scholarly journals Myogenic activity and serotonergic inhibition in the chromatophore network of the squidDosidicus gigas(family Ommastrephidae) andDoryteuthis opalescens(family Loliginidae)

2017 ◽  
Vol 220 (24) ◽  
pp. 4669-4680 ◽  
Author(s):  
Hannah E. Rosen ◽  
William F. Gilly
Keyword(s):  
2002 ◽  
Vol 283 (6) ◽  
pp. H2268-H2275 ◽  
Author(s):  
Rebecca J. Coulson ◽  
Naomi C. Chesler ◽  
Lisa Vitullo ◽  
Marilyn J. Cipolla

Passive (papaverine induced) and active (spontaneous pressure induced) biomechanical properties of ischemic and nonischemic rat middle cerebral arteries (MCAs) were studied under pressurized conditions in vitro. Ischemic (1 h of occlusion), contralateral, and sham-operated control MCAs were isolated from male Wistar rats ( n = 22) and pressurized using an arteriograph system that allowed control of transmural pressure (TMP) and measurement of lumen diameter and wall thickness. Three mechanical stiffness parameters were computed: overall passive stiffness (β), pressure-dependent modulus changes ( E inc,p), and smooth muscle cell (SMC) activity-dependent changes ( E inc,a). The β-value for ischemic vessels was increased compared with sham vessels (13.9 ± 1.7 vs. 9.1 ± 1.4, P < 0.05), indicating possible short-term remodeling due to ischemia. E inc,p increased with pressure in the passive vessels ( P < 0.05) but remained relatively constant in the active vessels for all vessel types, indicating that pressure-induced SMC contractile activity (i.e., myogenic reactivity) in cerebral arteries leads to the maintenance of a constant elastic modulus within the autoregulatory pressure range. E inc,a increased with pressure for all conditions, signifying that changes in stiffness are influenced by SMC activity and vascular tone.


2008 ◽  
pp. 57-61 ◽  
Author(s):  
I. V. Tikhonova ◽  
A. V. Tankanag ◽  
N. I. Kosyakova ◽  
N. K. Chemeris

Levels of inflammatory markers and skin microcirculation were studied in patients with chronic obstructive pulmonary disease. Proinflammatory cytokine concentrations and number of desquamated endothelial cells in blood flow were significant increased during exacerbation compared with controls. The increase in proinflammatory cytokine concentrations in exacerbation was accompanied by increased skin perfusion, increased oscil lation amplitudes in the frequency ranges of respiratory rhythm and higher endothelial activity compared with controls. In stable condition, the lev els of proinflammatory cytokines decreased compared with those in exacerbation. Myogenic activity was decreased twice in patients with stable con dition compared with healthy persons. The endothelialdependent vasodilation did not change and the endothelialindependent vasodilation increased in all patients compared with controls.


Development ◽  
1999 ◽  
Vol 126 (22) ◽  
pp. 4965-4976 ◽  
Author(s):  
A.J. Bendall ◽  
J. Ding ◽  
G. Hu ◽  
M.M. Shen ◽  
C. Abate-Shen

The migration of myogenic precursors to the vertebrate limb exemplifies a common problem in development - namely, how migratory cells that are committed to a specific lineage postpone terminal differentiation until they reach their destination. Here we show that in chicken embryos, expression of the Msx1 homeobox gene overlaps with Pax3 in migrating limb muscle precursors, which are committed myoblasts that do not express myogenic differentiation genes such as MyoD. We find that ectopic expression of Msx1 in the forelimb and somites of chicken embryos inhibits MyoD expression as well as muscle differentiation. Conversely, ectopic expression of Pax3 activates MyoD expression, while co-ectopic expression of Msx1 and Pax3 neutralizes their effects on MyoD. Moreover, we find that Msx1 represses and Pax3 activates MyoD regulatory elements in cell culture, while in combination, Msx1 and Pax3 oppose each other's trancriptional actions on MyoD. Finally, we show that the Msx1 protein interacts with Pax3 in vitro, thereby inhibiting DNA binding by Pax3. Thus, we propose that Msx1 antagonizes the myogenic activity of Pax3 in migrating limb muscle precursors via direct protein-protein interaction. Our results implicate functional antagonism through competitive protein-protein interactions as a mechanism for regulating the differentiation state of migrating cells.


2001 ◽  
Vol 281 (3) ◽  
pp. H1047-H1056 ◽  
Author(s):  
Timothy V. Murphy ◽  
Brian E. Spurrell ◽  
Michael A. Hill

Arterioles respond to increased transmural pressure with myogenic constriction. The present study investigated the role of tyrosine phosphorylation in myogenic activity. Cannulated segments of a rat cremaster arteriole were fixed under pressure, followed by incubation with fluorescein isothiocyanate (FITC)-conjugated anti-phosphotyrosine. Smooth muscle cell fluorescence intensity was measured with the use of confocal laser-scanning microscopy. Anti-phosphotyrosine fluorescence intensity in muscle cells of arterioles maintained at 100 mmHg was reduced by the tyrosine kinase inhibitor tyrphostin A47 (30 μM) and increased by the tyrosine phosphatase inhibitor pervanadate (100 μM). In time-course experiments, anti-phosphotyrosine fluorescence increased slowly (over 5 min) after an acute increase in intraluminal pressure, and was dissociated from myogenic contraction (within 1 min). In contrast, angiotensin II (0.1 μM) caused rapid constriction and increased tyrosine phosphorylation. Anti-phosphotyrosine fluorescence was also pressure dependent (10–100 mmHg). Abolition of myogenic activity, either through removal of extracellular Ca2+, or exposure to verapamil (5 μM) or forskolin (0.1 μM) caused a further increase in anti-phosphotyrosine fluorescence. We conclude that transmural pressure and/or wall tension in arterioles causes increased tyrosine phosphorylation; however, this is not involved in the acute phase of myogenic constriction but may be involved in later responses, such as sustained myogenic tone or mechanisms possibly related to growth.


