Facilitated diffusion of monosaccharides in smooth muscle of rat vas deferens in vitro

The suitability of rat vas deferens for investigating sugar transport in smooth muscle was determined in vitro, with the nonmetabolized glucose analog 3-O-methyl-D-glucose as test sugar. Vas deferens smooth muscle contains a facilitated diffusion system for monosaccharides, as shown by saturation of the transport sites and by competition between 3-O-methyl-D-glucose and D-glucose. The activity of the facilitated diffusion system could be enhanced by hyperosmolarity and by contractile activity, but frequency dependency could not be established. A high concentration of insulin (100 mU/mL) was required to stimulate sugar transport. As smooth muscle is not a primary tissue for the storage of energy reserves, it does not require large numbers of insulin receptors.

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A specific sugar transport mechanism in smooth muscle and its regulation

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y76-039 ◽

1976 ◽

Vol 54 (3) ◽

pp. 254-261 ◽

Cited By ~ 11

Author(s):

I. Bihler ◽

P. C. Sawh ◽

J. Elbrink

Keyword(s):

Smooth Muscle ◽

Sugar Transport ◽

Facilitated Diffusion ◽

Inhibitory Effects ◽

Rat Urinary Bladder ◽

Specificity And Sensitivity ◽

Rate Limiting ◽

Specific Sugar

The membrane transport of 3-O-methyl-D-glucose was studied in vitro in a smooth muscle, the detrusor of rat urinary bladder. Transport occurred by facilitated diffusion and showed the same chemical specificity and sensitivity to specific inhibitors as skeletal and cardiac muscle but its insulin sensitivity was smaller. Transport was increased by agents inhibiting the Na+ pump and was decreased by agents which increased Na+ and K+ gradients by apparently stimulating the Na+ pump. In accord with a rate limiting role of transport in glucose utilization, similar stimulating and inhibitory effects were seen when CO2 production from [14C]glucose was measured.

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Smooth muscle mechanical responses in vitro to bethanechol after progesterone in male rat.

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1978.235.4.e422 ◽

1978 ◽

Vol 235 (4) ◽

pp. E422 ◽

Cited By ~ 2

Author(s):

L A Bruce ◽

F M Behsudi ◽

I E Danhof

Keyword(s):

Smooth Muscle ◽

Contractile Activity ◽

Circular Muscle ◽

Male Rat ◽

Equal Weight ◽

Muscarinic Agonist ◽

Sprague Dawley ◽

Response Curves ◽

Dose Levels

Male Sprague-Dawley rats were pretreated subcutaneously with either progesterone (3 mg/kg per day) in a vehicle or a vehicle only for 3 days. Antral and gastroduodenal junctional tissues (GJT) were excised from both groups of animals and prepared for in vitro mechanical measurements. Responses from the circular muscle axis of these tissues were recorded with strain gauge transducers over a 30-min period. Chemical stimulation of the tissue was achieved with a muscarinic agonist, bethanechol chloride. Log-dose response curves suggested that untreated antral tissue generated stronger contractile activity than untreated GJT on an equal weight basis at bethanechol dose levels of 6.4 X 10(-6) M to 1 X 10(-4) M (P less than 0.005). Antral tissue and GJT contractile activity from the progesterone pretreated animals was significantly reduced (P less than 0.01) compared to the corresponding tissues from untreated animals at bethanechol dose levels of 6.4 X 10(-6) M and 1.28 X 10(-5) M. Progesterone pretreatment appeared to have little effect on the contractile frequency of either tissue. These results suggest possible progesteronic influences on contractile force in gastrointestinal smooth muscle.

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Simultaneous measurement of contractile effects in the circular and longitudinal smooth muscle of the rat vas deferens by drugs perfused externally or via the lumen

British Journal of Pharmacology ◽

10.1111/j.1476-5381.1985.tb11071.x ◽

1985 ◽

Vol 85 (4) ◽

pp. 737-746 ◽

Cited By ~ 4

Author(s):

Pedro A. Busatto ◽

Aron Jurkiewicz

Keyword(s):

Smooth Muscle ◽

Simultaneous Measurement ◽

Vas Deferens ◽

Rat Vas Deferens ◽

Longitudinal Smooth Muscle

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Electrophysiology of Syncytial Smooth Muscle

Journal of Experimental Neuroscience ◽

10.1177/1179069518821917 ◽

2019 ◽

Vol 13 ◽

pp. 117906951882191 ◽

Cited By ~ 4

Author(s):

Rohit Manchanda ◽

Shailesh Appukuttan ◽

Mithun Padmakumar

Keyword(s):

