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991.
The modulatory effect of myosin regulatory light chain phosphorylation in mammalian skeletal muscle, first documented as posttetanic potentiation of twitch tension, was subsequently shown to enhance the expression and development of tension at submaximal levels of activating calcium. Structural analyses demonstrated that thick filaments with phosphorylated myosin regulatory light chains appeared disordered: they lost the near-helical, periodic arrangement of myosin head characteristic of the relaxed state. We suggested that disordered heads may be more mobile than ordered heads and are likely to spend more time close to their binding sites on thin filaments. In this study we determined that the physiological effects of phosphorylation could be mimicked by decreasing the lattice spacing between the thick and the thin filaments, either by osmotic compression with dextran or by increasing the sarcomere length of permeabilized rabbit psoas fibers. Phosphorylation of regulatory light chains by incubation of permeabilized fibers with myosin light chain kinase and calmodulin, followed by low levels of activating calcium, potentiated tension development at resting or lower sarcomere lengths in the absence of dextran but had no additional effect on tension potentiation or development in fibers with decreased lattice spacing due to either osmotic compression or increased sarcomere length. 相似文献
992.
993.
The pathogenesis of cirrhotic cardiomyopathy remains unclear. Because ventricular contractility is dependent on the interplay of stimulatory beta-adrenergic and inhibitory muscarinic receptors, we aimed to examine a possible role of muscarinic M2 receptor overactivity in a rat model of cirrhotic cardiomyopathy. Cirrhosis was induced by bile duct ligation (BDL), while controls underwent sham operations. Contractile responses to the muscarinic agonist carbachol were measured in situ in the autonomic-denervated pithed rat and in vitro in isolated ventricular papillary muscles. Ventricular sarcolemmal plasma membranes were isolated by sucrose density gradients, and muscarinic receptor characteristics were studied using 1-[N-methyl-3H]scopolamine (NMS). Membrane adenylyl cyclase activity was tested by a protein binding assay. Maximum first time derivative of peak ventricular systolic pressure (+dP/dt) for sham-operated and cirrhotic rats at baseline was 3,599 +/- 296 versus 1,226 +/- 63 mm Hg/sec (P < .01). Maximum first time derivative of ventricular diastolic relaxation (-dP/dt) for sham and cirrhotic rats at basal levels was -3,040 +/- 235 versus -864 +/- 59 (P < .01). The +dP/dt(max), and -dP/dt(max) responses to carbachol were blunted in the cirrhotic rats. The cirrhotic papillary muscles showed significantly less inhibition to incremental doses of carbachol than control rat muscles. Likewise, isoproterenol-stimulated membrane adenylyl cyclase activity was significantly less inhibited by carbachol doses in the cirrhotic rats. Membrane M2 receptor density and binding affinity in cirrhotic rat hearts were similar to controls. We conclude that muscarinic responsiveness was blunted in cirrhotic hearts, but this was not caused by receptor down-regulation, suggesting changes in postreceptor factors. These changes in muscarinic function are likely compensatory, and M2 receptor overactivity is not involved in the genesis of cirrhotic cardiomyopathy. 相似文献
994.
BACKGROUND: Ischemic disorders of the retina and optic nerve head, which constitute a common cause of visual loss, are usually seen in patients with atherosclerosis. OBJECTIVE: To test the hypothesis that serotonin, which is released when platelets aggregate, may produce vasospasm in atherosclerotic monkeys and, thus, may contribute to the ischemic disorders and that short-term dietary treatment of atherosclerosis causes the propensity to vasospasm to subside. METHODS: We studied the response of retinal and posterior ciliary circulation to serotonin in 18 atherosclerotic (25 eyes) and 5 normal (8 eyes) cynomolgus monkeys. The eyes were evaluated by color fundus photography and fluorescein fundus angiography. The eyes were examined under basal conditions and, at a different time, during the intravenous infusion of serotonin. In 6 of the 18 atherosclerotic animals, the evaluation was repeated 5 to 12 months after discontinuing the atherogenic diet (ie, the regression group). RESULTS: Serotonin had no effect in normal monkeys. In 18 atherosclerotic monkeys, serotonin produced transient occlusion or delayed filling of the central retinal artery and/or posterior ciliary artery (PCA) in 9 eyes of 9 animals, involving the central retinal artery in 5, lateral PCA in 8, and medial PCA in 5, in various combinations. In 6 animals (6 eyes) of the regression group, the vasoconstrictor effect of serotonin was abolished completely, except in the medial PCA in 1 eye. CONCLUSIONS: Serotonin, in the presence of atherosclerotic lesions, can cause transient, complete occlusion or impaired blood flow in the central retinal artery and/or PCA. We speculate that this mechanism may play a role in the development of ischemic disorders of the retina and optic nerve head. Discontinuing the atherogenic diet abolished or markedly improved the serotonin-induced vasoconstriction within a few months. 相似文献
995.