2004 ◽  
Vol 286 (6) ◽  
pp. H2127-H2132 ◽  
Author(s):  
Marilyn J. Cipolla ◽  
Lisa Vitullo ◽  
John McKinnon

Eclampsia is thought to be similar to hypertensive encephalopathy, whereby acute elevations in intravascular pressure cause forced dilatation (FD) of intrinsic myogenic tone of cerebral arteries and arterioles, decreased cerebrovascular resistance, and hyperperfusion. In the present study, we tested the hypothesis that pregnancy and/or the postpartum period predispose cerebral arteries to FD by diminishing pressure-induced myogenic activity. We compared the reactivity to pressure (myogenic activity) as well as factors that modulate the level of tone of third-order branches (<200 μm) of the posterior cerebral artery (PCA) that were isolated from nonpregnant (NP, n = 7), late-pregnant (LP, 19 days, n = 10), and postpartum (PP, 3 days, n = 8) Sprague-Dawley rats under pressurized conditions. PCAs from all groups of animals developed spontaneous tone within the myogenic pressure range (50–150 mmHg) and constricted arteries at 100 mmHg (NP, 30 ± 3; LP, 39 ± 4; and PP, 42 ± 7%; P > 0.05). This level of myogenic activity was maintained in the NP arteries at all pressures; however, both LP and PP arteries dilated at considerably lower pressures compared with NP, which lowered the pressure at which FD occurred from >175 for NP to 146 ± 6.5 mmHg for LP ( P < 0.01 vs. NP) and 162 ± 7.7 mmHg for PP ( P < 0.01 vs. NP). The amount of myogenic tone was also significantly diminished at 175 mmHg compared with NP: percent tone for NP, LP, and PP animals were 35 ± 2, 11 ± 3 ( P < 0.01 vs. NP), and 20 ± 7% ( P < 0.01 vs. NP), respectively. Inhibition of nitric oxide (NO) with 0.1 mM Nω-nitro-l-arginine (l-NNA) caused constriction of all vessel types that was significantly increased in the PP arteries, which demonstrates significant basal NO production. Reactivity to 5-hydroxytryptamine (serotonin) was assessed in the presence of l-NNA and indomethacin. There was a differential response to serotonin: PCAs from NP animals dilated, whereas LP and PP arteries constricted. These results suggest that both pregnancy and the postpartum period predispose the cerebral circulation to FD at lower pressures, a response that may lower cerebrovascular resistance and promote hyperperfusion when blood pressure is elevated, as occurs during eclampsia.


Stroke ◽  
2006 ◽  
Vol 37 (3) ◽  
pp. 894-899 ◽  
Author(s):  
Matthew J. Maneen ◽  
Rachael Hannah ◽  
Lisa Vitullo ◽  
Nicole DeLance ◽  
Marilyn J. Cipolla

1999 ◽  
Vol 82 (3) ◽  
pp. 1339-1351 ◽  
Author(s):  
Colin G. Evans ◽  
Ferdinand S. Vilim ◽  
Orna Harish ◽  
Irving Kupfermann ◽  
Klaudiusz R. Weiss ◽  
...  

We observed fibers immunoreactive (IR) to serotonin (5-HT), the myomodulins (MMs), and FMRFamide on the I7-I10 complex in the marine mollusk Aplysia californica. The I7–I10 muscle complex, which produces radula opening, is innervated primarily by one motor neuron, B48. B48 is MM-IR and synthesizes authentic MMA. When B48 is stimulated in a physiological manner, cAMP levels are increased in opener muscles. cAMP increases also are seen when the MMs are applied to opener muscles but are not seen with application of the B48 primary neurotransmitter acetylcholine (ACh). Possible physiological sources of 5-HT and FMRFamide are discussed. When modulators are applied to resting opener muscles, changes in membrane potential are observed. Specifically, 5-HT, MMB, and low concentrations of MMA all depolarize muscle fibers. This depolarization is generally not sufficient to elicit myogenic activity in the absence of neural activity under “rest” conditions. However, if opener muscles are stretched beyond rest length, stretch- and modulator-induced depolarizations can summate and elicit contractions. This only occurs, however, if “depolarizing” modulators are applied alone. Thus other modulators (i.e., FMRFamide and high concentrations of MMA) hyperpolarize opener muscle fibers and can prevent depolarizing modulators from eliciting myogenic activity. All modulators tested affected parameters of motor neuron-elicited contractions of opener muscles. MMB and 5-HT increased contraction size over the range of concentrations tested, whereas MMA potentiated contractions when it was applied at lower concentrations but decreased contraction size at higher concentrations. FMRFamide decreased contraction size at all concentrations and did not affect relaxation rate. Additionally, the MMs and 5-HT increased muscle relaxation rate, decreased contraction latency, and decreased the rate at which tension was developed during motor neuron-elicited muscle contractions. Thus these modulators dramatically affect the ability of opener muscles to follow activity in the opener motor neuron B48. The possible physiological significance of these findings is discussed.


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