those with TnT(R92Q) and TnT(I79N) showed a moderate increase. The deletion mutant, TnT(In16), significantly decreased both the activation and the inhibition of force, and substantially decreased the activation and the inhibition of actin-Tm-activated myosin-ATPase activity. ATPase activation was also impaired by TnT(F110I), while its inhibition was reduced by TnT(R278C). The TnT(E163K) mutation had the smallest effect on the Ca(2+) sensitivity of force; however, it produced an elevated activation of the ATPase activity in reconstituted thin filaments. These observed changes in the Ca(2+) regulation of force development caused by these mutations would likely cause altered contractility and contribute to the development of FHC.

Amino Acid Sequence↗

PubMed1999

Is there a conflict between minimizing effort and energy expenditure with increasing velocities of muscle contraction in humans?

1. The present study examined the possibility that minimizing effort conflicts with minimizing energy expenditure at different velocities of muscle contraction during cycling. 2. Six normal subjects underwent incremental exercise on an electrically stabilized cycle ergometer. Power output increased by 45 W every 3 min to exhaustion at pedalling frequencies of 40, 60, 80 and 100 r.p.m. on separate days. Energy expenditure (oxygen uptake), leg effort and dyspnoea (Borg 0-10 scale) were measured in parallel at the end of each minute. 3. All six subjects completed 10 min of exercise achieving 180 W for all four pedalling frequencies. Two-way analysis of variance indicated that oxygen uptake (P < 0.0001), leg effort (P < 0.0001) and dyspnoea (P < 0.0001) increased with duration of exercise and power output; oxygen uptake (P < 0.0001) and leg effort (P < 0.05) were significantly different between pedalling frequencies; the interactions were not significant. Oxygen uptake was minimal at 60 r.p.m., and increased at both higher and lower pedalling frequencies. Both leg effort and dyspnoea were minimal at 80 r.p.m.; leg effort intensified at higher and lower pedalling frequencies; and dyspnoea was most intense at 100 r.p.m. 4. There was a conflict between minimization of energy expenditure and leg effort at power outputs less than 180 W. Minimizing effort occurred at the expense of an increase in energy expenditure.

Adult↗

PubMed1972

On the inhibition of muscle contraction caused by exposure to hypertonic solutions.

The evidence supporting a site of inhibition of excitation contraction (E-C) coupling near the plasma membrane (the "glycerol effect," the K(+)-potentiating effect) for muscle in hypertonic solution was reinvestigated. It was found, using whole frog sartorii, that there was a rehydration of muscle soaked in glycerol Ringer after 30 min and a large swelling (to 140% after 1 hr soaking) upon return of the muscle to normal Ringer, suggesting that significant amounts of glycerol enter the fibers during this time. While contrary to the original report of the glycerol effect, this finding was consistent with other studies involving the use of single fibers. Also reexamined was the potentiating effect of K(+) on the hypertonic inhibition of muscle contraction. It was found that muscles exposed to this KCl pretreatment swell so that they are less dehydrated in hypertonic solutions, thus accounting for the observed potentiation. After being treated instead with a K(2)-tartrate Ringer solution, muscles did not swell and, as determined with twitch recordings, did not display any potentiation in hypertonic solutions-even though the [K(+)] was higher than an osmotically equivalent KCl solution. The evidence was thus consistent with alternative hypotheses in which inhibition of contraction occurs at a later stage in E-C coupling or involves the contractile process itself.

Animals↗

PubMed2003

Tuning smooth muscle contraction by molecular motors.

As in striated muscle, smooth muscle cells (SMC) contract by Ca2+ activated cyclic interaction between actin and type II myosin. However, smooth muscle maintains tone at basal activating Ca2+ and low energetic cost during sustained activation. This review analyzes the regulation of phasic and tonic contraction of SMC on the molecular level. Type II myosin is the molecular motor also of smooth muscle contraction. Six myosin heavy chain (MHC) isoenzymes (four smooth muscle, two nonmuscle) and five myosin light chain (MLC) isoforms (two 17 kDa, two 20 kDa, one 23 kDa) are expressed in SMC. These myosin subunits could be generated by alternative splicing or by differential gene expression. Thus different myosin isoenzymes are generated which may be modified posttranslationally by phosphorylation, affecting the contractile state of the SMC. Furthermore, they may be part of distinct contractile systems which are targeted by different second messenger cascades and are recruited differentially during activation, electromechanical, and pharmacomechanical coupling. Low energy consumption, shortening velocity, and MLC20 phosphorylation at low Ca2+ activation levels during tone maintenance ("latch") could be explained by a switch from smooth muscle myosin to nonmuscle myosin activation upon prolonged activation.

Alternative Splicing↗

PubMed1988

Membrane currents that govern smooth muscle contraction in a ctenophore.

