Exercise training improves renal excretory responses to acute volume expansion in rats with heart failure

2006 ◽  
Vol 291 (6) ◽  
pp. F1148-F1156 ◽  
Author(s):  
Hong Zheng ◽  
Yi-Fan Li ◽  
Irving H. Zucker ◽  
Kaushik P. Patel
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Volume Expansion ◽  
Renal Sympathetic Nerve Activity ◽  
Beneficial Effects ◽  
Coronary Ligation ◽  
Ext Groups ◽  
Histological Data ◽  
Renal Responses ◽  
Renal Sympathetic

Experiments were performed to test the postulate that exercise training (ExT) improves the blunted renal excretory response to acute volume expansion (VE), in part, by normalizing the neural component of the volume reflex typically observed in chronic heart failure (HF). Diuretic and natriuretic responses to acute VE were examined in sedentary and ExT groups of rats with either HF or sham-operated controls. Experiments were performed in anesthetized (Inactin) rats 6 wk after coronary ligation surgery. Histological data indicated that there was a 34.9 ± 3.0% outer and 42.5 ± 3.2% inner infarct of the myocardium in the HF group. Sham rats had no observable damage to the myocardium. In sedentary rats with HF, VE produced a blunted diuresis (46% of sham) and natriuresis (35% of sham) compared with sham-operated control rats. However, acute VE-induced diuresis and natriuresis in ExT rats with HF were comparable to sham rats and significantly higher than sedentary HF rats. Renal denervation abolished the salutary effects of ExT on renal excretory response to acute VE in HF. Since glomerular filtration rates were not significantly different between the groups, renal hemodynamic changes may not account for the blunted renal responses in rats with HF. Additional experiments confirmed that renal sympathetic nerve activity responses to acute VE were blunted in sedentary HF rats; however, ExT normalized the renal sympathoinhibition in HF rats. These results confirm an impairment of neurally mediated excretory responses to acute VE in rats with HF. ExT restored the blunted excretory responses as well as the renal sympathoinhibitory response to acute VE in HF rats. Thus the beneficial effects of ExT on cardiovascular regulation in HF may be partly due to improvement of the neural component of volume reflex.

Neural influences on renal responses to acute volume expansion in rats with heart failure

1996 ◽  
Vol 271 (4) ◽  
pp. H1441-H1448 ◽  
Author(s):  
K. P. Patel ◽  
P. L. Zhang ◽  
P. K. Carmines
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Renal Nerve ◽  
Natriuretic Factor ◽  
Renal Nerve Activity ◽  
Neural Influences ◽  
Renal Responses ◽  
Renal Sympathetic ◽  
Atrial Natriuretic

Experiments were performed to test the postulate that neural influences underlie the suppressed excretory response to acute volume expansion (VE) typically observed 3-4 wk after myocardial infarction to induce chronic heart failure (CHF). Responses to VE were assessed in innervated (intact) and denervated (DNX) kidneys of anesthetized CHF rats and sham-operated controls. CHF rats exhibited blunted natriuretic responses to VE in both intact kidneys (35% of sham response) and DNX kidneys (55% of sham DNX response). CHF rats also displayed suppressed excretory responses to atrial natriuretic factor (0.25 microgram.kg-1.min-1 iv) in both intact kidneys (74% of sham response) and DNX kidneys (63% of sham DNX response). Additional experiments confirmed that the compliance of the venoatrial junction did not differ between sham rats (52 +/- 2 mmHg/microliter) and CHF rats (54-2 mmHg/microliter). The observations support the contention that both tonic renal sympathetic renal nerve activity and suppressed renal atrial natriuretic factor responsiveness likely contribute to the blunted excretory response to VE during CHF.

ANG II in the paraventricular nucleus potentiates the cardiac sympathetic afferent reflex in rats with heart failure

2004 ◽  
Vol 97 (5) ◽  
pp. 1746-1754 ◽  
Author(s):  
Guo-Qing Zhu ◽  
Lie Gao ◽  
Kuashik P. Patel ◽  
Irving H. Zucker ◽  
Wei Wang
Keyword(s):  
Heart Failure ◽  
Electrical Stimulation ◽  
Paraventricular Nucleus ◽  
Sham Group ◽  
Ang Ii ◽  
Renal Sympathetic Nerve Activity ◽  
Afferent Nerves ◽  
Coronary Ligation ◽  
Cardiac Sympathetic Afferent Reflex ◽  
Renal Sympathetic

