Active vascular smooth muscle tone and venous membrane potentials during hemorrhage

1980 ◽  
Vol 238 (2) ◽  
pp. H144-H152
Author(s):  
W. J. Stekiel ◽  
W. J. Willems ◽  
D. R. Harder ◽  
J. H. Lombard
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Tone ◽  
Muscle Tone ◽  
Venous Pressure ◽  
Membrane Potentials ◽  
Intracellular Membrane ◽  
Small Intestinal ◽  
Vascular Smooth Muscle Tone

To clarify mechanisms leading to failure of compensatory vascular tone in splanchnic blood vessels during prolonged hypotensive stress, anesthetized rats were maintained at a constant mean arterial pressure of 35 mmHg by hemorrhage into an external reservoir until 40% autoinfusion of maximum bled volume. In vivo intracellular membrane potentials (Em) of small intestinal mesenteric veins (300--500 micrometers) were measured before and during the compensatory (bleedout) and decompensatory (autinfusion) phases of the hypotensive period to assess the state of vascular smooth muscle (VSM) excitation. During the compensatory phase, Em decreased from -41 +/- 1 mV (prehemorrhage) to -31 +/- 2 mV, and small venous pressures decreased significantly. The onset of cardiovascular decompensation was associated with hyperpolarization (-53 +/- 3 mV), vasodilation, and return of venous pressure to control levels. Although direct electrical stimulation of the VSM and norepinephrine suffusion still produced constriction late in the hypotensive period, venoconstrictor responses to perivascular nerve stimulation failed progressively. This study indicates that failure of adrenergic neuromuscular transmission contributes significantly to the loss of compensatory VSM tone during hemorrhage.

scholarly journals Modulation of temperature-induced tone by vasoconstrictor agents

1999 ◽  
Vol 86 (3) ◽  
pp. 963-969 ◽  
Author(s):  
Michael P. Massett ◽  
Stephen J. Lewis ◽  
James N. Bates ◽  
Kevin C. Kregel
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Tone ◽  
Muscle Tone ◽  
Vascular Ring ◽  
Bath Temperature ◽  
Mesenteric Arteries ◽  
Contractile Responses ◽  
Tension Generation ◽  
Vascular Smooth Muscle Tone

One of the primary cardiovascular adjustments to hyperthermia is a sympathetically mediated increase in vascular resistance in the viscera. Nonneural factors such as a change in vascular tone or reactivity may also contribute to this response. Therefore, the aim of this study was to determine whether vascular smooth muscle tone is altered during heating to physiologically relevant temperatures >37°C. Gradually increasing bath temperature from 37°C (normothermia) to 43°C (severe hyperthermia) produced graded contractions in vascular ring segments from rat mesenteric arteries and thoracic aortae. In untreated rings these contractions were relatively small, whereas hyperthermia elicited near-maximal increases in tension when rings were constricted with phenylephrine or KCl before heating. In phenylephrine-treated mesenteric arterial rings, the contractile responses to heating were markedly attenuated by the Ca2+channel antagonists nifedipine and diltiazem. Diltiazem also blocked the contractile responses to heating in thoracic aortic rings. These results demonstrate that hyperthermia has a limited effect on tension generation in rat vascular smooth muscle in the absence of vascular tone. However, in the presence of agonist-induced tone, tension generation during heating is markedly enhanced and dependent on extracellular Ca2+. In conclusion, these data suggest that local regulation of vascular tone can contribute to the hemodynamic adjustments to hyperthermia.

Vasoconstrictors and nitrovasodilators reciprocally regulate the Na+-K+-2Cl−cotransporter in rat aorta

1999 ◽  
Vol 276 (6) ◽  
pp. C1383-C1390 ◽  
Author(s):  
Fatma Akar ◽  
Elizabeth Skinner ◽  
Janet D. Klein ◽  
Madhumita Jena ◽  
Richard J. Paul ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Tone ◽  
Smooth Muscle Contraction ◽  
Rat Aorta ◽  
Regulatory Function ◽  
Ang Ii ◽  
Vascular Smooth Muscle Tone

Little is known about the function and regulation of the Na+-K+-2Cl−cotransporter NKCC1 in vascular smooth muscle. The activity of NKCC1 was measured as the bumetanide-sensitive efflux of86Rb+from intact smooth muscle of the rat aorta. Hypertonic shrinkage (440 mosmol/kgH2O) rapidly doubled cotransporter activity, consistent with its volume-regulatory function. NKCC1 was also acutely activated by the vasoconstrictors ANG II (52%), phenylephrine (50%), endothelin (53%), and 30 mM KCl (54%). Both nitric oxide and nitroprusside inhibited basal NKCC1 activity (39 and 34%, respectively), and nitroprusside completely reversed the stimulation by phenylephrine. The phosphorylation of NKCC1 was increased by hypertonic shrinkage, phenylephrine, and KCl and was reduced by nitroprusside. The inhibition of NKCC1 significantly reduced the contraction of rat aorta induced by phenylephrine (63% at 10 nM, 26% at 30 nM) but not by KCl. We conclude that the Na+-K+-2Cl−cotransporter in vascular smooth muscle is reciprocally regulated by vasoconstrictors and nitrovasodilators and contributes to smooth muscle contraction, indicating that alterations in NKCC1 could influence vascular smooth muscle tone in vivo.

