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Treatment of cerebral small vessel disease with relaxin
Author(s) -
Chan SiuLung,
Cipolla Marilyn
Publication year - 2013
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.27.1_supplement.709.1
Subject(s) - relaxin , medicine , endocrinology , perfusion , parenchyma , white matter , cardiology , blood pressure , hormone , pathology , magnetic resonance imaging , radiology
Cerebral small vessel disease (SVD) associated with hypertension is a common cause of vascular cognitive impairment thought to be due to inward remodeling of brain parenchymal arterioles (PA) and white matter hypoperfusion. Here, we examined structural remodeling of PA in spontaneous hypertensive (SHR) and Wistar‐Kyoto rats (WKY; n=8/group) and if treatment with relaxin (4 μg/hr, osmotic pump for 2 wks), a peptide hormone shown to selectively enlarge PA, could reverse structural remodeling in SHR. PA were dissected from the brain parenchyma and studied pressurized in an arteriograph for passive structural measurements. PA from SHR had significantly smaller inner and outer diameters than WKY (49±3 vs. 58±3 μm and 62±3 vs. 71±3 μm at 60 mmHg; p<0.01) that was reversed by relaxin treatment (56±4 and 67±4 μm; p<0.01 vs. SHR). Relaxin treatment of SHR also increased PA distensibility (34±3 vs. 10±2 % in SHR at 60 mmHg; p<0.01) without affecting blood pressure (MAP with and without relaxin in SHR: 140±5 vs.138±2 mmHg). In summary, chronic hypertension caused inward remodeling in PA that was reversed by relaxin treatment. The effect of relaxin on PA diameter and distensibility may improve perfusion to the white matter in chronic hypertension and thus may improve cerebral SVD. This study is supported by NIH NS045940 and HL095488.