scholarly journals Role of Corticotrophin-Releasing Factor in Effects of Leptin on Sympathetic Nerve Activity and Arterial Pressure

Hypertension ◽  
2001 ◽  
Vol 38 (3) ◽  
pp. 384-388 ◽  
Author(s):  
Marcelo L.G. Correia ◽  
Donald A. Morgan ◽  
Jennifer L. Mitchell ◽  
William I. Sivitz ◽  
Allyn L. Mark ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Corticotrophin Releasing Factor

Osmolality: a physiological long-term regulator of lumbar sympathetic nerve activity and arterial pressure

1999 ◽  
Vol 276 (6) ◽  
pp. R1579-R1586 ◽  
Author(s):  
Karie E. Scrogin ◽  
Eugene T. Grygielko ◽  
Virginia L. Brooks
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Cumulative Effect ◽  
Physiological Changes ◽  
Progressive Reduction ◽  
Nerve Activity

Acute infusion of hypertonic fluid increases mean arterial pressure (MAP) in part by elevating nonrenal sympathetic activity. However, it is not known whether chronic, physiological increases in osmolality also increase sympathetic activity. To test this hypothesis, MAP, heart rate (HR), and lumbar sympathetic nerve activity (LSNA) were measured in conscious, 48-h water-deprived rats (WD) during a progressive reduction in osmolality produced by a 2-h systemic infusion (0.12 ml/min) of 5% dextrose in water (5DW). Water deprivation significantly increased osmolality (308 ± 2 vs. 290 ± 2 mosmol/kgH2O, P < 0.001), HR (453 ± 7 vs. 421 ± 10 beats/min, P < 0.05), and LSNA (63.5 ± 1.8 vs. 51.9 ± 3.8% baroreflex maximum, P < 0.01). Two hours of 5DW infusion reduced osmolality (−15 ± 5 mosmol/kgH2O), LSNA (−23 ± 3% baseline), and MAP (−10 ± 1 mmHg). To evaluate the role of vasopressin in these changes, rats were pretreated with a V1-vasopressin receptor antagonist. The antagonist lowered MAP (−5 ± 1 mmHg) and elevated HR (32 ± 7 beats/min) and LSNA (11 ± 3% baseline) in WD ( P < 0.05), but not in water-replete, rats. 5DW infusion had a similar cumulative effect on all variables in V1-blocked WD rats, but had no effect in water-replete rats. Infusion of the same volume of normal saline in WD rats did not change osmolality, LSNA or MAP. Together these data indicate that, in dehydrated rats, vasopressin supports MAP and suppresses LSNA and HR and that physiological changes in osmolality directly influence sympathetic activity and blood pressure independently of changes in vasopressin and blood volume.

Dynamic interactions between arterial pressure and sympathetic nerve activity: role of arterial baroreceptors

2003 ◽  
Vol 285 (4) ◽  
pp. R834-R841 ◽  
Author(s):  
Claude Julien ◽  
Bruno Chapuis ◽  
Yong Cheng ◽  
Christian Barrès
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Noise Sources ◽  
Nerve Activity ◽  
Pass Filter ◽  
Low Pass Filter ◽  
Mayer Waves ◽  
Arterial Baroreceptors

The role of arterial baroreceptors in controlling arterial pressure (AP) variability through changes in sympathetic nerve activity was examined in conscious rats. AP and renal sympathetic nerve activity (RSNA) were measured continuously during 1-h periods in freely behaving rats that had been subjected to sinoaortic baroreceptor denervation (SAD) or a sham operation 2 wk before study ( n = 10 in each group). Fast Fourier transform analysis revealed that chronic SAD did not alter high-frequency (0.75-5 Hz) respiratory-related oscillations of mean AP (MAP) and RSNA, decreased by ∼50% spectral power of both variables in the midfrequency band (MF, 0.27-0.74 Hz) containing the so-called Mayer waves, and induced an eightfold increase in MAP power without altering RSNA power in the low-frequency band (0.005-0.27 Hz). In both groups of rats, coherence between RSNA and MAP was maximal in the MF band and was usually weak at lower frequencies. In SAD rats, the transfer function from RSNA to MAP showed the characteristics of a second-order low-pass filter containing a fixed time delay (∼0.5 s). These results indicate that arterial baroreceptors are not involved in production of respiratory-related oscillations of RSNA but play a major role in the genesis of synchronous oscillations of MAP and RSNA at the frequency of Mayer waves. The weak coupling between slow fluctuations of RSNA and MAP in sham-operated and SAD rats points to the interference of noise sources unrelated to RSNA affecting MAP and of noise sources unrelated to MAP affecting RSNA.

Problems, possibilities, and pitfalls in studying the arterial baroreflexes’ influence over long-term control of blood pressure

2005 ◽  
Vol 288 (4) ◽  
pp. R837-R845 ◽  
Author(s):  
Carolyn J. Barrett ◽  
Simon C. Malpas
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Critical Role ◽  
Pressure Control ◽  
Arterial Baroreflex ◽  
Nerve Activity ◽  
The Many

While there is no disputing the critical role of baroreflexes in buffering rapid changes in arterial pressure, their role in long-term pressure control has become an area of controversy. Recent experiments using novel techniques have challenged the traditional view that arterial baroreflexes are not involved in setting chronic arterial pressure levels. Resetting of the arterial baroreflex, often used as an argument against the arterial baroreflex playing a role in long-term pressure control is rarely complete. The arterial baroreflex is just one of the many neural, hormonal, and intrinsic mechanisms involved in arterial pressure control and while the removal of the arterial baroreflex alone has little effect on mean arterial pressure it is too simplistic to suggest that the baroreflex has no role in long-term pressure control. Renal sympathetic nerve activity appears to be particularly resistant to resetting in response to ANG II-induced hypertension. Given the important role of the kidneys in long-term pressure control, we suggest there is a clear need to develop experimental techniques whereby sympathetic nerve activity to the kidneys and other organs can be monitored over periods of weeks to months.

scholarly journals Hypothalamic mTORC1 Signaling Controls Sympathetic Nerve Activity and Arterial Pressure and Mediates Leptin Effects

2013 ◽  
Vol 17 (4) ◽  
pp. 599-606 ◽  
Author(s):  
Shannon M. Harlan ◽  
Deng-Fu Guo ◽  
Donald A. Morgan ◽  
Caroline Fernandes-Santos ◽  
Kamal Rahmouni
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Mtorc1 Signaling
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