The Beauty and the Beast: Aspects of the Autonomic Nervous System

Sympathetic nerve activity is altered and is a prognostic factor for many cardiovascular diseases such as hypertension, coronary syndromes, and congestive heart failure. Therefore, the selection of vasoactive drugs for the treatment of these diseases should also take into consideration their effects on the sympathetic nervous system.

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Angiotensin receptor antagonist improves cardiac reflex control of renal sodium handling in heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1998.274.2.h636 ◽

1998 ◽

Vol 274 (2) ◽

pp. H636-H641 ◽

Cited By ~ 21

Author(s):

Gerald F. Dibona ◽

Susan Y. Jones ◽

Linda L. Sawin

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Right Atrial ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic Nerve ◽

Renal Sodium Handling ◽

Renal Sympathetic

In rats with congestive heart failure, type 1 angiotensin II receptor antagonist treatment (losartan) decreases basal renal sympathetic nerve activity and improves arterial baroreflex regulation of renal sympathetic nerve activity. This investigation examined the effect of losartan on cardiac baroreflex regulation of renal sympathetic nerve activity and renal sodium handling in rats with congestive heart failure. Losartan treatment decreased arterial pressure from 120 ± 3 to 93 ± 5 mmHg and increased the afferent (from 0.95 ± 0.21 to 2.22 ± 0.42% Δafferent vagal nerve activity/mmHg mean right atrial pressure, P < 0.05) and overall gain (from −1.14 ± 0.19 to −4.20 ± 0.39% Δrenal sympathetic nerve activity/mmHg mean right atrial pressure, P < 0.05) of the cardiac baroreflex. During isotonic saline volume loading, urinary sodium excretion increased from 2.4 ± 0.8 to 10.5 ± 1.3 μeq/min in vehicle-treated rats (excretion of 52 ± 3% of the load) and from 3.0 ± 1.0 to 15.1 ± 1.8 μeq/min in losartan-treated rats (excretion of 65 ± 4% of the load, P < 0.05). When rats were changed from a low- to a high-sodium diet, cumulative sodium balance over 5 days was 7.8 ± 0.6 meq in vehicle-treated rats and 4.2 ± 0.4 meq in losartan-treated rats ( P < 0.05). In congestive heart failure, losartan treatment improved cardiac baroreflex regulation of renal sympathetic nerve activity, which was associated with improved ability to excrete acute and chronic sodium loads.

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Arterial pressure lability and renal sympathetic nerve activity are dissociated in SAD rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1992.263.3.r639 ◽

1992 ◽

Vol 263 (3) ◽

pp. R639-R646 ◽

Cited By ~ 17

Author(s):

C. Barres ◽

S. J. Lewis ◽

H. J. Jacob ◽

M. J. Brody

Keyword(s):

Nervous System ◽

Sympathetic Nervous System ◽

Arterial Pressure ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

High Variability ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Sympathetic Nervous ◽

Renal Sympathetic

The purpose of this study was to determine whether the sympathetic nervous system drives the high variability of arterial pressure (AP) observed after sinoaortic denervation (SAD) in rats. One or fourteen days after SAD, rats were instrumented chronically to record mean AP (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) in the conscious unrestrained state. Acute SAD increased MAP, HR, RSNA, and variability of MAP and decreased variability of both HR and RSNA. In rats with chronic SAD, variability of MAP remained high, whereas MAP, HR, RSNA, and variability of HR and RSNA returned to normal levels. Correlation analysis showed that, in sham-operated rats, AP and RSNA were negatively correlated in 90% of cases. In contrast, rats with both acute and chronic SAD exhibited only 30% negative and 25% positive correlations. These results indicate that 1) low AP variability in intact rats results from baroreflex-mediated inversely related fluctuations in RSNA and HR and 2) high variability of AP after acute and chronic SAD is correlated infrequently with RSNA. Because lability is reduced by interventions that block the sympathetic nervous system, we conclude that lability of AP associated with SAD appears to be mediated largely by a permissive role of sympathetic activity.

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