Smooth Muscle ◽

Action Potentials ◽

Signal Analysis ◽

Computational Models ◽

Vas Deferens ◽

Contractile Activity ◽

Smooth Muscles ◽

Biophysical Analysis ◽

Recent Developments ◽

The Many

As in other excitable tissues, two classes of electrical signals are of fundamental importance to the functioning of smooth muscles: junction potentials, which arise from neurotransmission and represent the initiation of excitation (or in some instances inhibition) of the tissue, and spikes or action potentials, which represent the accomplishment of excitation and lead on to contractile activity. Unlike the case in skeletal muscle and in neurons, junction potentials and spikes in smooth muscle have been poorly understood in relation to the electrical properties of the tissue and in terms of their spatiotemporal spread within it. This owes principally to the experimental difficulties involved in making precise electrical recordings from smooth muscles and also to two inherent features of this class of muscle, ie, the syncytial organization of its cells and the distributed innervation they receive, which renders their biophysical analysis problematic. In this review, we outline the development of hypotheses and knowledge on junction potentials and spikes in syncytial smooth muscle, showing how our concepts have frequently undergone radical changes and how recent developments hold promise in unraveling some of the many puzzles that remain. We focus especially on computational models and signal analysis approaches. We take as illustrative examples the smooth muscles of two organs with distinct functional characteristics, the vas deferens and urinary bladder, while also touching on features of electrical functioning in the smooth muscles of other organs.

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Effect of NO donors on protein phosphorylation in intact vascular and nonvascular smooth muscles

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2001.280.4.h1565 ◽

2001 ◽

Vol 280 (4) ◽

pp. H1565-H1580 ◽

Cited By ~ 8

Author(s):

James K. Hennan ◽

Jack Diamond

Keyword(s):

Smooth Muscle ◽

Protein Kinase ◽

Protein Phosphorylation ◽

Vas Deferens ◽

Smooth Muscles ◽

Rat Aorta ◽

Rat Vas Deferens ◽

Two Dimensional Gel Electrophoresis ◽

Relaxant Response ◽

Underlying Mechanisms

It is generally well accepted that nitrovasodilator-induced relaxation of vascular smooth muscle involves elevation of cGMP and activation of a specific cGMP-dependent protein kinase [protein kinase G (PKG)]. However, the protein targets of PKG and the underlying mechanisms by which this kinase leads to a relaxant response have not been elucidated. Several types of smooth muscle, including rat myometrium and vas deferens, are not relaxed by sodium nitroprusside, even at concentrations that produce marked elevation of cGMP and activation of PKG. The main objective of our studies was to compare PKG-mediated protein phosphorylation in intact rat aorta, rat myometrium, and rat vas deferens using two-dimensional gel electrophoresis. In intact rat aorta, seven PKG substrates were detected during relaxation of the tissue. None of the PKG substrates identified in the rat aorta appeared to be phosphorylated in the myometrium or vas deferens after administration of various cGMP-elevating agents. Thus the failure of the rat myometrium and rat vas deferens to relax in the face of cGMP elevation and PKG activation may be due to a lack of PKG substrate phosphorylation.

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Ca2+ handling properties of microsomal subfractions of rat vas deferens smooth muscle

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y84-011 ◽

1984 ◽

Vol 62 (1) ◽

pp. 76-79 ◽

Cited By ~ 1

Author(s):

A. K. Grover ◽

C. Y. Kwan

Keyword(s):

Smooth Muscle ◽

Concentration Dependence ◽

Vas Deferens ◽

Membrane Vesicles ◽

Rat Vas Deferens ◽

Enzyme Marker ◽

Isopycnic Centrifugation ◽

Stimulation Of ◽

Ph Profiles

The rat vas deferens smooth muscle microsomes on isopycnic centrifugation gave two fractions, namely F2 (15–30% sucrose) and F3 (30–40% sucrose), with comparable ATP-dependent azide-insensitive Ca2+-uptake capacities, although these fractions differed from each other in various enzyme marker activities. The fractions F2 and F3 also show similar pH profiles for the ATP-independent and ATP-dependent Ca2+ uptake, and similar ionized Ca2+-concentration dependence for the ATP-dependent Ca2+ uptake. However, the fractions F2 and F3 differ from each other in that: (a) F3 shows higher permeability to Ca2+, and (b) F3 shows higher stimulation of the ATP-dependent Ca2+ uptake by oxalate. The F3 fraction can also be used to obtain membrane vesicles loaded with Ca2+ oxalate in the presence of ATP. However, the yield of the Ca2+ oxalate enriched fraction is too low to permit their further characterization.

