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

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.