Ctenophores are transparent marine organisms that swim by means of beating cilia; they are the simplest animals with individual muscle fibres. Predatory species, such as Beroe ovata, have particularly well-developed muscles and are capable of an elaborate feeding response. When Beroe contacts its prey, the mouth opens, the body shortens, the pharynx expands, the prey is engulfed and the lips then close tightly. How this sequence, which lasts 1 s, is accomplished is unclear. The muscles concerned are structurally uniform and are innervated at each end by a neuronal nerve net with no centre for coordination. Isolated muscle cells studied under voltage-clamp provide a solution to this puzzle. We find that different groups of muscle cells have different time-dependent membrane currents. Because muscle contraction depends upon calcium entry during each action potential, these different currents produce different patterns of contraction. We conclude that in a simple animal such as a ctenophore, a sophisticated set of membrane conductances can compensate for the absence of an elaborate system of effectors.

4-Aminopyridine↗

PubMed1988

Effect of removal of epithelium on antigen-induced smooth muscle contraction and mediator release from guinea pig isolated trachea.

We examined the effect of removal of the epithelium on antigen-induced smooth muscle contraction and the release of mediators of inflammation from superfused, sensitized guinea-pig tracheal spirals in vitro. The epithelium was stripped from one-half of each trachea by mechanical means, and immunologic responses were evaluated by paired analysis. Removing the epithelium potentiated antigen-induced contraction, as reflected by a 5-fold leftward shift in the antigen dose-response curve, but the maximum response to antigen was not altered. This potentiation was not inhibited by pretreating the tissues with indomethacin (5 X 10(-6) M). At maximum concentrations of antigen removing the epithelium had no effect on the magnitude or kinetics of release of immunoreactive sulfidopeptide leukotrienes, prostaglandin (PG) D2, PGF2 alpha or thromboxane B2. Removing the epithelium did, however, significantly decrease the release of PGE and 6-keto-PGF1 alpha, a prostacyclin metabolite. Antigen-induced histamine release was enhanced by removing the epithelium; this effect varied inversely with antigen concentration. Selectively exposing either the luminal or serosal surface of an intact, superfused trachea to antigen resulted in the release of less than 5% of the total tissue histamine. Removing the epithelium from the intact trachea increased histamine release to approximately 25% following luminal but not serosal exposure to antigen. These studies demonstrate that the tracheal epithelium can act to inhibit antigen-induced airway contraction in vitro. This may in part reflect the role of the intact epithelium as a diffusion barrier which can limit the rate of influx of antigen molecules and thereby influence tissue mast cell activation.

Animals↗

PubMed2001

Endothelin-1 enhances eicosanoids-induced coronary smooth muscle contraction by activating specific protein kinase C isoforms.

Endothelin-1 (ET-1), a potent vasoconstrictor, has been implicated in the pathogenesis of coronary vasospasm by enhancing coronary vasoconstriction to vasoactive eicosanoids; however, the cellular mechanisms involved are unclear. We investigated whether physiological concentrations of ET-1 enhance coronary smooth muscle contraction to vasoactive eicosanoids by activating specific protein kinase C (PKC) isoforms. Cell contraction was measured in single smooth muscle cells isolated from porcine coronary arteries, intracellular free Ca(2+) ([Ca(2+)](i)) was measured in fura-2-loaded cells, and the cytosolic and particulate fractions were examined for PKC activity and reactivity with isoform-specific anti-PKC antibodies using Western blots. In Hanks' solution (1 mmol/L Ca(2+)), ET-1 (10 pmol/L) did not increase basal [Ca(2+)](i) (81+/-2 nmol/L), but it did cause cell contraction (9%) that was inhibited by GF109203X (10(-6) mol/L), an inhibitor of Ca(2+)-dependent and Ca(2+)-indpendent PKC isoforms. The vasoactive eicosanoid prostaglandin F(2alpha) (PGF(2alpha), 10(-7) mol/L) caused increases in cell contraction (11%) and [Ca(2+)](i) (108+/-7 nmol/L) that were inhibited by the Ca(2+) channel blocker diltiazem (10(-6) mol/L). Pretreatment with ET-1 (10 pmol/L) for 10 minutes enhanced cell contraction to PGF(2alpha) (35%) with no additional increase in [Ca(2+)](i) (112+/-8 nmol/L). Direct activation of PKC by phorbol 12,13-dibutyrate (PDBu, 10(-7) mol/L) caused cell contraction (10%) and enhanced PGF(2alpha) contraction (33%) with no additional increase in [Ca(2+)](i) (115+/-7 nmol/L). The ET-1-induced enhancement of PGF(2alpha) contraction was inhibited by Gö6976 (10(-6) mol/L), an inhibitor of Ca(2+)-dependent PKC isoforms. Both ET-1 and PDBu caused an increase in PKC activity in the particulate fraction and a decrease in the cytosolic fraction and increased the particulate/cytosolic PKC activity ratio. Western blots revealed the Ca(2+)-dependent alpha-PKC and the Ca(2+)-independent delta-, epsilon-, and zeta-PKC isoforms. In resting tissues, alpha- and epsilon-PKC were mainly cytosolic, delta-PKC was mainly in the particulate fraction, and zeta-PKC was equally distributed in the cytosolic and particulate fraction. ET-1 (10 pmol/L) alone or PDBu (10(-7) mol/L) alone caused translocation of epsilon-PKC from the cytosolic to the particulate fraction, localized delta-PKC more in the particulate fraction, but did not change the distribution of zeta-PKC. PGF(2alpha) (10(-7) mol/L) alone did not change PKC activity. In tissues pretreated with ET-1 or PDBu, PGF(2alpha) caused additional increases in alpha-PKC activity. Thus, the enhancement of PGF(2alpha)-induced coronary smooth muscle contraction by physiological concentrations of ET-1 involves activation and translocation of alpha-PKC in addition to delta- and epsilon-PKC isoforms, and this may represent one possible cellular mechanism by which ET-1 could enhance coronary vasoconstriction to vasoactive eicosanoids in coronary vasospasm.

