Longitudinal differences in vascular control mechanisms in isolated resistance arteries of the rat cremaster muscle.
The purpose of this study was to determine if there are intrinsic differences in resting tone, vascular reactivity, myogenic responses, and neurogenic vasoconstriction between the large and small feeder arteries and first order arterioles (1A) of the rat cremaster muscle. The pudic-epigastric artery (PEA), external spermatic artery (ESA), and 1A were isolated and changes in vessel diameter were recorded in response to: (1) increases in intralumenal pressure, (2) inhibition of nitric oxide synthase (NOS), (3) norepinephrine (NE), (4) acetylcholine (ACh), and (5) perivascular nerve stimulation. Vessel responses to Ca(2+)-free physiological salt solution were measured to assess resting tone, which was significantly greater in the ESA and 1A compared to the PEA. NE caused a significant constriction of all vessels, with 1A exhibiting the greatest sensitivity. NOS inhibition did not alter vascular sensitivity to NE, but enhanced resting tone in ESA and 1A. ACh induced significant dilation in ESA and 1A, with minimal effect on PEA. The myogenic response was not different between ESA and 1A, but was minimal in PEA. Perivascular nerve stimulation induced a significant vasoconstriction in all vessels tested. These results suggest that the relative importance of different vascular control mechanisms varies substantially at different levels of the cremasteric arterial network and that the ESA and 1A may be the major site of active vascular regulation upstream from the cremaster muscle microcirculation.
Sylvester
F A
FA
Department of Physiology, Medical College of Wisconsin, Milwaukee, 53226, USA.
Frisbee
J C
JC
Lombard
J H
JH
D000818:Animals; D001158:Arteries / Q000294:innervation / Q000502:physiology*; D001341:Autonomic Nervous System / Q000502:physiology; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014655:Vascular Resistance / Q000502:physiology*