Chronic heart failure (CHF) is characterized by sympathoexcitation, and the cardiac sympathetic afferent reflex (CSAR) is a sympathoexcitatory reflex. Our previous studies have shown that the CSAR was enhanced in CHF. In addition, central angiotensin II (ANG II) is an important modulator of this reflex. This study was performed to determine whether the CSAR evoked by stimulation of cardiac sympathetic afferent nerves (CSAN) in rats with coronary ligation-induced CHF is enhanced by ANG II in the paraventricular nucleus (PVN). Under α-chloralose and urethane anesthesia, renal sympathetic nerve activity (RSNA) was recorded. The RSNA responses to electrical stimulation (5, 10, 20, and 30 Hz) of the CSAN were evaluated. Bilateral microinjection of the AT1-receptor antagonist losartan (50 nmol) into the PVN had no significant effects in the sham group, but it abolished the enhanced RSNA response to stimulation in the CHF group. Unilateral microinjection of three doses of ANG II (0.03, 0.3, and 3 nmol) into the PVN resulted in dose-related increases in the RSNA responses to stimulation. Although ANG II also potentiated the RSNA response to electrical stimulation in sham rats, the RSNA responses to stimulation after ANG II into the PVN in rats with CHF were much greater than in sham rats. The effects of ANG II were prevented by pretreatment with losartan into the PVN in CHF rats. These results suggest that the central gain of the CSAR is enhanced in rats with coronary ligation-induced CHF and that ANG II in the PVN augments the CSAR evoked by CSAN, which is mediated by the central angiotensin AT1 receptors in rats with CHF.

scholarly journals Exercise training normalizes enhanced glutamate-mediated sympathetic activation from the PVN in heart failure

2008 ◽  
Vol 294 (6) ◽  
pp. R1863-R1872 ◽  
Author(s):  
Allison C. Kleiber ◽  
Hong Zheng ◽  
Harold D. Schultz ◽  
Jacob D. Peuler ◽  
Kaushik P. Patel
Keyword(s):  
Heart Failure ◽  
Exercise Training ◽  
Treadmill Running ◽  
Coronary Artery Ligation ◽  
Sympathetic Outflow ◽  
Receptor Subunit ◽  
Artery Ligation ◽  
Renal Sympathetic Nerve Activity ◽  
Subunit Mrna ◽  
Ext Groups

Exercise training (ExT) normalizes the increased sympathetic outflow in heart failure (HF), but the mechanisms are not known. We hypothesized that ExT would normalize the augmented glutamatergic mechanisms mediated by N-methyl-d-aspartic acid (NMDA) receptors within the paraventricular nucleus (PVN) that occur with HF. Four groups of rats were used: 1) sham-operated (Sham) sedentary (Sed), 2) Sham ExT, 3) HF Sed, and 4) HF ExT. HF was induced by left coronary artery ligation, and ExT consisted of 3 wk of treadmill running. In α-chloralose-urethane-anesthetized rats, the increase in renal sympathetic nerve activity in response to the highest dose of NMDA (200 pmol) injected into the PVN in the HF Sed group was approximately twice that of the Sham Sed group. In the HF ExT group the response was not different from the Sham Sed and Sham ExT groups. Relative NMDA NR1 receptor subunit mRNA expression was 63% higher in the HF Sed group compared with the Sham Sed group but in the HF ExT group was not different from the Sham Sed and Sham ExT groups. NR1 receptor subunit protein expression was increased 87% in the HF Sed group compared with the Sham Sed group but in the HF ExT group was not significantly different from the Sham Sed and Sham ExT groups. Thus one mechanism by which ExT alleviates elevated sympathetic outflow in HF may be through normalization of glutamatergic mechanisms within the PVN.

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.

scholarly journals Exercise training attenuates chemoreflex-mediated reductions of renal blood flow in heart failure

2015 ◽  
Vol 309 (2) ◽  
pp. H259-H266 ◽  
Author(s):  
Noah J. Marcus ◽  
Carolin Pügge ◽  
Jai Mediratta ◽  
Alicia M. Schiller ◽  
Rodrigo Del Rio ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Exercise Training ◽  
Renal Blood Flow ◽  
Carotid Body ◽  
Sympathetic Nerve Activity ◽  
Renal Perfusion ◽  
Renal Sympathetic Nerve Activity ◽  
Fractional Shortening ◽  
Renal Sympathetic

In chronic heart failure (CHF), carotid body chemoreceptor (CBC) activity is increased and contributes to increased tonic and hypoxia-evoked elevation in renal sympathetic nerve activity (RSNA). Elevated RSNA and reduced renal perfusion may contribute to development of the cardio-renal syndrome in CHF. Exercise training (EXT) has been shown to abrogate CBC-mediated increases in RSNA in experimental heart failure; however, the effect of EXT on CBC control of renal blood flow (RBF) is undetermined. We hypothesized that CBCs contribute to tonic reductions in RBF in CHF, that stimulation of the CBC with hypoxia would result in exaggerated reductions in RBF, and that these responses would be attenuated with EXT. RBF was measured in CHF-sedentary (SED), CHF-EXT, CHF-carotid body denervation (CBD), and CHF-renal denervation (RDNX) groups. We measured RBF at rest and in response to hypoxia (FiO2 10%). All animals exhibited similar reductions in ejection fraction and fractional shortening as well as increases in ventricular systolic and diastolic volumes. Resting RBF was lower in CHF-SED (29 ± 2 ml/min) than in CHF-EXT animals (46 ± 2 ml/min, P < 0.05) or in CHF-CBD animals (42 ± 6 ml/min, P < 0.05). In CHF-SED, RBF decreased during hypoxia, and this was prevented in CHF-EXT animals. Both CBD and RDNX abolished the RBF response to hypoxia in CHF. Mean arterial pressure increased in response to hypoxia in CHF-SED, but was prevented by EXT, CBD, and RDNX. EXT is effective in attenuating chemoreflex-mediated tonic and hypoxia-evoked reductions in RBF in CHF.

