A comparison of angiotensin-converting enzyme inhibitors, calcium antagonists, beta-blockers and diuretic agents on reactive hyperemia in patients with essential hypertension: a multicenter study
Yukihito Higashi, MD, PhD*,
Shota Sasaki, MD*,
Keigo Nakagawa, MD*,
Tomohiro Ueda, MD*,
Atsunori Yoshimizu, MD*,
Satoshi Kurisu, MD*,
Hideo Matsuura, MD, PhD*,
Goro Kajiyama, MD, PhD* and
Tetsuya Oshima, MD, PhD
* First Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima, Japan
Department of Clinical Laboratory Medicine, Hiroshima University School of Medicine, Hiroshima, Japan

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Figure 1 Forearm blood flow at rest and during reactive hyperemia in the normotensive control subjects (n = 47), hypertensive patients treated with calcium antagonists (n = 175), ACE inhibitors (n = 51), beta-blockers (n = 14) and diuretic agents (n = 10) and untreated hypertensive patients (n = 46). Reactive hyperemia was impaired in hypertensive patients as compared with normotensive subjects (p < 0.01). Reactive hyperemia was greater in hypertensive patients treated with ACE inhibitors than in those treated with calcium antagonists (p < 0.01), beta-blockers (p < 0.01) and diuretic agents (p < 0.05) and untreated hypertensive patients (p < 0.01). Reactive hyperemia was similar among calcium antagonist, beta-blocker, diuretic agent and untreated groups.
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Figure 2 Maximal forearm blood flow after the sublingual administration of NTG in normotensive control subjects (n = 47), hypertensive patients treated with calcium antagonists (n = 175), ACE inhibitors (n = 51), beta-blockers (n = 14) and diuretic agents (n = 10) and untreated hypertensive patients (n = 46). Nitroglycerin-induced vasodilation was similar in all six groups.
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Figure 3 Forearm blood flow at rest and during reactive hyperemia after the administration of L-NMMA, an NO synthase inhibitor, or indomethacin, a prostaglandin synthesis inhibitor, in hypertensive patients treated with ACE inhibitors (n = 13) or other agents (n = 15) and in untreated hypertensive patients (n = 18). L-NMMA abolished the enhancement of reactive hyperemia in hypertensive patients treated with ACE inhibitors (top). Indomethacin did not affect reactive hyperemia in any group (bottom).
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