Baroreflex control of renal sympathetic nerve activity is preserved in heart failure despite reduced arterial baroreceptor sensitivity.

Dibner-Dunlap, Mark E.; Thames, Marc D.

doi:10.1161/01.res.65.6.1526

Cited by 94 publications

(64 citation statements)

References 38 publications

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“…30,[32][33][34][35] Our results were compatible with these reports. The precise mechanism of reduced BRS was studied in animals with experimental heart failure, and it was shown that, in addition to reduced sensitivity of the baroreceptors themselves, a decrease in the reactivity of vagal afferents, sympathetic efferents, and peripheral effectors was also responsible for impairment of this reflex arc, but most authors have found an association of reduced BRS with decreased vagal afferent neural activity.…”

Section: Relationship Between Brs and Humoral Factors In Heart Failuresupporting

confidence: 93%

“…The precise mechanism of reduced BRS was studied in animals with experimental heart failure, and it was shown that, in addition to reduced sensitivity of the baroreceptors themselves, a decrease in the reactivity of vagal afferents, sympathetic efferents, and peripheral effectors was also responsible for impairment of this reflex arc, but most authors have found an association of reduced BRS with decreased vagal afferent neural activity. [29][30][31][32]36 This abnormality of BRS in heart failure has been thought to be functional rather than organic because heart transplantation 34 and the control of heart failure 35 improved BRS. In the present study, we found no significant correlation between a decrease of BRS and overactivation of sympathetic nervous system, but a direct relationship was observed between a low BRS and an increased ANP level.…”

Section: Relationship Between Brs and Humoral Factors In Heart Failurementioning

confidence: 99%

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Correlation Between Atrial Natriuretic Peptide and Baroreflex Sensitivity in Patients With Congestive Heart Failure

et al. 1999

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Section: Relationship Between Brs and Humoral Factors In Heart Failuresupporting

confidence: 93%

Section: Relationship Between Brs and Humoral Factors In Heart Failurementioning

confidence: 99%

Correlation Between Atrial Natriuretic Peptide and Baroreflex Sensitivity in Patients With Congestive Heart Failure

et al. 1999

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“…The normal control of CSNA by the arterial baroref lex indicates that the impaired response of HR must be because of depressed parasympathetic control, as described (26,27). Studies in humans (28,29) and animal models of HF (30,31) support the concept that the arterial baroref lex control of SNA is not altered in HF. However, there is evidence from studies in rabbits that the baroref lex control of RSNA is desensitized in HF (24,25,32).…”

Section: Discussionmentioning

confidence: 87%

“…Although all animal models have limitations, the animal model of pacing-induced HF has been used extensively and shows the symptoms of HF seen clinically, including decreased ventricular function and intense neurohumoral activation (30,33). Importantly, the level of neurohumoral activation in pacing models of HF closely parallels that seen in human HF patient populations (34).…”

Section: Discussionmentioning

confidence: 99%

Basis for the preferential activation of cardiac sympathetic nerve activity in heart failure

Ramchandra

Hood

Denton

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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In heart failure (HF) , sympathetic nerve activity is increased. Measurements in HF patients of cardiac norepinephrine spillover, reflecting cardiac sympathetic nerve activity (CSNA), indicate that it is increased earlier and to a greater extent than sympathetic activity to other organs. This has important consequences because it worsens prognosis, provoking arrhythmias and sudden death. To elucidate the mechanisms responsible for the activation of CSNA in HF, we made simultaneous direct neural recordings of CSNA and renal SNA (RSNA) in two groups of conscious sheep: normal animals and animals in HF induced by chronic, rapid ventricular pacing. In normal animals, the level of activity, measured as burst incidence (bursts of pulse related activity/100 heart beats), was significantly lower for CSNA (30 ؎ 5%) than for RSNA (94 ؎ 2%). Furthermore, the resting level of CSNA, relative to its maximum achieved while baroreceptors were unloaded by reducing arterial pressure, was set at a much lower percentage than RSNA. In HF, burst incidence of CSNA increased from 30 to 91%, whereas burst incidence of RSNA remained unaltered at 95%. The sensitivity of the control of both CSNA and RSNA by the arterial baroreflex remained unchanged in HF. These data show that, in the normal state, the resting level of CSNA is set at a lower level than RSNA, but in HF, the resting levels of SNA to both organs are close to their maxima. This finding provides an explanation for the preferential increase in cardiac norepinephrine spillover observed in HF.arterial baroreflex ͉ renal sympathetic nerve activity ͉ sheep H eart failure (HF) is associated with an increase in sympathetic nerve activity (SNA) that shows a large regional heterogeneity in the extent to which activity increases. The level of SNA to different organs may be estimated by measurements of regional norepinephrine (NE) spillover, and it has been observed that in HF there is a greater increase in NE spillover from the heart than the kidney, and no change from the gut (1, 2). This increase in cardiac NE spillover occurs at an earlier stage of HF than it does to other organs (3, 4), again suggesting a preferential stimulation of cardiac SNA (CSNA) in HF. The increase in CSNA in HF is detrimental as it can promote the progression of the disease and leads to development of arrhythmias and sudden death (5). The mechanisms accounting for the increase in CSNA in HF are poorly understood.One explanation for the preferential increase in cardiac NE spillover in HF is that, in the normal state, the resting levels of CSNA and renal SNA (RSNA) are similar, but in HF, sympathetic activity increases more to the heart than to the kidney. An alternative explanation is that the resting level of CSNA is set at a lower level compared with that to other organs, such the kidney, and in HF, both CSNA and RSNA increase to near maximum levels. Both explanations seem plausible, but the resting levels of CSNA and RSNA have not been simultaneously recorded in the normal state and compared with activities ...

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“…There is accumulating evidence suggesting that arterial baroreceptor-mediated control and cardiopulmonary receptor-mediated control are altered in both human [10][11][12][13] and experimental heart failure, [14][15][16] but there are few studies concerning the compensatory process after acute left ventricular overloading. We previously demonstrated that left ventricular function progressively deteriorated, along with myocardial -adrenergic receptor down-regulation, depletion of catecholamines and an increase in plasma norepinephrine level, during the first week after production of aortic regurgitation (AR) in rabbits.…”

mentioning

confidence: 99%

Baroreceptor Sensitivity During the Compensatory Phase of Left Ventricular Overloading

et al. 1998

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Baroreflex control of renal sympathetic nerve activity is preserved in heart failure despite reduced arterial baroreceptor sensitivity.

Cited by 94 publications

References 38 publications

Correlation Between Atrial Natriuretic Peptide and Baroreflex Sensitivity in Patients With Congestive Heart Failure

Correlation Between Atrial Natriuretic Peptide and Baroreflex Sensitivity in Patients With Congestive Heart Failure

Basis for the preferential activation of cardiac sympathetic nerve activity in heart failure

Baroreceptor Sensitivity During the Compensatory Phase of Left Ventricular Overloading

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