Splanchnic vasoconstriction in heat-stressed men: role of renin-angiotensin system

Authors:
  • PEP. Escourrou
    P. Escourrou
  • PFP. R. Freund
    P. R. Freund
  • LRL. B. Rowell
    L. B. Rowell
  • DJD. G. Johnson
    D. G. Johnson
  • BMBrendan D. McNeely
    Brendan D. McNeely
  • RMRobert D. Meade
    Robert D. Meade
  • NFNaoto Fujii
    Naoto Fujii
  • ASAndrew J. E. Seely
    Andrew J. E. Seely
  • RSRonald J. Sigal
    Ronald J. Sigal
  • GKGlen P. Kenny
    Glen P. Kenny
  • JLJoshua F. Lee
    Joshua F. Lee
  • MHMichelle L. Harrison
    Michelle L. Harrison
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Abstract
We conducted a two-part study to determine whether the renin-angiotensin system contributes to the rise in splanchnic vascular resistance (SVR) during heat stress (rectal temperature was raised 1 degree C). In experiment 1 (control) seven men on a normal salt diet were directly heated (water-perfused suits) for 40–50 min. Arterial pressure (85 Torr) was unchanged; plasma renin activity (PRA) rose from 102 to 239 ng angiotensin I.100 ml-1.3 h-1; and SVR increased 73% (from 63 to 109 units). Experiment 2 was a repetition of experiment 1 on the same subjects, except that propranolol (10 mg iv) was given at the onset of heating to block renin release. Propranolol attenuated the rise in heart rate and reduced mean arterial pressure from 82 to 72 Torr; it blocked the rise in PRA with heating in two subjects, reduced it in three, but increased it in two. Although changes in SVR paralleled those in PRA in three subjects, SVR still rose 60% (from 58 to 99 units) after PRA rise was blocked. In both experiments, plasma norepinephrine concentration rose indicating increased sympathetic nervous activity. During mild heat stress, increased PRA is not a major factor in the increase of SVR.