SS Khan J Forrester 《Canadian Metallurgical Quarterly》1997,337(17):1243; author reply 1244-1243; author reply 1245
996.
S Gründer D Firsov SS Chang NF Jaeger I Gautschi L Schild RP Lifton BC Rossier 《Canadian Metallurgical Quarterly》1997,16(5):899-907
Pseudohypoaldosteronism type 1 (PHA-1) is an inherited disease characterized by severe neonatal salt-wasting and caused by mutations in subunits of the amiloride-sensitive epithelial sodium channel (ENaC). A missense mutation (G37S) of the human ENaC beta subunit that causes loss of ENaC function and PHA-1 replaces a glycine that is conserved in the N-terminus of all members of the ENaC gene family. We now report an investigation of the mechanism of channel inactivation by this mutation. Homologous mutations, introduced into alpha, beta or gamma subunits, all significantly reduce macroscopic sodium channel currents recorded in Xenopus laevis oocytes. Quantitative determination of the number of channel molecules present at the cell surface showed no significant differences in surface expression of mutant compared with wild-type channels. Single channel conductances and ion selectivities of the mutant channels were identical to that of wild-type. These results suggest that the decrease in macroscopic Na currents is due to a decrease in channel open probability (P(o)), suggesting that mutations of a conserved glycine in the N-terminus of ENaC subunits change ENaC channel gating, which would explain the disease pathophysiology. Single channel recordings of channels containing the mutant alpha subunit (alphaG95S) directly demonstrate a striking reduction in P(o). We propose that this mutation favors a gating mode characterized by short-open and long-closed times. We suggest that determination of the gating mode of ENaC is a key regulator of channel activity. 相似文献
997.
SS Wing N Bédard C Morales P Hingamp J Trasler 《Canadian Metallurgical Quarterly》1996,16(8):4064-4072
The Saccharomyces cerevisiae ubiquitin-conjugating enzymes (E2s) UBC4 and UBC5 are essential for degradation of short-lived and abnormal proteins. We previously identified rat cDNAs encoding two E2s with strong sequence similarity to UBC4 and UBC5. These E2 isoforms are widely expressed in rat tissues, consistent with a fundamental cellular function for these E2s. We now report a new isoform, 8A, which despite having >91% amino acid identity with the other isoforms, shows several novel features. Expression of the 8A isoform appears restricted to the testis, is absent in early life, but is induced during puberty. Hypophysectomy reduced expression of the 8A isoform. In situ hybridization studies indicated that 8A mRNA is expressed mainly in round spermatids. Immunoblot analyses showed that 8A protein is found not only in subfractions of germ cells enriched in round spermatids but also in subfractions containing residual bodies extruded from more mature elongated spermatids, indicating that the protein possesses a longer half-life than the mRNA. Unlike all previously identified mammalian and plant homologs of S. cerevisiae UBC4, which possess a basic pI, the 8A isoform is unique in possessing an acidic pI. The small differences in sequence between the 8A isoform and other rat isoforms conferred differences in biochemical function. The 8A isoform was less effective than an isoform with a basic pI or ineffective in conjugating ubiquitin to certain fractions of testis proteins. Thus, although multiple isoforms of a specific E2 may exist to ensure performance of a critical cellular function, our data demonstrate, for the first time, that multiple genes also permit highly specialized regulation of expression of specific isoforms and that subtle differences in E2 primary structure can dictate conjugation of ubiquitin to different subsets of cellular proteins. 相似文献
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