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Decrease in cardiovascular stress reactivity in AT 1A receptor knockout mice is stimulus intensity ‐ dependent
Author(s) -
Mayorov Dmitry,
Chavez Carolina A,
Choy Kwok H
Publication year - 2010
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.24.1_supplement.623.15
Subject(s) - endocrinology , phenylephrine , medicine , stimulation , shaker , agonist , stimulus (psychology) , knockout mouse , receptor , chemistry , blood pressure , psychology , physics , quantum mechanics , vibration , psychotherapist
Angiotensin AT 1A receptor knockout (AT 1A −/− ) mice have attenuated blood pressure (BP) responses to intense aversive stimuli including restraint or footshock. Conversely, BP responses to less intense aversive events, such as novelty or handling, appear to be unaltered in AT 1A −/− mice. In the present study, we examined whether this complexity relates to the intensity of aversive stimulation. AT 1A −/− (n=7) and AT 1A +/+ mice (n=7) were implanted with BP telemetry devices and subjected to 5‐min shaker stress of different intensities (40, 80 and 160 rpm). Shaker stress increased BP in an intensity‐dependent manner in AT 1A +/+ mice (+21±3, +25±3 and +33±2 mmHg, respectively). The BP rises during the low‐ and mid‐ intensity shaker were not altered in AT 1A −/− mice, whereas that to high‐intensity shaker was reduced by 25%. This reduction could not be ascribed to attenuated vascular reactivity to intense sympathetic stimulation, because intraperitoneal administration of the α 1 ‐adrenoreceptor agonist phenylephrine (0.1–5 μg/g) dose‐dependently increased BP in both strains, and these increases were similar at all doses tested. These data suggest that AT 1A receptors are essential for the full expression of the BP response to high‐ but not low‐aversive stimuli in mice. This selectivity appears to relate primarily to alterations in central stress processing rather than sympathetic vascular reactivity. NHMRC (Australia)