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Role of vascular dysfunction in prostate tumor perfusion during exercise
Author(s) -
McCullough Danielle J.,
Siemann Dietmar W,
Behnke Bradley J
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1136.15
Subject(s) - vasoconstriction , perfusion , prostate , medicine , endocrinology , vasodilation , norepinephrine , myogenic contraction , vascular resistance , adrenergic , in vivo , blood pressure , biology , cancer , smooth muscle , receptor , microbiology and biotechnology , dopamine
During exercise, blood flow to inactive tissues is reduced through changes in vascular tone elicited largely by the autonomic nervous system. However, in tumors the reduced innervation of feed arteries and possibly blunted adrenergic vasoconstriction may lead to an increased tumor perfusion during exercise. We used control (CON; n=16) and prostate tumor bearing (TB; n=14) Copenhagen rats to test the hypothesis that α‐adrenergic (via norepinephrine; NE) and myogenic vasoconstrictor responses are diminished in the prostatic tumor feed arteries (PTA), resulting in an increased tumor perfusion during exercise. Dunning R‐3327 MatLyLu tumor cells (10 4 ) were injected into the ventral prostates of rats. PTA and prostate arteries (CON) were studied in vitro and exposed to cumulative additions of NE (10 −9 to 10 −4 M) and increases in intraluminal pressure (myogenic response; 0 to 135 cmH 2 O). In vivo quantification of perfused tumor vessels during rest and acute exercise (treadmill; 5 min) was determined using Hoechst‐33342 staining. Both α‐adrenergic (7 ± 6% vs. 88 ± 2%, p<0.05) and myogenic vasoconstriction were blunted in PTA versus CON, while the number of PTA perfused increased ~113% with exercise. These data suggest that dysfunction in the PTA results in an inability to augment vascular resistance during exercise, resulting in an enhanced tumor perfusion. Supp.: NIH (AG‐31317) & Florida Biomed. Res. Prog. (1BN‐02).