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How calcium signals in myocytes and pericytes are integrated across in situ microvascular networks and control microvascular tone.

Borysova L, Wray S, Eisner DA, Burdyga T - Cell Calcium (2013)

Bottom Line: Ca2+ signals vary between distributing arcade and downstream transverse and precapillary arterioles, are modified by agonists, with sympathetic agonists being ineffective beyond transverse arterioles.Increases of Ca2+ in pericytes and myocytes constrict all vessels except capillaries.These data reveal the structural and signalling specializations allowing blood flow to be regulated by myocytes and pericytes.

View Article: PubMed Central - PubMed

Affiliation: Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Crown Street, L69 3BX, UK.

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Ca2+ signalling and myocyte mediated constriction induced by PE, AVP and ET-1 in different sections of arteriolar network in situ. (A) Images of in situ ureteric AA (i), TA (ii), and PA (iii) in radial sections taken before (top panel) and during (bottom panel) exposure to 5 nM AVP. (B) Ca2+ oscillations and diameter changes of AA induced by 1 and 5 μM PE. Cell 1 (solid line) is responding throughout and cell 2 (dotted line) only when the concentration of PE was increased to 5 μM. (C) Mean data showing vasoconstriction produced by a single cell contraction (black bar) and high frequency Ca2+ oscillations caused by maximal concentration of PE (green bar), AVP (yellow bar), and ET-1 (cyan bar) in all sections of arteriolar network. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of the article.)
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fig0020: Ca2+ signalling and myocyte mediated constriction induced by PE, AVP and ET-1 in different sections of arteriolar network in situ. (A) Images of in situ ureteric AA (i), TA (ii), and PA (iii) in radial sections taken before (top panel) and during (bottom panel) exposure to 5 nM AVP. (B) Ca2+ oscillations and diameter changes of AA induced by 1 and 5 μM PE. Cell 1 (solid line) is responding throughout and cell 2 (dotted line) only when the concentration of PE was increased to 5 μM. (C) Mean data showing vasoconstriction produced by a single cell contraction (black bar) and high frequency Ca2+ oscillations caused by maximal concentration of PE (green bar), AVP (yellow bar), and ET-1 (cyan bar) in all sections of arteriolar network. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of the article.)

Mentions: The aim of experiments such as that illustrated in Fig. 4 was to investigate whether the observed calcium signals were sufficient to close or constrict the vessels or produce vasomotion (Supplementary Movie 6). Fig. 4B shows that low frequency (<0.05 Hz) Ca2+ oscillations induced by a low concentration of PE (1 μM) resulted in only uncoordinated transient twitching of individual myocytes associated with local vasomotion. Similar results were seen with low concentrations of AVP and ET-1 throughout the arteriolar network. We found that the functional impact of single cell contraction depended upon the diameter of the microvessel and was maximal in the smallest vessels; thus in the precapillary arterioles contraction of one cell was sufficient to produce occlusion (Fig. 4C, black bar), but this was not the case in larger diameter vessels. Increasing the agonist concentration increased the frequency of oscillations (Fig. 4B and C) and thence constriction. The higher frequency of Ca2+ oscillations in the myocytes of transverse and precapillary arterioles induced a substantially greater arteriolar constriction (Fig. 4C; Supplementary Movie 6).


How calcium signals in myocytes and pericytes are integrated across in situ microvascular networks and control microvascular tone.

Borysova L, Wray S, Eisner DA, Burdyga T - Cell Calcium (2013)

Ca2+ signalling and myocyte mediated constriction induced by PE, AVP and ET-1 in different sections of arteriolar network in situ. (A) Images of in situ ureteric AA (i), TA (ii), and PA (iii) in radial sections taken before (top panel) and during (bottom panel) exposure to 5 nM AVP. (B) Ca2+ oscillations and diameter changes of AA induced by 1 and 5 μM PE. Cell 1 (solid line) is responding throughout and cell 2 (dotted line) only when the concentration of PE was increased to 5 μM. (C) Mean data showing vasoconstriction produced by a single cell contraction (black bar) and high frequency Ca2+ oscillations caused by maximal concentration of PE (green bar), AVP (yellow bar), and ET-1 (cyan bar) in all sections of arteriolar network. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of the article.)
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3775125&req=5

fig0020: Ca2+ signalling and myocyte mediated constriction induced by PE, AVP and ET-1 in different sections of arteriolar network in situ. (A) Images of in situ ureteric AA (i), TA (ii), and PA (iii) in radial sections taken before (top panel) and during (bottom panel) exposure to 5 nM AVP. (B) Ca2+ oscillations and diameter changes of AA induced by 1 and 5 μM PE. Cell 1 (solid line) is responding throughout and cell 2 (dotted line) only when the concentration of PE was increased to 5 μM. (C) Mean data showing vasoconstriction produced by a single cell contraction (black bar) and high frequency Ca2+ oscillations caused by maximal concentration of PE (green bar), AVP (yellow bar), and ET-1 (cyan bar) in all sections of arteriolar network. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of the article.)
Mentions: The aim of experiments such as that illustrated in Fig. 4 was to investigate whether the observed calcium signals were sufficient to close or constrict the vessels or produce vasomotion (Supplementary Movie 6). Fig. 4B shows that low frequency (<0.05 Hz) Ca2+ oscillations induced by a low concentration of PE (1 μM) resulted in only uncoordinated transient twitching of individual myocytes associated with local vasomotion. Similar results were seen with low concentrations of AVP and ET-1 throughout the arteriolar network. We found that the functional impact of single cell contraction depended upon the diameter of the microvessel and was maximal in the smallest vessels; thus in the precapillary arterioles contraction of one cell was sufficient to produce occlusion (Fig. 4C, black bar), but this was not the case in larger diameter vessels. Increasing the agonist concentration increased the frequency of oscillations (Fig. 4B and C) and thence constriction. The higher frequency of Ca2+ oscillations in the myocytes of transverse and precapillary arterioles induced a substantially greater arteriolar constriction (Fig. 4C; Supplementary Movie 6).

Bottom Line: Ca2+ signals vary between distributing arcade and downstream transverse and precapillary arterioles, are modified by agonists, with sympathetic agonists being ineffective beyond transverse arterioles.Increases of Ca2+ in pericytes and myocytes constrict all vessels except capillaries.These data reveal the structural and signalling specializations allowing blood flow to be regulated by myocytes and pericytes.

View Article: PubMed Central - PubMed

Affiliation: Department of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Crown Street, L69 3BX, UK.

Show MeSH
Related in: MedlinePlus