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Effects of mechanical unloading on vasoconstriction dynamics in mesenteric resistance vessels

Bradley J. Behnke, Rhonda D. Prisby, Michael D. Delp

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Abstract

Cephalic fluid shifts inducedby head-down tilt and microgravity alter cardiovascular regulation, resulting in an attenuated ability to regulate blood pressure with sudden postural changes and possibly resulting in orthostatic hypotension. PURPOSE We tested the hypothesis that, consequent to mechanical unloading, mesenteric resistance arteries would demonstrate blunted vasoconstriction dynamics (i.e., slower rate of constriction) versus that of vessels from control animals. METHODS Mesenteric resistance arteries from control (C) and 14-day head-down tail suspension (HDT) rats (6 mo. male Sprague-Dawley) were isolated, cannulated and the rate and magnitude of vasoconstriction to norepinephrine (10−4 M) was quantified via real-time, frame-by-frame analysis (30 frames/s) of luminal diameter. RESULTS Upon exposure to NE, vessels from HDT demonstrated a longer delay before the onset of constriction (HDT, 1.8 ± 0.2 vs. C, 0.9 ± 0.1 s) and a reduced rate of constriction (HDT, 8.4 ± 2.1 vs. C, 13.6 ± 2.6 μm/s). In addition, the time to the steady-state constriction (i.e., no further changes in luminal diameter) was longer in the vessels from HDT rats (HDT, 11.4 ± 1.0 vs. C, 8.0 ± 0.5 s). DISCUSSION These results (i.e., slower rate of vasoconstriction) may provide a mechanistic basis for the increased rate of post-flight orthostatic intolerance. Supported by NASA grant NCC2-1166.

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Cephalic fluid shifts inducedby head-down tilt and microgravity alter cardiovascular regulation, resulting in an attenuated ability to regulate blood pressure with sudden postural changes and possibly resulting in orthostatic hypotension. PURPOSE We tested the hypothesis that, consequent to mechanical unloading, mesenteric resistance arteries would demonstrate blunted vasoconstriction dynamics (i.e., slower rate of constriction) versus that of vessels from control animals. METHODS Mesenteric resistance arteries from control (C) and 14-day head-down tail suspension (HDT) rats (6 mo. male Sprague-Dawley) were isolated, cannulated and the rate and magnitude of vasoconstriction to norepinephrine (10−4 M) was quantified via real-time, frame-by-frame analysis (30 frames/s) of luminal diameter. RESULTS Upon exposure to NE, vessels from HDT demonstrated a longer delay before the onset of constriction (HDT, 1.8 ± 0.2 vs. C, 0.9 ± 0.1 s) and a reduced rate of constriction (HDT, 8.4 ± 2.1 vs. C, 13.6 ± 2.6 μm/s). In addition, the time to the steady-state constriction (i.e., no further changes in luminal diameter) was longer in the vessels from HDT rats (HDT, 11.4 ± 1.0 vs. C, 8.0 ± 0.5 s). DISCUSSION These results (i.e., slower rate of vasoconstriction) may provide a mechanistic basis for the increased rate of post-flight orthostatic intolerance. Supported by NASA grant NCC2-1166.

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Available abstract

Cephalic fluid shifts inducedby head-down tilt and microgravity alter cardiovascular regulation, resulting in an attenuated ability to regulate blood pressure with sudden postural changes and possibly resulting in orthostatic hypotension. PURPOSE We tested the hypothesis that, consequent to mechanical unloading, mesenteric resistance arteries would demonstrate blunted vasoconstriction dynamics (i.e., slower rate of constriction) versus that of vessels from control animals. METHODS Mesenteric resistance arteries from control (C) and 14-day head-down tail suspension (HDT) rats (6 mo. male Sprague-Dawley) were isolated, cannulated and the rate and magnitude of vasoconstriction to norepinephrine (10−4 M) was quantified via real-time, frame-by-frame analysis (30 frames/s) of luminal diameter. RESULTS Upon exposure to NE, vessels from HDT demonstrated a longer delay before the onset of constriction (HDT, 1.8 ± 0.2 vs. C, 0.9 ± 0.1 s) and a reduced rate of constriction (HDT, 8.4 ± 2.1 vs. C, 13.6 ± 2.6 μm/s). In addition, the time to the steady-state constriction (i.e., no further changes in luminal diameter) was longer in the vessels from HDT rats (HDT, 11.4 ± 1.0 vs. C, 8.0 ± 0.5 s). DISCUSSION These results (i.e., slower rate of vasoconstriction) may provide a mechanistic basis for the increased rate of post-flight orthostatic intolerance. Supported by NASA grant NCC2-1166.

Key concepts: Vasoconstriction, Constriction, Vascular resistance, Internal medicine, Medicine, Mesenteric arteries, Orthostatic vital signs, Cardiology

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