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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 pericyte mediated constriction of precapillary arterioles, capillaries and postcapillary venules. (A) Images of PA (i), capillary (ii), and AV in tangential (iii) and radial (iv) optical sections before (top) and during (bottom) exposure to 5 nM ET-1. (B) Ca2+ transients induced by 5 nM AVP, 5 nM ET-1 and 60 mM KCl in pericytes of all sections of “pericytic” microvessels: PA, capillaries, CV and AV. (C and D) Pericyte Ca2+ transients and changes in diameter at pericyte site of the PA and the capillary induced by AVP (5 nM) and ET-1 (5 nM). (E) Ca2+ transients measured from two different pericytes (1 and 2) and reduction in the diameter of the AV induced by AVP (5 nM) and ET-1 (5 nM). (F) Mean data showing vasoconstriction at pericyte site of PA, TV and AV caused by AVP (yellow bar) and ET-1 (cyan bar).
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fig0015: Ca2+ signalling and pericyte mediated constriction of precapillary arterioles, capillaries and postcapillary venules. (A) Images of PA (i), capillary (ii), and AV in tangential (iii) and radial (iv) optical sections before (top) and during (bottom) exposure to 5 nM ET-1. (B) Ca2+ transients induced by 5 nM AVP, 5 nM ET-1 and 60 mM KCl in pericytes of all sections of “pericytic” microvessels: PA, capillaries, CV and AV. (C and D) Pericyte Ca2+ transients and changes in diameter at pericyte site of the PA and the capillary induced by AVP (5 nM) and ET-1 (5 nM). (E) Ca2+ transients measured from two different pericytes (1 and 2) and reduction in the diameter of the AV induced by AVP (5 nM) and ET-1 (5 nM). (F) Mean data showing vasoconstriction at pericyte site of PA, TV and AV caused by AVP (yellow bar) and ET-1 (cyan bar).

Mentions: In contrast to the data from smooth muscle cells, the responses seen in pericytes did not depend on location (n = 11–28). Thus increases of Ca2+ to AVP and ET-1 were seen at all locations but no pericytes in any vessel responded to PE or caffeine (Fig. 3A and B; Table 1; Supplementary Movie 5). Pericytes responded in an agonist specific manner to AVP and ET-1 (Fig. 3B). At low concentrations (1 nM), AVP produced either no response or elicited a single Ca2+ oscillation in all sections of pericytic microvessels (Table 1). At higher concentrations of AVP (5 nM) the signal changed from one oscillation to several in most pericytes throughout the network (Fig. 3E), with frequencies of 0.02–0.03 Hz (n = 18). In contrast to AVP, in all pericytes, ET-1 (1–5 nM) caused a single Ca2+ transient which decayed very slowly (Fig. 3B–E). Examination of Figs. 2 and 3 shows that there are obvious differences between the characteristics of the Ca2+ signals in myocytes and pericytes. Next we wished to investigate if these patterns of Ca2+ oscillations, which varied between vessels, led to differing functional responses in the microcirculatory vessels.


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 pericyte mediated constriction of precapillary arterioles, capillaries and postcapillary venules. (A) Images of PA (i), capillary (ii), and AV in tangential (iii) and radial (iv) optical sections before (top) and during (bottom) exposure to 5 nM ET-1. (B) Ca2+ transients induced by 5 nM AVP, 5 nM ET-1 and 60 mM KCl in pericytes of all sections of “pericytic” microvessels: PA, capillaries, CV and AV. (C and D) Pericyte Ca2+ transients and changes in diameter at pericyte site of the PA and the capillary induced by AVP (5 nM) and ET-1 (5 nM). (E) Ca2+ transients measured from two different pericytes (1 and 2) and reduction in the diameter of the AV induced by AVP (5 nM) and ET-1 (5 nM). (F) Mean data showing vasoconstriction at pericyte site of PA, TV and AV caused by AVP (yellow bar) and ET-1 (cyan bar).
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fig0015: Ca2+ signalling and pericyte mediated constriction of precapillary arterioles, capillaries and postcapillary venules. (A) Images of PA (i), capillary (ii), and AV in tangential (iii) and radial (iv) optical sections before (top) and during (bottom) exposure to 5 nM ET-1. (B) Ca2+ transients induced by 5 nM AVP, 5 nM ET-1 and 60 mM KCl in pericytes of all sections of “pericytic” microvessels: PA, capillaries, CV and AV. (C and D) Pericyte Ca2+ transients and changes in diameter at pericyte site of the PA and the capillary induced by AVP (5 nM) and ET-1 (5 nM). (E) Ca2+ transients measured from two different pericytes (1 and 2) and reduction in the diameter of the AV induced by AVP (5 nM) and ET-1 (5 nM). (F) Mean data showing vasoconstriction at pericyte site of PA, TV and AV caused by AVP (yellow bar) and ET-1 (cyan bar).
Mentions: In contrast to the data from smooth muscle cells, the responses seen in pericytes did not depend on location (n = 11–28). Thus increases of Ca2+ to AVP and ET-1 were seen at all locations but no pericytes in any vessel responded to PE or caffeine (Fig. 3A and B; Table 1; Supplementary Movie 5). Pericytes responded in an agonist specific manner to AVP and ET-1 (Fig. 3B). At low concentrations (1 nM), AVP produced either no response or elicited a single Ca2+ oscillation in all sections of pericytic microvessels (Table 1). At higher concentrations of AVP (5 nM) the signal changed from one oscillation to several in most pericytes throughout the network (Fig. 3E), with frequencies of 0.02–0.03 Hz (n = 18). In contrast to AVP, in all pericytes, ET-1 (1–5 nM) caused a single Ca2+ transient which decayed very slowly (Fig. 3B–E). Examination of Figs. 2 and 3 shows that there are obvious differences between the characteristics of the Ca2+ signals in myocytes and pericytes. Next we wished to investigate if these patterns of Ca2+ oscillations, which varied between vessels, led to differing functional responses in the microcirculatory vessels.

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