Regulation of glycogenolysis in human skeletal muscle

1989 ◽  
Vol 67 (6) ◽  
pp. 2243-2248 ◽  
Author(s):  
J. M. Ren ◽  
E. Hultman
Keyword(s):  
Electrical Stimulation ◽  
Inorganic Phosphate ◽  
Quadriceps Muscle ◽  
Stimulation Period ◽  
Blood Flow Occlusion ◽  
Flow Occlusion ◽  
Observation Period ◽  
Stimulation Of ◽  
Occlusion Period

The role of inorganic phosphate on the regulation of glycogenolysis in resting and contracting muscle was studied in human quadriceps muscle. Increased Pi content was achieved by intermittent electrical stimulation of the muscle followed by occlusion of the blood flow. Occlusion resulted in the maintenance of a high Pi content over a 60-s observation period during which the muscle was either at rest or was stimulated electrically. The study was performed with and without infusion of epinephrine (EPI). In the absence of EPI the phosphorylase a fraction was 50% immediately at the end of the initial stimulation period, declining to 22% after 60 s. With EPI corresponding values for phosphorylase a were 91% initially, 56% after 30 s, and 33% after 60 s, respectively. In both cases the Pi content was increased by approximately 35 mmol/kg dry muscle during the stimulation and remained constant during the occlusion. In neither of these situations was significant degradation of glycogen observed during the occlusion. In the study performed with electrical stimulation during the occlusion period, muscle glycogen degradation was observed both with and without EPI. Phosphorylase a fractions and Pi contents in this study were similar to those observed when muscle was rested over the 60-s occlusion period. The paradox of a high Pi content and extensive transformation of phosphorylase to the a form but low glycogenolytic activity points to additional factors in the regulation of glycogen breakdown.

Protein kinase Cε and the antiadrenergic action of adenosine in rat ventricular myocytes

2004 ◽  
Vol 287 (4) ◽  
pp. H1721-H1729 ◽  
Author(s):  
Koji Miyazaki ◽  
Satoshi Komatsu ◽  
Mitsuo Ikebe ◽  
Richard A. Fenton ◽  
James G. Dobson
Keyword(s):  
Electrical Stimulation ◽  
Protein Kinase ◽  
Ventricular Myocytes ◽  
Adrenergic Agonist ◽  
Inhibitory Peptide ◽  
Rat Ventricular Myocytes ◽  
Adult Rat ◽  
Tubular System ◽  
Stimulation Of

Adenosine-induced antiadrenergic effects in the heart are mediated by adenosine A1 receptors (A1R). The role of PKCε in the antiadrenergic action of adenosine was explored with adult rat ventricular myocytes in which PKCε was overexpressed. Myocytes were transfected with a pEGFP-N1 vector in the presence or absence of a PKCε construct and compared with normal myocytes. The extent of myocyte shortening elicited by electrical stimulation of quiescent normal and transfected myocytes was recorded with video imaging. PKCε was found localized primarily in transverse tubules. The A1R agonist chlorocyclopentyladenosine (CCPA) at 1 μM rendered an enhanced localization of PKCε in the t-tubular system. The β-adrenergic agonist isoproterenol (Iso; 0.4 μM) elicited a 29–36% increase in myocyte shortening in all three groups. Although CCPA significantly reduced the Iso-produced increase in shortening in all three groups, the reduction caused by CCPA was greatest with PKCε overexpression. The CCPA reduction of the Iso-elicited shortening was eliminated in the presence of a PKCε inhibitory peptide. These results suggest that the translocation of PKCε to the t-tubular system plays an important role in A1R-mediated antiadrenergic actions in the heart.

Norepinephrine uptake as an indicator of cardiac reinnervation in dogs

1978 ◽  
Vol 235 (3) ◽  
pp. H289-H294 ◽  
Author(s):  
M. P. Kaye ◽  
G. M. Tyce
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Nerves ◽  
Progressive Increase ◽  
Canine Heart ◽  
Storage Mechanism ◽  
Specific Membrane ◽  
Heart Uptake ◽  
Membrane Mechanism ◽  
Stimulation Of

To study the possible role of uptake of [3H]norepinephrine ([3H]NE) as an indicator of sympathetic reinnervation of the surgically denervated canine heart, uptake was determined from multiple areas of hearts at various stages of reinnervation (1--6 mo), and these data were correlated with myocardial catecholamine content and functional response of the heart to electrical stimulation of the sympathetic nerves. Our experiments confirm that NE content correlates poorly with the degree of reinnervation of the previously denervated canine heart. There is, however, a progressive increase of [3H]NE uptake from 1 mo to 6 mo, at which time uptake has returned to approximately 57% of control values in the left atrium. The development of the storage mechanism lags far behind the specific-membrane mechanism for uptake in the reinnervating surgically denervated canine heart.

