scholarly journals Role of the endothelium in regulation of contractile and dilatatory reactions of the aorta in rats with experimental hypothyrosis

2002 ◽  
Vol 48 (1) ◽  
pp. 41-44
Author(s):  
L. M. Lobanok ◽  
L. S. Luksha ◽  
N. G. Solovyova ◽  
I. I. Krylova
Keyword(s):  
Smooth Muscle ◽  
Functional Activity ◽  
Adrenergic Receptor ◽  
Female Rats ◽  
Receptor System ◽  
Vascular Stenosis ◽  
Main Determinants ◽  
Arterial Tone ◽  
Adrenergic And Cholinergic Receptors

The role of endothelium in regulation of the functional activity of vessels in experimental hypothyrosis was studied during different periods of ontogenesis. The study was carried out on isolated segments of the aorta from young (1 month) and adult (4-5 months) female rats. Hypothyrosis was induced by addition of thyrostatic mercasolil to the ration. Vascular stenosis was induced by norepinephrine, dilatation by carbacholine. The specific features in the mechanisms regulating arterial tone of euthyroid rats in the early ontogenesis are explained by a lower basal level of NO and specificity and/or density of adrenergic and cholinergic receptors, characteristic of this age. Reactions of arteries to norepinephrine and carbacholine in hypothyrosis are largely determined by age, modification of adrenergic receptor system of smooth-muscle cells, and endothelial function. A lower level of basal NO synthesis, characteristic of young hypothyroid animals, can be regarded as one of the main determinants of vasoconstrictive effect stimulation in hypothyrosis.

β2-Adrenergic Receptor Agonists and cAMP Arrest Human Cultured Airway Smooth Muscle Cells in the G1 Phase of the Cell Cycle: Role of Proteasome Degradation of Cyclin D1

1999 ◽  
Vol 56 (5) ◽  
pp. 1079-1086 ◽  
Author(s):  
Alastair G. Stewart ◽  
Trudi Harris ◽  
Darren J. Fernandes ◽  
Leslie C. Schachte ◽  
Valentina Koutsoubos ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cyclin D1 ◽  
Airway Smooth Muscle ◽  
Adrenergic Receptor ◽  
G1 Phase ◽  
Airway Smooth Muscle Cells ◽  
Β2 Adrenergic Receptor

Mechanisms of protein kinase C regulation of airway contractility

1989 ◽  
Vol 66 (4) ◽  
pp. 1935-1941 ◽  
Author(s):  
C. M. Schramm ◽  
M. M. Grunstein
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Functional Activity ◽  
Phorbol Esters ◽  
Isometric Tension ◽  
Channel Blockers ◽  
Kinase C ◽  
Higher Doses

To elucidate the role of protein kinase C (PK-C) in regulating airway contractility, the effects of PK-C activation with phorbol esters, 12-deoxyphorbol 13-isobutyrate (DPB), and phorbol 12-myristate 13-acetate (PMA), and with the diacylglycerol analogue 1-oleoyl-2-acetate-rac-glycerol (OAG) were separately evaluated in isolated rabbit tracheal smooth muscle (TSM) segments. The latter agents produced dual and opposing contractile effects, with DPB being the most potent. Lower doses of DPB (less than or equal to 10(-6) M) elicited significant increases in isometric tension in both untreated TSM, as well as in TSM half-maximally precontracted with methacholine. These potentiated TSM contractions were inhibited by the Ca2+ channel blockers, nifedipine (10(-4) M) and diltiazem (10(-5) M). In contrast, higher doses of DPB (greater than or equal to 10(-6) M) induced airway relaxation, which was ablated by preinhibition of the electrogenic Na+-K+ pump with ouabain (5 x 10(-6) M) or K+-free buffer. Indeed, in separate experiments DPB (10(-7) M) was found to significantly potentiate the functional activity of the Na+-K+ pump, an effect occurring independent of inhibition of Na+-H+ exchange with amiloride (10(-4) M) or extracellular Ca2+ influx with nifedipine (10(-4) M).(ABSTRACT TRUNCATED AT 250 WORDS)

Cocaine-Induced Supersensitivity in the Human Umbilical Artery

1974 ◽  
Vol 52 (3) ◽  
pp. 687-698 ◽  
Author(s):  
R. J. Reiffenstein ◽  
C. R. Triggle
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Adrenergic Receptor ◽  
Umbilical Artery ◽  
Sympathetic Innervation ◽  
Receptor System ◽  
Human Umbilical Artery ◽  
Uptake Of Noradrenaline ◽  
The Mean ◽  
Selective Increase

Cocaine (3.3 × 10−7 – 3.3 × 10−5 M) has no effect on the uptake of noradrenaline by the smooth muscle cells of the human umbilical artery but was found to potentiate the mean effective dose (ED50) responses of isolated helical strips of human umbilical artery to noradrenaline (3 × 10−5 M), and, to a lesser degree, 5-hydroxytryptamine (3.65 × 10−4 M), but had no effect on the response to KCl (40 mM) or histamine (1.8 × 10−6 M). Concentrations of cocaine above 1.7 × 10−4 M were found to antagonize ED50 responses to all the agonists tested. Because the preparation used in these studies does not receive sympathetic innervation, the effect of cocaine is likely to be mediated by an action at the level of the muscle. This selective increase in the response mediated by noradrenaline may be explained by an allosteric alteration of the α-adrenergic receptor system and/or a semiselective increase in smooth muscle sensitivity.

scholarly journals The Role of the Tumor Supressor‐p53 in Alpha1D‐Adrenergic Receptor (AR) Induce Apoptosis in Vascular Smooth Muscle Cells