Animals↗

PubMed1992

Neurally mediated renal vasoconstriction during isometric muscle contraction in cats.

The aim of this study was to determine if the reflex increase in renal sympathetic nerve activity (RSNA) during static (isometric) muscle contraction evokes renal vasoconstriction and decreases renal blood flow. RSNA, renal blood flow velocity, and arterial pressure were measured simultaneously during isometric contraction of the hindlimb triceps surae muscle in eight chloralose-anesthetized cats. A 1-min contraction was evoked by stimulating the peripheral ends of the cut L7 and S1 ventral roots. RSNA and mean arterial pressure (MAP) increased 41 +/- 14% (SE) and 50 +/- 10 mmHg during static contraction, whereas mean renal blood flow velocity (MRBV) decreased 14 +/- 5%. Calculated renal vascular resistance increased 73 +/- 20% during the contraction. The increase in RSNA preceded the decrease in MRBV by 20 s. Passive mechanical stretch of the muscle increased RSNA 21 +/- 12% but did not alter MRBV. Renal denervation abolished the decrease in MRBV during isometric contraction but only attenuated the rise in MAP. Cutting the L4-S1 dorsal roots or muscle paralysis abolished the MRBV and MAP responses. Thus reflex stimulation of RSNA from the contracting muscle can induce renal vasoconstriction and decrease renal blood flow.

Animals↗

PubMed1989

Cardiovascular sympathetic hypofunction in muscle contraction headache and migraine.

There have been some recent reports proposing that muscle contraction headache (MCH) and migraine are similar and may have a common etiology. It has been hypothesized that derangement of the autonomic nervous system (ANS) plays an important role in the pathogenesis of migraine. However, reports on the ANS function in MCH have rarely been submitted. Therefore, in this report, MCH patients were investigated as well as migraine patients. The cardiovascular reflex responses by orthostatic test, isometric work test and the pulse rate (R-R interval) variation in fifteen MCH patients and fifteen migraine patients were recorded during headache-free intervals. The plasma norepinephrine (NE) levels were also measured throughout the orthostatic tests. Fifteen healthy subjects served as the age-matched control group. In the MCH group and the migraine group, blood pressure immediately after going from the supine to the erect position decreased more significantly than in the control group. The basal NE level was significantly low in both the MCH group and the migraine group, in comparison with the control group. MCH patients as well as migraine patients showed cardiovascular sympathetic hypofunction.

Adult↗

PubMed2001

High levels of docosahexaenoic acid (22:6n-3)-containing phospholipids in high-frequency contraction muscles of hummingbirds and rattlesnakes.

Phospholipids containing docosahexaenoic acid (22:6n-3) have been proposed to be required as conformational cofactors for the functional assembly of membrane proteins such as rhodopsin, ion pumps and the various complexes of the mitochondrial electron transport chain (Infante, 1987, Mol. Cell. Biochem. 74, 111-116; Infante and Huszagh, 2000, FEBS Lett. 468, 1-5). This hypothesis predicts that high-frequency contraction muscles, which are endowed with a high content of sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) and mitochondrial respiration enzymes, would have higher concentrations of 22:6n-3-containing phospholipids when compared with other muscles in the same species known to have a much lower contraction frequency. We have analyzed the fatty acid composition of ruby-throated hummingbird (Archilochus colubris) pectoral and leg muscles and of rattlesnake (Crotalus atrox) shaker and ventral muscles. We have found that hummingbird pectoral muscles, which are high contraction frequency muscles with the highest known respiratory rate among vertebrates, have a 22:6n-3 concentration of 20.8% vs. 4.9% for the low frequency leg muscles. Similarly, rattler muscles in rattlesnakes, also high contraction frequency muscles, have a higher 22:6n-3 concentration than that of their ventral muscles (15.1% vs. 10.6%, respectively). These results are consistent with a specific molecular role for 22:6n-3-containing phospholipids, as proposed.

Animals↗