Amelioration of depressed cardiopulmonary reflex control of sympathetic nerve activity by short-term exercise training in male rabbits with heart failure

2003 ◽  
Vol 95 (5) ◽  
pp. 1883-1888 ◽  
Author(s):  
R. U. Pliquett ◽  
K. G. Cornish ◽  
K. P. Patel ◽  
H. D. Schultz ◽  
J. D. Peuler ◽  
...  
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Sympathetic Nerve ◽  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Reflex Response ◽  
Nerve Activity ◽  
Reflex Regulation

The reflex regulation of sympathetic nerve activity has been demonstrated to be impaired in the chronic heart failure (CHF) state compared with the normal condition (Liu JL, Murakami H, and Zucker IH. Circ Res 82: 496–502, 1998). Exercise training (Ex) appears to be beneficial to patients with CHF and has been shown to reduce sympathetic outflow in this disease state (Hambrecht R, Hilbrich L, Erbs S, Gielen S, Fiehn E, Schoene N, and Schuler G. J Am Coll Cardiol 35: 706–713, 2000). We tested the hypothesis that Ex corrects the reduced cardiopulmonary (CP) reflex response to volume expansion in the CHF state. Normal, normal with Ex, CHF, and CHF with Ex (CHF-Ex) groups ( n = 10–21) of male New Zealand White rabbits were studied. CHF was induced by chronic ventricular pacing. Rabbits were instrumented to record left ventricular end-diastolic pressure (LVEDP), left ventricular end-diastolic diameter (LVEDD), and renal sympathetic nerve activity (RSNA). Experiments were carried out with the animals in the conscious state. Volume expansion was performed with 6% dextran in normal saline at a rate of 5 ml/min to ∼20% of estimated plasma volume without any significant effect on mean arterial pressure being exhibited. The relationships between RSNA and LVEDP and between RSNA and LVEDD were determined by linear regression; the slopes served as an index of CP reflex sensitivity. Normal rabbits exhibited a CP reflex sensitivity of -8.4 ± 1.5%Δ RSNA/mmHg. This value fell to 0.0 ± 1.3%Δ RSNA/mmHg in CHF rabbits ( P < 0.001). Ex increased CP reflex sensitivity to -5.0 ± 0.7%Δ RSNA/mmHg in CHF-Ex rabbits ( P < 0.05 compared with CHF). A similar trend was seen when related to the change in LVEDD. Furthermore, resting RSNA expressed as a percentage of maximum RSNA in response to cigarette smoke was also normalized by Ex in rabbits with CHF. Ex had no effect on these parameters in normal rabbits. These data confirm an impairment of CP reflex sensitivity and sympathoexcitation in CHF vs. normal animals. Ex substantially restored both CP reflex sensitivity and baseline RSNA in CHF animals. Thus Ex beneficially affects reflex regulation in CHF, thereby lowering resting sympathetic nerve activity.

scholarly journals Impact of gender on benefits of exercise training on sympathetic nerve activity and muscle blood flow in heart failure

2009 ◽  
Vol 12 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Ligia M. Antunes-Correa ◽  
Ruth C. Melo ◽  
Thais S. Nobre ◽  
Linda M. Ueno ◽  
Fabio G.M. Franco ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Exercise Training ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Blood Flow ◽  
Nerve Activity

Exercise training reduces sympathetic nerve activity in heart failure patients treated with carvedilol

2007 ◽  
Vol 9 (6-7) ◽  
pp. 630-636 ◽  
Author(s):  
Raffael Fraga ◽  
Fábio G. Franco ◽  
Fabiana Roveda ◽  
Luciana N.J. de Matos ◽  
Ana M.F.W. Braga ◽  
...  
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Heart Failure Patients

scholarly journals Responses of cardiac sympathetic nerve activity to changes in circulating volume differ in normal and heart failure sheep

2008 ◽  
Vol 295 (3) ◽  
pp. R719-R726 ◽  
Author(s):  
Rohit Ramchandra ◽  
Sally G. Hood ◽  
Anna M. D. Watson ◽  
Clive N. May
Keyword(s):  
Heart Failure ◽  
Normal State ◽  
Sympathetic Nerve ◽  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Cardiac Sympathetic Nerve ◽  
Volume Depletion ◽  
Nerve Activity ◽  
Cardiac Sympathetic Nerve Activity