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Reversal of enhanced muscle glucose transport after exercise: roles of insulin and glucose

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1990.259.5.e685 ◽

1990 ◽

Vol 259 (5) ◽

pp. E685-E691 ◽

Cited By ~ 22

Author(s):

E. A. Gulve ◽

G. D. Cartee ◽

J. R. Zierath ◽

V. M. Corpus ◽

J. O. Holloszy

Keyword(s):

Skeletal Muscle ◽

Insulin Sensitivity ◽

Glucose Transport ◽

Transport Process ◽

Sugar Transport ◽

Transport Activity ◽

High Concentration ◽

Exercise Induced ◽

Muscle Glucose Transport

Exercise stimulates insulin-independent glucose transport in skeletal muscle and also increases the sensitivity of the glucose transport process in muscle to insulin. A previous study [D. A. Young, H. Wallberg-Henriksson, M. D. Sleeper, and J. O. Holloszy. Am. J. Physiol. 253 (Endocrinol. Metab. 16): E331–E335, 1987] showed that the exercise-induced increase in glucose transport activity disappears rapidly when rat epitrochlearis muscles are incubated for 3 h in vitro in the absence of insulin and that 7.5 microU/ml insulin in the incubation medium apparently slowed the loss of enhanced sugar transport. We examined whether addition of insulin several hours after exercise increases glucose transport to the same extent as continuous insulin exposure. Addition of 7.5 microU/ml insulin 2.5 h after exercise (when glucose transport has returned to basal levels) increased sugar transport to the same level as that which resulted from continuous insulin exposure. This finding provides evidence for an increase in insulin sensitivity rather than a slowing of reversal of the exercise-induced increase in insulin-independent glucose transport activity. Glucose transport was enhanced only at submaximal, not at maximal, insulin concentrations. Exposure to a high concentration of glucose and a low insulin concentration reduced the exercise-induced increase in insulin-sensitive glucose transport. Incubation with a high concentration of 2-deoxy-D-glucose (2-DG) did not alter the increase in insulin sensitivity, even though a large amount of 2-DG entered the muscle and was phosphorylated.(ABSTRACT TRUNCATED AT 250 WORDS)

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Resolvin D1 reverses reactivity and Ca2+ sensitivity induced by ET-1, TNF-α, and IL-6 in the human pulmonary artery

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00452.2014 ◽

2014 ◽

Vol 307 (11) ◽

pp. H1547-H1558 ◽

Cited By ~ 18

Author(s):

Roddy Hiram ◽

Edmond Rizcallah ◽

Chantal Sirois ◽

Marco Sirois ◽

Caroline Morin ◽

...

Keyword(s):

Smooth Muscle ◽

Pulmonary Artery ◽

Contractile Activity ◽

Transmembrane Protein ◽

Pulmonary Arteries ◽

Resolvin D1 ◽

Endothelin 1 ◽

Inflammatory Status ◽

Tnf Α

Pulmonary hypertension (PH) is a rare and progressive disease characterized by an inflammatory status and vessel wall remodeling, resulting in increased pulmonary artery resistance. During the last decade, treatments have been proposed; most of them target the endothelial pathways that stimulate smooth muscle cell relaxation. However, PH remains associated with significant morbidity. We hypothesized that inflammation plays a crucial role in the severity of the abnormal vasoconstriction in PH. The goal of this study was to assess the effects of resolvin D1 (RvD1), a potent anti-inflammatory agent, on the pharmacological reactivity of human pulmonary arteries (HPAs) via an in vitro model of induced hyperreactivity. The effects of RvD1 and monoacylglyceride compounds were measured on contractile activity and Ca2+ sensitivity developed by HPAs that had been pretreated (or not) under proinflammatory conditions with either 10 ng/ml TNF-α or 10 ng/ml IL-6 or under hyperreactive conditions with 5 nM endothelin-1. The results demonstrated that, compared with controls, 24-h pretreatment with TNF-α, IL-6, or endothelin-1 increased reactivity and Ca2+ sensitivity of HPAs as revealed by agonist challenges with 80 mM KCl, 1 μM serotonin (5-hydroxytryptamine), 30 nM U-46619, and 1 μM phorbol 12,13-dibutyrate. However, 300 nM RvD1 as well as 1 μM monoacylglyceride-docosapentaenoic acid monoglyceride strongly reversed the overresponsiveness induced by both proinflammatory and hyperreactive treatments. In pretreated pulmonary artery smooth muscle cells, Western blot analyses revealed that RvD1 treatment decreased the phosphorylation level of CPI-17 and expression of transmembrane protein member 16A while increasing the detection of G protein-coupled receptor 32. The present data demonstrate that RvD1, a trihydroxylated docosahexaenoic acid derivative, decreases induced overreactivity in HPAs via a reduction in CPI-17 phosphorylation and transmembrane protein member 16A expression.

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