Modulation of vascular tone by neutrophils: dependence on endothelial integrity

1989 ◽  
Vol 257 (4) ◽  
pp. H1315-H1320
Author(s):  
J. L. Mehta ◽  
D. L. Lawson ◽  
W. W. Nichols ◽  
P. Mehta
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Relaxant ◽  
Muscle Tone ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Smooth Muscle Tone ◽  
High Concentrations ◽  
Vascular Smooth Muscle Tone ◽  
Smooth Muscle Relaxant

To determine the influence of polymorphonuclear leukocytes (PMNLs) on vascular smooth muscle tone, isolated human PMNLs (10(4)–10(7) cells/ml) were suspended in a tissue bath with precontracted rat aortic rings with or without endothelium. PMNLs in low concentrations (10(4) and 10(5) cells/ml) caused a mild contraction, and in higher concentrations (10(6) and 10(7) cells/ml) caused a modest relaxation of aortic rings with intact endothelium. In contrast, PMNLs caused a potent concentration-dependent relaxation of deendothelialized rings (P less than 0.01 compared with rings with intact endothelium). The PMNL-induced vascular smooth muscle relaxation was abolished by both hemoglobin and methylene blue and potentiated by both superoxide dismutase and captopril. Although suspension of PMNLs caused release of eicosanoids, thromboxane A2 and prostacyclin, from rings with intact endothelium, neither indomethacin nor the TxA2-endoperoxide receptor antagonist SQ 29548 modified the effects of PMNLs on vascular smooth muscle tone. These observations suggest that unstimulated PMNLs generate a smooth muscle relaxant, which has biological characteristics similar to the endothelium-derived relaxing factor. Since the activity of this PMNL-derived smooth muscle relaxant is more pronounced in deendothelialized vascular segments, it appears that endothelium provides a barrier against vasorelaxation by high concentrations of PMNLs.

PI3-kinase/Akt modulates vascular smooth muscle tone via cAMP signaling pathways

2001 ◽  
Vol 91 (4) ◽  
pp. 1819-1827 ◽  
Author(s):  
Padmini Komalavilas ◽  
Shyamal Mehta ◽  
Christopher J. Wingard ◽  
Daniel T. Dransfield ◽  
Jyoti Bhalla ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Vascular Smooth Muscle ◽  
Cyclic Nucleotide ◽  
Muscle Tone ◽  
Pi3 Kinase ◽  
Dependent Protein Kinase ◽  
Smooth Muscle Tone ◽  
Dependent Protein ◽  
Vascular Smooth Muscle Tone

Phosphatidylinositol 3-kinase (PI3-kinase) activates protein kinase B (also known as Akt), which phosphorylates and activates a cyclic nucleotide phosphodiesterase 3B. Increases in cyclic nucleotide concentrations inhibit agonist-induced contraction of vascular smooth muscle. Thus we hypothesized that the PI3-kinase/Akt pathway may regulate vascular smooth muscle tone. In unstimulated, intact bovine carotid artery smooth muscle, the basal phosphorylation of Akt was higher than that in cultured smooth muscle cells. The phosphorylation of Akt decreases in a time-dependent manner when incubated with the PI3-kinase inhibitor, LY-294002. Agonist (serotonin)-, phorbol ester (phorbol 12,13-dibutyrate; PDBu)-, and depolarization (KCl)-induced contractions of vascular smooth muscles were all inhibited in a dose-dependent fashion by LY-294002. However, LY-294002 did not inhibit serotonin- or PDBu-induced increases in myosin light chain phosphorylation or total O2 consumption, suggesting that inhibition of contraction was not mediated by reversal or inhibition of the pathways that lead to smooth muscle activation and contraction. Treatment of vascular smooth muscle with LY-294002 increased the activity of cAMP-dependent protein kinase and increased the phosphorylation of the cAMP-dependent protein kinase substrate heat shock protein 20 (HSP20). These data suggest that activation of the PI3-kinase/Akt pathway in unstimulated smooth muscle may modulate vascular smooth muscle tone (allow agonist-induced contraction) through inhibition of the cyclic nucleotide/HSP20 pathway and suggest that cyclic nucleotide-dependent inhibition of contraction is dissociated from the myosin light chain contractile regulatory pathways.

Effects of Calcium on Vascular Smooth Muscle Tone

1990 ◽  
Vol 3 (10_Pt_2) ◽  
pp. 291S-298S ◽  
Author(s):  
Kathleen G. Morgan ◽  
Eiichi Suematsu
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Muscle Tone ◽  
Smooth Muscle Tone ◽  
Vascular Smooth Muscle Tone
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