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Muscle metaboreflex‐induced increases in ventricular performance are limited in hypertension due to exaggerated coronary vasoconstriction
Author(s) -
Spranger Marty D.,
SalaMercado Javier A.,
Kaur Jasdeep,
AbuHamdah Rania,
O'Leary Donal S.
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.1118.16
Subject(s) - cardiology , medicine , vasoconstriction , hemodynamics , blood flow , blood pressure , anesthesia
Increases in myocardial O2 consumption mainly occur via increases in coronary blood flow (CBF) inasmuch as cardiac O2 extraction is high even at rest. However, during exercise sympathetically‐mediated constrictor tone can limit increases in CBF. Increased sympathetic activity during exercise may stem from muscle metaboreflex activation (MMA). Sympathetic activity is often elevated even at rest in subjects with hypertension (HTN). We tested whether HTN causes exaggerated coronary vasoconstriction during mild exercise with MMA which thereby limits increases in CBF and ventricular performance. MMA was achieved by reducing hindlimb blood flow in canines by ~60% during treadmill exercise before and after α1‐adrenergic blockade. Experiments were repeated in the same animals following the induction of HTN (2K1C) which increased mean arterial pressure from 94.7 ± 3.8 to 130.5 ± 11.0 mmHg. In HTN, MMA‐induced increases in CBF, left ventricular dP/dtmax and cardiac output were markedly reduced to only 37 ± 12%, 26 ± 16% and 17 ± 8% of the changes observed in control. In this setting, α1‐blockade nearly restored these responses to the levels observed when normotensive. We conclude that in HTN, exaggerated MMA‐induced increases in sympathetic activity functionally vasoconstrict the coronary vasculature impairing increases in CBF which limits O2 delivery and ventricular performance. NIH HL‐ 55743 and HL‐095819