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Aldosterone impairs baroreflex sensitivity in humans
Author(s) -
Monahan Kevin D.,
Leuenberger Urs A.,
Dyckman Damian J.,
Ray Chester A.
Publication year - 2006
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.20.5.a1428-b
Animal studies suggest that acute and chronic aldosterone administration impairs baroreflex sensitivity (BRS). In several human cardiovascular disease states aldosterone levels are elevated (e.g., congestive heart failure and renovascular hypertension) and baroreflex dysfunction occurs. It is unknown if these events are mechanistically linked. We tested the hypothesis that aldosterone impairs baroreflex control of cardiac period (cardiovagal BRS) and muscle sympathetic nerve activity (MSNA: sympathetic BRS) in humans. BRS was determined (modified Oxford technique) in 16 young subjects (25±1 yr) before (Pre) and 30 min after (Post) beginning either an aldosterone infusion (12 pmol/kg/min) or saline infusion (control). Cardiovagal BRS was quantified from the systolic blood pressure (BP)‐RR interval relation and sympathetic BRS from the diastolic BP‐MSNA relation. Aldosterone infusion increased aldosterone levels ~4‐fold (8.7±1.3 vs. 32.8±4.8 ng/dl for Pre and Post, respectively; P<0.01). Aldosterone did not change heart rate (58±3 vs. 59±3 beats/min), but increased mean BP (84±3 vs. 86±4 mmHg; P<0.05) and MSNA at rest (9±2 vs. 11±1 bursts/min; P=0.07). Both cardiovagal (18.9±2.3 vs. 15.6±1.2 ms/mmHg) and sympathetic BRS (−4.4±0.4 vs. −3.0±0.4 au/beat/mmHg) were decreased by aldosterone infusion (P<0.05). In contrast in control subjects neither cardiovagal nor sympathetic BRS were changed (Pre vs. Post). These data support the concept that aldosterone impairs cardiovagal and sympathetic BRS in humans. Therefore, aldosterone may be an important determinant of BRS in health and disease. Support: NIH DC006459 , HL77670, M01 RR10732; NSBRI CA00404