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Jennifer Leigh Smith ◽  
Mary Lolis García‐Cazarín ◽  
Linda A Simmerman ◽  
Robert W Hadley ◽  
Michael T Piascik
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Adrenergic Receptor ◽  
Muscle Cells ◽  
Tumor Supressor

Liver glycogenolysis during exercise in adrenodemedullated male and female rats

1986 ◽  
Vol 251 (6) ◽  
pp. R1151-R1155
Author(s):  
W. W. Winder ◽  
S. F. Loy ◽  
D. S. Burke ◽  
S. J. Hawkes
Keyword(s):  
Adrenergic Receptor ◽  
Mature Female ◽  
Female Rats ◽  
Male Rats ◽  
Plasma Epinephrine ◽  
Male And Female ◽  
Male And Female Rats ◽  
Liver Glycogenolysis ◽  
Stimulation Of

Previous studies have shown that adrenodemedullation has no effect on the rate of liver glycogenolysis during exercise in male rats. Mature female rats have been reported to have a higher hepatic beta-adrenergic receptor activity than do male rats of the same age. The present study was undertaken to determine the role of plasma epinephrine in stimulating liver glycogenolysis during exercise in female rats. Both male and female rats were adrenodemedullated or sham operated. Three weeks later rats were run for 60 min at 21 m/min up a 15% grade. The rate of liver glycogenolysis during exercise was not affected by adrenodemedullation in either female rats or male rats. Hepatic adenosine 3',5'-cyclic monophosphate increased to approximately the same extent in sham operated as in adrenodemedullated female rats during exercise. Adrenodemedullation caused a significant reduction in the amount of glycogen utilized by the soleus muscle and in the degree of hyperglycemia during exercise. We conclude that epinephrine is unessential for stimulation of liver glycogenolysis during exercise in either male or female rats.

Regulation of alpha 1B-adrenergic receptor half-life: protein synthesis dependence and effect of norepinephrine

1994 ◽  
Vol 266 (3) ◽  
pp. C771-C775 ◽  
Author(s):  
N. J. Izzo ◽  
W. S. Colucci
Keyword(s):  
Protein Synthesis ◽  
Smooth Muscle ◽  
Half Life ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Independent Method ◽  
Unexpected Finding ◽  
Disappearance Rate ◽  
Aortic Smooth Muscle

Agonist-mediated down-regulation of alpha 1B-adrenergic receptors (AAR) may involve a decrease in synthesis, an increase in degradation, or a combination of the two mechanisms. Norepinephrine (NE) causes downregulation of AAR in rabbit aortic smooth muscle cells (RbSMC). To study the role of receptor degradation in this phenomenon, we studied the half-life (t1/2) of the AAR under basal conditions and during exposure to NE. We first determined the disappearance rate of AAR in the presence of cycloheximide, a commonly used method for measuring receptor t1/2. By this approach, the basal t1/2 was surprisingly long, 172 +/- 20 h. In contrast, the t1/2 in NE-treated cells was 11.8 +/- 0.3 h, suggesting that either NE decreased the t1/2 of AAR or cycloheximide increased the basal t1/2. To distinguish these possibilities, basal receptor t1/2 was determined by a second, independent method based on the repopulation of AAR after irreversible alkylation with chloroethylclonidine. This approach indicated a basal t1/2 (7.4 +/- 0.2 h) that was similar to the t1/2 with NE but more than 20-fold shorter than the t1/2 with cycloheximide. We conclude that in RbSMC NE-induced downregulation of AAR occurs without a decrease in receptor t1/2. The unexpected finding that cycloheximide markedly increases the basal t1/2 of the AAR further indicates that the t1/2 of the AAR is regulated, at least in part, by a short-lived protein that may regulate and/or mediate receptor degradation.

Ca2+-independent PLA2 controls endothelial store-operated Ca2+ entry and vascular tone in intact aorta

2008 ◽  
Vol 295 (6) ◽  
pp. H2466-H2474 ◽  
Author(s):  
François-Xavier Boittin ◽  
Françoise Gribi ◽  
Karima Serir ◽  
Jean-Louis Bény
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Muscle Relaxation ◽  
Physiological Mechanism ◽  
Smooth Muscle Relaxation ◽  
No Production ◽  
Arterial Tone ◽  
Endothelium Dependent Relaxation ◽  
Stimulation Of

During an agonist stimulation of endothelial cells, the sustained Ca2+ entry occurring through store-operated channels has been shown to significantly contribute to smooth muscle relaxation through the release of relaxing factors such as nitric oxide (NO). However, the mechanisms linking Ca2+ stores depletion to the opening of such channels are still elusive. We have used Ca2+ and tension measurements in intact aortic strips to investigate the role of the Ca2+-independent isoform of phospholipase A2 (iPLA2) in endothelial store-operated Ca2+ entry and endothelium-dependent relaxation of smooth muscle. We provide evidence that iPLA2 is involved in the activation of endothelial store-operated Ca2+ entry when Ca2+ stores are artificially depleted. We also show that the sustained store-operated Ca2+ entry occurring during physiological stimulation of endothelial cells with the circulating hormone ATP is due to iPLA2 activation and significantly contributes to the amplitude and duration of ATP-induced endothelium-dependent relaxation. Consistently, both iPLA2 metabolites arachidonic acid and lysophosphatidylcholine were found to stimulate Ca2+ entry in native endothelial cells. However, only the latter triggered endothelium-dependent relaxation through NO release, suggesting that lysophosphatidylcholine produced by iPLA2 upon Ca2+ stores depletion may act as an intracellular messenger that stimulates store-operated Ca2+ entry and subsequent NO production in endothelial cells. Finally, we found that ACh-induced endothelium relaxation also depends on iPLA2 activation, suggesting that the iPLA2-dependent control of endothelial store-operated Ca2+ entry is a key physiological mechanism regulating arterial tone.

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