title: Diameter dependence of myogenic tone of human pial arteries. Possible relation to distensibility.
abstract: OBJECTIVE
  Responses to changes in intraluminal pressure of isolated human pial arteries (200 to 1200 microns i.d.) obtained from patients undergoing neurosurgery were measured.
  
  
  METHODS
  The vessels were cannulated and pressurized (60 mm Hg); vascular diameter and intraluminal pressure were recorded simultaneously. After spontaneous development of steady state tone, intraluminal pressure was changed to both higher and lower levels in random sequence.
  
  
  RESULTS
  Human pial arteries exhibited myogenic responses and maintained their diameter over the pressure range of 20 to 100 mm Hg. The level of myogenic tone observed at 30 mm Hg did not vary significantly with artery diameter. In contrast, at 60 and 90 mm Hg, the extent of myogenic tone increased as the diameter decreased (up to 70% to 80% of maximum in 200-microns i.d. arteries). The arteries contracted to KCl 30 mmol/L, norepinephrine 1 mumol/L, and vasopressin 0.1 mumol/L and relaxed to acetylcholine 3 mumol/L. The extent of these responses did not vary with the diameter of the artery. Arterial distensibility, represented by the slope of the tangent of the passive pressure-diameter curve at lower pressures (5 to 50 mm Hg), increased as arteries became smaller. This is consistent with the possibility that the level of myogenic tone is related to vessel distensibility. Human omental arteries of comparable size did not develop myogenic tone but contracted to KCl and norepinephrine and relaxed to acetylcholine to an extent similar to pial arteries.
  
  
  CONCLUSIONS
  There is a specific gradient of myogenic responsiveness in human pial arteries that varies inversely with their diameter. This tone does not develop in all vascular beds. These levels of tone in the pial circulation would be expected to be of profound functional significance by allowing blood flow to vary widely.
authors.affiliation: Totman Laboratory for Human Cerebrovascular Research, Department of Pharmacology, University of Vermont, Burlington 05405-0068, USA.
authors.forename: N
authors.initials: N
authors.lastname: Thorin-Trescases
authors.forename: T
authors.initials: T
authors.lastname: Bartolotta
authors.forename: N
authors.initials: N
authors.lastname: Hyman
authors.forename: P L
authors.initials: PL
authors.lastname: Penar
authors.forename: C L
authors.initials: CL
authors.lastname: Walters
authors.forename: R D
authors.initials: RD
authors.lastname: Bevan
authors.forename: J A
authors.initials: JA
authors.lastname: Bevan
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000375:Aging / Q000502:physiology; D001158:Arteries / Q000502:physiology; D004548:Elasticity; D005260:Female; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D008875:Middle Aged; D009129:Muscle Tonus / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009852:Omentum / Q000098:blood supply; D010841:Pia Mater / Q000098:blood supply*; D011312:Pressure; D014666:Vasomotor System / Q000502:physiology*