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The Role of Macrophage Migration Inhibitory Factor (MIF) in the Paraventricular Nucleus (PVN) During Acute Stress
Author(s) -
Erdos Benedek,
Clifton Rebekah,
McCowan Michael L.,
Sumners Colin,
Scheuer Deborah A.
Publication year - 2012
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.26.1_supplement.1091.72
Subject(s) - endocrinology , medicine , baroreflex , downregulation and upregulation , macrophage migration inhibitory factor , angiotensin ii , blood pressure , inhibitory postsynaptic potential , sympathetic nervous system , chemistry , heart rate , cytokine , biochemistry , gene
We previously demonstrated that MIF is upregulated by angiotensin II (AngII) in the PVN of normotensive animals and counteracts the pressor action of AngII. In contrast, AngII fails to upregulate MIF in spontaneously hypertensive (SHR) rats, but overexpression of MIF reduces blood pressure (BP) in SHRs. Here, we investigated whether MIF is involved in BP regulation in normotensive Sprague‐Dawley (SD) rats during acute stress and under resting conditions. BP was measured with telemetry and AAV2‐GFP (n=8) or AAV2‐MIF (n=8) was injected bilaterally into the PVN. Responses to 1hr restraint stress (RS) and 15 min water stress (WS, 1cm deep, 25 °C) were evaluated. Unlike in SHRs, MIF overexpression had no effect on baseline BP in SD rats, and did not influence the amplitude of BP and HR responses to RS or WS. However, recovery time following WS was shorter in MIF‐ vs GFP‐treated rats (24±2 vs 30±3 min). In addition, spontaneous baroreflex sensitivity (sBRS) analyzed by the sequence method tended to increase following MIF treatment (from 1.74±0.14 to 1.94±0.15 ms/mmHg, P=0.07), while power in the LF range of BP variability spectrum indicating sympathetic nervous system influence on vasculature tended to decrease (from 2.83±0.32 to 2.48±0.24 mmHg 2 ; P=0.06). In conclusion, in normotensive animals, MIF overexpression has only subtle effects on BP regulatory mechanisms. Supported by NIH #HL93186 (MPI).