Efferent-mediated protection from acoustic overexposure: relation to slow effects of olivocochlear stimulation

1995 ◽  
Vol 73 (2) ◽  
pp. 506-514 ◽  
Author(s):  
E. R. Reiter ◽  
M. C. Liberman
Keyword(s):  
Electrical Stimulation ◽  
Inner Ear ◽  
Guinea Pigs ◽  
Threshold Shift ◽  
Exposure Condition ◽  
Protective Effects ◽  
Acoustic Overstimulation ◽  
Different Levels ◽  
Stimulation Of

1. The present study attempts to resolve discrepancies in the reported role of olivocochlear (OC) efferent activation in protecting the inner ear from acoustic overstimulation: in previous studies, activating the OC system in guinea pigs reduced the threshold shift caused by 1 min monaural exposure to a 10-kHz tone; whereas unilateral OC activation in cats had no effect on threshold shifts following binaural exposure to a 10 min 6-kHz tone. 2. In this study, anesthetized and curarized guinea pigs were exposed either monaurally or binaurally to tones of different duration (1-5 min), frequency (6 to 10 kHz) and intensity (105-118 dB SPL). For each exposure condition, threshold shifts were compared among ears with different levels of OC activation: in some cases, the OC bundle (OCB) was electrically stimulated during (and/or before) the acoustic overexposure; in others, the OCB was cut before the exposure; in control cases, the OCB was neither cut nor electrically stimulated. 3. Electrical stimulation of the OCB delivered simultaneously with acoustic overstimulation produced significant reductions in threshold shift only for acoustic exposures at higher frequencies (8 and 10 kHz) and shorter durations (1 and 2 min). The protective effects on 1-min exposures could be extinguished by prior stimulation of the OCB, i.e., if the OC stimulation was turned on 4 min before the acoustic overexposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of periaqueductal gray in the pressor response produced by central injections of angiotensin II

1993 ◽  
Vol 265 (5) ◽  
pp. R1052-R1059
Author(s):  
L. R. Portis ◽  
S. J. Lewis ◽  
M. J. Brody
Keyword(s):  
Electrical Stimulation ◽  
Angiotensin Ii ◽  
Fluorescent Dyes ◽  
Pressor Response ◽  
Periaqueductal Gray ◽  
Ang Ii ◽  
Hemodynamic Responses ◽  
Anesthetized Rats ◽  
Stimulation Of

The present studies were undertaken to determine the role of rostral periaqueductal gray (PAG) in mediating the pressor effect produced by intracerebroventricular (icv) injection of angiotensin II (ANG II, 200 ng). Two functionally and anatomically distinct sites were identified in rostral PAG: a dorsomedial site involved in the hemodynamic responses produced by electrical stimulation of the anteroventral third ventricle (AV3V) region and a ventromedial site required for the pressor response elicited by icv administration of ANG II. In Saffan-anesthetized rats, injection of lidocaine (LIDO, 4%) in dorsomedial PAG, but not in ventromedial PAG, significantly attenuated the decrease in hindquarter resistance (HQR) produced by electrical stimulation of the AV3V region, and the poststimulatory increase in mean arterial pressure (MAP) and HQR. The injection of LIDO in ventromedial PAG had no effect on the hemodynamic responses produced by electrical stimulation of the AV3V region in anesthetized rats but significantly attenuated the pressor response produced by icv administration of ANG II in conscious rats. The hypothesis that these two sites receive separate projections was addressed by microinjecting two retrogradely transported fluorescent dyes, Fluoro-Gold and Fast Blue. The anatomic findings suggest that separation of the pathways activated by electrical and chemical stimulation of the AV3V region occurs at the level of rostral PAG.

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