Factors controlling cardiac sympathetic nerve activity (CSNA) in the normal state and those causing the large increase in activity in heart failure (HF) remain unclear. We hypothesized from previous clinical findings that activation of cardiac mechanoreceptors by the increased blood volume in HF may stimulate sympathetic nerve activity (SNA), particularly to the heart via cardiocardiac reflexes. To investigate the effect of volume expansion and depletion on CSNA we have made multiunit recordings of CSNA in conscious normal sheep and sheep paced into HF. In HF sheep ( n = 9) compared with normal sheep ( n = 9), resting levels of CSNA were significantly higher (34 ± 5 vs. 93 ± 2 bursts/100 heart beats, P < 0.05), mean arterial pressure was lower (76 ± 3 vs. 87 ± 2 mmHg; P < 0.05), and central venous pressure (CVP) was greater (3.0 ± 1.0 vs. 0.0 ± 1.0 mmHg; P < 0.05). In normal sheep ( n = 6), hemorrhage (400 ml over 30 min) was associated with a significant increase in CSNA (179 ± 16%) with a decrease in CVP (2.7 ± 0.7 mmHg). Volume expansion (400 ml Gelofusine over 30 min) significantly decreased CSNA (35 ± 12%) and increased CVP (4.7 ± 1.0 mmHg). In HF sheep ( n = 6) the responses of CSNA to both volume expansion and hemorrhage were severely blunted with no significant changes in CSNA or heart rate with either stimulus. In summary, these studies in a large conscious mammal demonstrate that in the normal state directly recorded CSNA increased with volume depletion and decreased with volume loading. In contrast, both of these responses were severely blunted in HF with no significant changes in CSNA during either hemorrhage or volume expansion.

scholarly journals Chronic AT1 receptor blockade normalizes NMDA-mediated changes in renal sympathetic nerve activity and NR1 expression within the PVN in rats with heart failure

2010 ◽  
Vol 298 (5) ◽  
pp. H1546-H1555 ◽  
Author(s):  
Allison C. Kleiber ◽  
Hong Zheng ◽  
Neeru M. Sharma ◽  
Kaushik P. Patel
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Protein Expression ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Receptor Blockade ◽  
Ang Ii ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic

Exercise training normalizes enhanced glutamatergic mechanisms within the paraventricular nucleus (PVN) concomitant with the normalization of increased plasma ANG II levels in rats with heart failure (HF). We tested whether ANG II type 1 (AT1) receptors are involved in the normalization of PVN glutamatergic mechanisms using chronic AT1 receptor blockade with losartan (Los; 50 mg·kg−1·day−1 in drinking water for 3 wk). Left ventricular end-diastolic pressure was increased in both HF + vehicle (Veh) and HF + Los groups compared with sham-operated animals (Sham group), although it was significantly attenuated in the HF + Los group compared with the HF + Veh group. The effect of Los on cardiac function was similar to exercise training. At the highest dose of N-methyl-d-aspartate (NMDA; 200 pmol) injected into the PVN, the increase in renal sympathetic nerve activity was 93 ± 13% in the HF + Veh group, which was significantly higher ( P < 0.05) than the increase in the Sham + Veh (45 ± 2%) and HF + Los (47 ± 2%) groups. Relative NMDA receptor subunit NR1 mRNA expression within the PVN was increased 120% in the HF + Veh group compared with the Sham + Veh group ( P < 0.05) but was significantly attenuated in the HF + Los group compared with the HF + Veh group ( P < 0.05). NR1 protein expression increased 87% in the HF + Veh group compared with the Sham + Veh group but was significantly attenuated in the HF + Los group compared with the HF + Veh group ( P < 0.05). Furthermore, in in vitro experiments using neuronal NG-108 cells, we found that ANG II treatment stimulated NR1 protein expression and that Los significantly ameliorated the NR1 expression induced by ANG II. These data are consistent with our hypothesis that chronic AT1 receptor blockade normalizes glutamatergic mechanisms within the PVN in rats with HF.

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