Hypertension compromises functional hyperemia in hamster feed arteries

Abstract

We tested whether hypertension reduces ascending vasodilation of feed arteries (FA) in response to skeletal muscle contraction. Diameter and RBC velocity were recorded in FA supplying the retractor muscle of spontaneously hypertensive (SHH) and normotensive hamsters (NH) during rhythmic contractions [40 Hz: 200 ms every 2 s for 1 min]. Blood flow into muscles was thereby evaluated concomitant with muscle force production. Neither resting nor maximal (SNP dilation) FA diameter (NH 87±4 and 122±5 μ m vs SHH, 86±7 and 114±6 μ m, respectively) or blood flow (NH, 46±10 and 170±18 nl/s vs SHH, 63±15 179±35 nl/s, respectively) were different between strains, nor was integrated muscle force production (NH, 3.0±0.2 N*sec vs SHH, 2.6±0.2 N*sec). Nevertheless, functional dilation of FA (10±2 μ m; n=12) in SHH was attenuated (p<0.05) vs. NH (16±2 μ m n=14). Impaired functional dilation of FA was underscored by a 61% decrease in hyperemic response of SHH vs NH (56±8 vs 35±7 nl/s, respectively; p<0.05). Blockade of AT-1 receptors (losartan, 10 μ M) increased FA dilation (from 6±2 to 14±2 μ m; p<0.05; n=4) and hyperemia (from 22±18 to 42±23 nl/s; p<0.05) to muscle contraction in the SHH. In accord with recent findings (AJP 288:H861–70, 2005) we suggest that compromised functional hyperemia in SHH reflects an AT-1-dependent decrease in the conduction of vasodilation into FA from intramuscular arterioles. UA FSG, NIH HL58732, NIH HL56786