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Lisinopril Improves Cutaneous Microvascular Function in Hypertensive Men and Women
Author(s) -
Craighead Daniel,
Kenney W Larry,
Alexander Lacy
Publication year - 2015
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.29.1_supplement.994.1
Subject(s) - lisinopril , vasodilation , medicine , endocrinology , microdialysis , angiotensin converting enzyme , nitric oxide , endothelial dysfunction , sodium nitroprusside , arginase , acetylcholine , chemistry , pharmacology , blood pressure , arginine , biochemistry , amino acid , central nervous system
Hypertension is a chronic disease that induces microvascular dysfunction through upregulation of arginase and inducible nitric oxide synthase (iNOS) resulting in a loss of endothelial (e)NOS‐dependent vasodilation. Angiotensin converting enzyme inhibitors may have off‐target beneficial vascular effects on endothelial signaling and microvessel structure. We hypothesized that treatment with Lisinopril (>3 month) would improve cutaneous microvascular function in hypertensive adults. Four intradermal microdialysis fibers were placed in the forearm skin of 6 controlled hypertensive subjects (Lisinopril (LIS): MAP 94 mmHg), 9 hypertensive (HTN: MAP 111 mmHg) and 10 age matched normotensive (NTN: MAP 86 mmHg) subjects. Ringer's solution (control), 20mM L‐NAME (NOS inhibited), 0.1mM 1400w (iNOS inhibited), and 5mM BEC (arginase inhibited) were perfused through the fibers. Red cell flux was measured by laser‐Doppler flowmetry (LDF) during an acetylcholine (ACh) dose‐response (0.01mM‐100mM ACh). Cutaneous vascular conductance (CVC=LDF/MAP) was calculated and normalized to a percent of maximum (%CVC max : 28mM SNP). SNP‐induced maximum vasodilation (CVC max ) was also assessed. There were no differences in ACh‐induced vasodilation between the LIS and NTN groups. LIS treatment improved %CVC max responses to ACh compared to unmedicated HTN (all ACh doses 蠅 1mM p<0.05). Neither iNOS nor arginase inhibition altered the %CVC max response to ACh in the LIS group (vs. control site). CVC max was attenuated in HTN (1.57 ± 0.6 vs NTN 1.75 ± 0.6, p<0.05) and not improved in LIS (1.64 ± 0.5, p=0.33). These data suggest that pharmacotherapy for essential hypertension with Lisinopril improves eNOS‐dependent but not SNP‐induced maximal vasodilation in hypertensive adults. NIH R01 HL089302