scholarly journals Exercise training improves peripheral chemoreflex function in heart failure rabbits

2008 ◽  
Vol 105 (3) ◽  
pp. 782-790 ◽  
Author(s):  
Yu-Long Li ◽  
Yanfeng Ding ◽  
Chad Agnew ◽  
Harold D. Schultz
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Exercise Training ◽  
Ang Ii ◽  
Renal Sympathetic Nerve Activity ◽  
Chemoreflex Sensitivity ◽  
Peripheral Chemoreflex ◽  
Oxide Synthase ◽  
Renal Sympathetic

An enhancement of peripheral chemoreflex sensitivity contributes to sympathetic hyperactivity in chronic heart failure (CHF) rabbits. The enhanced chemoreflex function in CHF involves augmented carotid body (CB) chemoreceptor activity via upregulation of the angiotensin II (ANG II) type 1 (AT1)-receptor pathway and downregulation of the neuronal nitric oxide synthase (nNOS)-nitric oxide (NO) pathway in the CB. Here we investigated whether exercise training (EXT) normalizes the enhanced peripheral chemoreflex function in CHF rabbits and possible mechanisms mediating this effect. EXT partially, but not fully, normalized the exaggerated baseline renal sympathetic nerve activity (RSNA) and the response of RSNA to hypoxia in CHF rabbits. EXT also decreased the baseline CB nerve single-fiber discharge (4.9 ± 0.4 vs. 7.7 ± 0.4 imp/s at Po2 = 103 ± 2.3 Torr) and the response to hypoxia (20.6 ± 1.1 vs. 36.3 ± 1.3 imp/s at Po2 = 41 ± 2.2 Torr) from CB chemoreceptors in CHF rabbits, which could be reversed by treatment of the CB with ANG II or a nNOS inhibitor. Our results also showed that NO concentration and protein expression of nNOS were increased in the CBs from EXT + CHF rabbits, compared with that in CHF rabbits. On the other hand, elevated ANG II concentration and AT1-receptor overexpression of the CBs in CHF state were blunted by EXT. These results indicate that EXT normalizes the CB chemoreflex in CHF by preventing an increase in afferent CB chemoreceptor activity. EXT reverses the alterations in the nNOS-NO and ANG II-AT1-receptor pathways in the CB responsible for chemoreceptor sensitization in CHF.

Impairment of cardiopulmonary baroreflexes during the newborn period

1995 ◽  
Vol 268 (3) ◽  
pp. H1343-H1351
Author(s):  
D. C. Merrill ◽  
O. J. McWeeny ◽  
J. L. Segar ◽  
J. E. Robillard
Keyword(s):  
Volume Expansion ◽  
Sympathetic Nerve Activity ◽  
Right Atrial ◽  
Arterial Baroreflex ◽  
Newborn Period ◽  
Renal Sympathetic Nerve Activity ◽  
Dextran 70 ◽  
Reflex Control ◽  
Renal Responses ◽  
Renal Sympathetic

The present study was designed to characterize the maturation of cardiopulmonary reflex control of renal sympathetic nerve activity (RSNA) independent of influences from the arterial baroreflex. Studies were conducted in conscious newborn lambs (3- to 7-days-old) (n = 16) and older lambs (6- to 8-wk-old) (n = 18). All animals underwent either sinoaortic denervation (SAD) or a sham procedure. Hemodynamic, humoral, neural, and renal responses to volume expansion (6% Dextran 70, 0.7 ml.kg-1.min-1 x 60 min) were recorded. Volume expansion resulted in a significant decrease (P < 0.05) in RSNA in intact newborn (-28.1 +/- 5.3% change from control) and older lambs (-19.4 +/- 10.1%). SAD totally abolished the sympathetic inhibition seen with volume expansion in newborn lambs (-3.6 +/- 5.7%) but not in older lambs (-25.6 +/- 8.4%). Right atrial pressure increased in a similar fashion in both newborn (intact: 5.6 +/- 0.5 mmHg; SAD: 6.1 +/- 0.8 mmHg) and older lambs (intact: 5.2 +/- 0.9 mmHg; SAD: 5.3 +/- 0.9 mmHg) and was not altered by SAD. The reflex bradycardia seen with volume expansion in newborn lambs was blocked by SAD. The present study demonstrates that, during the newborn period, the RSNA and heart rate responses to volume expansion are dependent mainly on the integrity of the arterial baroreflex. Furthermore, these studies suggest that cardiopulmonary reflex control of RSNA in response to volume expansion is impaired early in life and increases with maturation.

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