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Decreased angiotensin II response but unaltered cardiovascular pressor response to infused norepinephrine after sodium restriction and converting enzyme inhibition
Author(s) -
Mills Paul J,
Dimsdale Joel E,
Ziegler Michael G,
Nelesen Richard A,
Brown Marvin R
Publication year - 1993
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.1993.50
Subject(s) - captopril , norepinephrine , medicine , endocrinology , angiotensin ii , angiotensin converting enzyme , pressor response , adrenergic , renin–angiotensin system , pharmacology , chemistry , blood pressure , dopamine , heart rate , receptor
Although studies indicate that converting enzyme inhibitors such as captopril influence α‐adrenergic physiology, the data on α‐adrenergic physiology is inconsistent. This study therefore examined the effects of captopril (50 mg/day for 5 days) during sodium restriction on the pressor response and on angiotensin II and neuropeptide Y levels to infused norepinephrine (0.01 to 0.1 μg/kg/min) in 17 hypertensive and 27 normotensive subjects. Angiotensin II increased significantly in response to infused norepinephrine during placebo administration (p < 0.001) but not during captopril administration (p = 0.15). Neuropeptide Y levels decreased in response to captopril (p = 0.02). Despite these changes the pressor response to infused norepinephrine was unchanged with captopril. These data support the conclusion that the antihypertensive action of captopril is unrelated to alterations in norepinephrine‐mediated α‐adrenergic pressor regulation. The finding of a decrease in neuropeptide Y levels may have relevance to the therapeutic effects of captopril. Clinical Pharmacology and Therapeutics (1993) 53, 450–456; doi: 10.1038/clpt.1993.50