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The restoration of cerebrovascular myogenic function after hemorrhagic stroke development in stroke prone hypertensive rats
Author(s) -
Smeda John Stanislaw,
Daneshtalab Noriko
Publication year - 2009
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.23.1_supplement.933.10
Subject(s) - stroke (engine) , medicine , nifedipine , constriction , blood pressure , depolarization , losartan , endocrinology , myograph , anesthesia , angiotensin ii , cardiology , calcium , artery , engineering , mechanical engineering
Hemorrhagic stroke (HS) development in Kyoto Wistar stroke prone hypertensive rats (SHRsp) is associated with the loss of pressure dependent constriction (PDC) in middle cerebral arteries (MCAs). We attempted to restore PDC by administering oral Captopril (CAP, 50 mg/kg/day) or Losartan (LOS, 35 mg/kg/day) treatment after stroke. MCAs were studied using a pressure myograph. MCAs from SHRsp with HS did not elicit constriction to a 100 mmHg pressure step or in response to PKC activation (phorbol dibutyrate 1μM, with 3μM nifedipine). Elevations in [K + ] o (80mM) produced depolarization with attenuated constriction. The MCAs from post stroke SHRsp also could not utilize the sarcoplasmic release of Ca 2+ to produce constraction (vasopressin 0.12 μM, with 3μM nifedipine). Post stroke CAP or LOS treatment restored these functions to pre‐stroke levels within 7 days without altering blood pressure. These functions deteriorated after 30 days of CAP treatment but were maintained past 100 days of LOS treatment. We believe that the loss of PDC after HS is produced by a dysfunctional PKC system and the presence of voltage gated Ca 2+ channel that exhibits an attenuated response to depolarization. The enhanced ability of LOS to restore these functions after HS may be related to the physiological benefits of maintaining high plasma angiotensin II in combination with AT‐1 receptor blockade.