Differences in pericyte contractile function in rat cardiac and skeletal muscle microvasculatures

Ronald Tilton, Charles Kilo, Joseph R. Williamson, Donald W. Murch

Research output: Contribution to journalArticle

104 Citations (Scopus)

Abstract

In order to evaluate contractile activity of pericytes, rat hearts and hindlimbs were perfused separately with angiotensin (1 μg/ml), norepinephrine (1 μg/ml), or vasopressin (10-3 U/ml) for 3 min, fixed by perfusion, then processed for electron microscopy and morphometry. An electronic planimeter was employed to quantify configurational alterations (buckling) of endothelium between pericyte processes which provided an index of pericyte contraction (PCI). Inherent in this technique is the assumption that contracting pericytes distort and convolute endothelial cell membranes (increasing the PCI) abutting pericytes, but do not affect endothelial configuration elsewhere around the capillary circumference. PCI values were virtually identical in control hearts and skeletal muscle and in low-flow hindlimb perfusions (101.2 ± 0.3% (SD), 101.2 ± 0.7%, and 102.3 ± 0.8%, respectively). All three vasoactive agents increased perfusion pressure significantly in both hearts and hindlimbs with one exception (norepinephrine produced a slight pressure drop in hearts). While perfusion with vasoactive agents had no effect on the cardiac PCI, skeletal PCI values were markedly elevated for all three vasoactive agents (124.1 ± 8.2, 118.7 ± 4.9, and 120.2 ± 6.8% for angiotensin, norepinephrine, and vasopressin, respectively). Marked buckling of endothelium in apposition with pericytes and the absence of such changes elsewhere in the vessel wall were documented in morphologic studies of drug-perfused skeletal muscle. In both control hearts and hindlimbs and drug-perfused hearts, endothelial configuration in apposition with pericytes did not differ from the rest of the vessel. These observations, together with ultrastructural and morphometric data documenting much more extensive interaction between pericytes and endothelium in skeletal than in cardiac muscle, strongly suggest that pericytes in rat hindlimb skeletal muscle constrict in response to selected vasoactive agents while those in cardiac muscle do not.

Original languageEnglish (US)
Pages (from-to)336-352
Number of pages17
JournalMicrovascular Research
Volume18
Issue number3
DOIs
StatePublished - 1979
Externally publishedYes

Fingerprint

Pericytes
Microvessels
Muscle
Rats
Myocardium
Skeletal Muscle
Hindlimb
Perfusion
Endothelium
Norepinephrine
Angiotensins
Vasopressins
Buckling
Planimeters
Pressure
Endothelial cells
Cell membranes
Pharmaceutical Preparations
Electron microscopy
Pressure drop

ASJC Scopus subject areas

  • Biochemistry
  • Cardiology and Cardiovascular Medicine

Cite this

Differences in pericyte contractile function in rat cardiac and skeletal muscle microvasculatures. / Tilton, Ronald; Kilo, Charles; Williamson, Joseph R.; Murch, Donald W.

In: Microvascular Research, Vol. 18, No. 3, 1979, p. 336-352.

Research output: Contribution to journalArticle

Tilton, Ronald ; Kilo, Charles ; Williamson, Joseph R. ; Murch, Donald W. / Differences in pericyte contractile function in rat cardiac and skeletal muscle microvasculatures. In: Microvascular Research. 1979 ; Vol. 18, No. 3. pp. 336-352.
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abstract = "In order to evaluate contractile activity of pericytes, rat hearts and hindlimbs were perfused separately with angiotensin (1 μg/ml), norepinephrine (1 μg/ml), or vasopressin (10-3 U/ml) for 3 min, fixed by perfusion, then processed for electron microscopy and morphometry. An electronic planimeter was employed to quantify configurational alterations (buckling) of endothelium between pericyte processes which provided an index of pericyte contraction (PCI). Inherent in this technique is the assumption that contracting pericytes distort and convolute endothelial cell membranes (increasing the PCI) abutting pericytes, but do not affect endothelial configuration elsewhere around the capillary circumference. PCI values were virtually identical in control hearts and skeletal muscle and in low-flow hindlimb perfusions (101.2 ± 0.3{\%} (SD), 101.2 ± 0.7{\%}, and 102.3 ± 0.8{\%}, respectively). All three vasoactive agents increased perfusion pressure significantly in both hearts and hindlimbs with one exception (norepinephrine produced a slight pressure drop in hearts). While perfusion with vasoactive agents had no effect on the cardiac PCI, skeletal PCI values were markedly elevated for all three vasoactive agents (124.1 ± 8.2, 118.7 ± 4.9, and 120.2 ± 6.8{\%} for angiotensin, norepinephrine, and vasopressin, respectively). Marked buckling of endothelium in apposition with pericytes and the absence of such changes elsewhere in the vessel wall were documented in morphologic studies of drug-perfused skeletal muscle. In both control hearts and hindlimbs and drug-perfused hearts, endothelial configuration in apposition with pericytes did not differ from the rest of the vessel. These observations, together with ultrastructural and morphometric data documenting much more extensive interaction between pericytes and endothelium in skeletal than in cardiac muscle, strongly suggest that pericytes in rat hindlimb skeletal muscle constrict in response to selected vasoactive agents while those in cardiac muscle do not.",
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