Arterial and arteriolar contributions to skeletal muscle functional hyperemia in spontaneously hypertensive rats.

During contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR), arteriolar dilation is of normal magnitude but tissue PO2 is significantly depressed relative to normotensive [Wistar-Kyoto (WKY)] rats. This study examined the possibility that this low PO2 results from suppressed dilation of the upstream arterial feed vessels and a limitation of muscle blood flow. Contraction-induced changes in vascular resistances (R) and conductances (G) were calculated for upstream (Rup, Gup), microvascular (Rst, Gst), and downstream (Rdown, Gdown) vascular segments from measurements of pressure and flow in the rostral feed artery and vein. Feed arteries were smaller in SHR than in WKY rats at rest and after contractions (rest, 63.0 +/- 2.6 vs. 86.0 +/- 4.8 microns; 2 Hz 84.0 +/- 4.5 vs. 111.0 +/- 7.3 microns; 8 Hz, 130.0 +/- 5.9 vs. 144.0 +/- 7.1 microns). However, relative increases [times control (xCT)] in diameter and flow were greater in SHR (8 Hz diam, 2.080 +/- 0.072 vs. 1.690 +/- 0.042 xCT; 8 Hz flow, 15.700 +/- 2.057 vs. 8.170 +/- 0.752 xCT). In both groups, Rup and Rst decreased 60-70 and 85-90% after 2- and 8-Hz contractions, respectively. However, segmental vascular conductances increased more in SHR than in WKY rats (8 Hz: Gup, 18.50 +/- 3.76 vs. 8.00 +/- 1.26 xCT; Gst, 19.90 +/- 3.73 vs. 10.10 +/- 0.96 xCT; Gdown, 8.80 +/- 1.70 vs. 5.50 +/- 0.88 xCT). Therefore, upstream arterial dilation is not suppressed during muscle contractions in SHR, and deficits in muscle blood flow and oxygen delivery cannot account for the abnormally low tissue PO2 observed during muscle contractions in SHR.