Hypertension attenuates cell-to-cell communication in hamster retractor muscle feed arteries.
This study examined whether hypertension attenuated cell-to-cell communication in skeletal muscle resistance arteries. Briefly, arteries feeding the retractor muscle of normotensive and hypertensive hamsters were cannulated, pressurized, and superfused with a physiological saline solution. Cell-to-cell communication was functionally assessed by application of vasoactive stimuli (via micropipette) to a small portion of a feed artery while diameter at sites distal to the point of agent application was monitored. In keeping with past observations, discrete application of a smooth muscle depolarizing agent (phenylephrine or KCl) elicited a localized vasoconstriction that conducted poorly along feed arteries from normotensive hamsters. In contrast, acetylcholine, an agent known to hyperpolarize endothelial cells, elicited a vasodilation in normotensive feed arteries that conducted with little decay. Whereas smooth muscle depolarizing agents continued to elicit a localized response, conduction of endothelium-dependent vasodilation was attenuated in hypertensive hamsters. This decrease occurred in the absence of changes in vessel reactivity to intravascular pressure or to global application of phenylephrine, U-46619, or acetylcholine. We propose, on the basis of these physiological observations, quantitative mRNA measurements of connexins 37, 40, 43, and 45, and analysis of the literature, that an increase in endothelial-to-endothelial or smooth muscle-to-endothelial coupling resistance is likely responsible for hypertension-induced impairment in vascular communication. We hypothesize that this attenuation could contribute to the rise in total peripheral resistance characteristically observed in hypertension.
Kurjiaka
David T
DT
Department of Biological Sciences, Ohio University, Athens, Ohio, USA.
Bender
Shawn B
SB
Nye
Darin D
DD
Wiehler
William B
WB
Welsh
Donald G
DG
D000818:Animals; D001158:Arteries / Q000166:cytology* / Q000502:physiology*; D002450:Cell Communication / Q000502:physiology*; D017630:Connexins / Q000235:genetics; D006224:Cricetinae; D004730:Endothelium, Vascular / Q000166:cytology / Q000502:physiology; D017629:Gap Junctions / Q000502:physiology; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology*; D018482:Muscle, Skeletal / Q000098:blood supply*; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000502:physiology; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014664:Vasodilation / Q000502:physiology
D017630:Connexins; D012333:RNA, Messenger