Baroreceptor mechanisms controlling sympathetic nervous rhythms of central origin

1975 ◽  
Vol 228 (4) ◽  
pp. 1002-1003 ◽  
Author(s):  
DG Taylor ◽  
tgl Gebber

A study was made in the anesthetized cat of the slow wave of sympathetic nervous discharge (SND) locked in a 1:1 relation to the cardiac cycle (3 cycle/s periodicity). SND was recorded from the preganglionic splanchnic and postganglionic renal nerves. The data contradict the generally accepted view that the slow wave occurs as the direct result of a waxing and waning of baroreceptor nervous discharge. Although baroreceptor denervation unlocked the phase relations between SND and the cardiac cycle, the slow wave persisted and its duration was not changed. Furthermore, the slow wave was aborted by stimuli delivered to the baroreceptor nerves or paramedian reticular nucleus during a time span which accounted for less than 1 percent of the cardiac cycle. It is concluded that the 3 cycle/s periodicity of SND is representative of a vasomotor rhythm of central origin which is entrained to the cardiac cycle by the baroreceptor reflexes. The sympathoinhibitory effect leading to the entrainment of the slow wave is mediated in the brainstem. ta spinal component of baroreceptor-induced sympathoinhibition also was demonstrated.

1976 ◽  
Vol 230 (2) ◽  
pp. 263-270 ◽  
Author(s):  
GL Gebber

The phase relations between the cardiac cycle and sympathetic nervous discharge (SND) were studied with an average-response computer in the anesthetized cat. Maximum SND occurred during early diastole at heart rates between 3 and 4 beats/s. Dramatic shifts in the phase relations between SND and the cardiac cycle accompanied the decrease in heart rate produced by stimulation of the distal end of the cut right vagus nerve. The point of maximum SND was shifted from early diastole to near peak systole and then into the late diastolic phase of the preceding cardiac cycle as heart rate was progressively lowered to 2 beats/s. These observations indicate that synchronization of SND during each cardiac cycle is not the simple consequence of the waxing and waning of baroreceptor nerve activity. Rather, 1:1 locking of bursts of SND to the cardiac cycle is explained on the basis of entrainment by the baroreceptor reflexes of a sympathetic rhythm of central origin. An inhibitory-phasing hypothesis is proposed to account for entrainment. In addition, two components (spinal and brainstem) of sympathoinhibition associated with the pulse-synchronous discharge of the carotid sinus nerve were revealed when the 1:1 relationship between bursts of SND and the cardiac cycle was disrupted at heart rates below 2 beats/s.


1992 ◽  
Vol 262 (6) ◽  
pp. E763-E778 ◽  
Author(s):  
I. A. Reid

The renin-angiotensin system plays an important role in the regulation of arterial blood pressure and in the development of some forms of clinical and experimental hypertension. It is an important blood pressure control system in its own right but also interacts extensively with other blood pressure control systems, including the sympathetic nervous system and the baroreceptor reflexes. Angiotensin (ANG) II exerts several actions on the sympathetic nervous system. These include a central action to increase sympathetic outflow, stimulatory effects on sympathetic ganglia and the adrenal medulla, and actions at sympathetic nerve endings that serve to facilitate sympathetic neurotransmission. ANG II also interacts with baroreceptor reflexes. For example, it acts centrally to modulate the baroreflex control of heart rate, and this accounts for its ability to increase blood pressure without causing a reflex bradycardia. The physiological significance of these actions of ANG II is not fully understood. Most evidence indicates that the actions of ANG to enhance sympathetic activity do not contribute significantly to the pressor response to exogenous ANG II. On the other hand, there is considerable evidence that the actions of endogenous ANG II on the sympathetic nervous system enhance the cardiovascular responses elicited by activation of the sympathetic nervous system.


Author(s):  
J. L. Gill

Property owners in New Zealand obtain indemnity against loss or damage occurring as a direct result of earthquake shock or earthquake fire under a compulsory extension to a contract of fire insurance. A special earthquake and war damage premium is levied under fire insurance contracts made in New Zealand and is paid by the insurer into a fund which is administered by the Commission under the Earthquake and War Damage Act 1944.


2015 ◽  
Vol 308 (8) ◽  
pp. R708-R713 ◽  
Author(s):  
Rodrigo Maranon ◽  
Roberta Lima ◽  
Frank T. Spradley ◽  
Jussara M. do Carmo ◽  
Howei Zhang ◽  
...  

Women with polycystic ovary syndrome (PCOS) have hyperandrogenemia and increased prevalence of risk factors for cardiovascular disease, including elevated blood pressure. We recently characterized a hyperandrogenemic female rat (HAF) model of PCOS [chronic dihydrotestosterone (DHT) beginning at 4 wk of age] that exhibits similar characteristics as women with PCOS. In the present studies we tested the hypotheses that the elevated blood pressure in HAF rats is mediated in part by sympathetic activation, renal nerves, and melanocortin-4 receptor (MC4R) activation. Adrenergic blockade with terazosin and propranolol or renal denervation reduced mean arterial pressure (MAP by telemetry) in HAF rats but not controls. Hypothalamic MC4R expression was higher in HAF rats than controls, and central nervous system MC4R antagonism with SHU-9119 (1 nmol/h icv) reduced MAP in HAF rats. Taking a genetic approach, MC4R null and wild-type (WT) female rats were treated with DHT or placebo from 5 to 16 wk of age. MC4R null rats were obese and had higher MAP than WT control rats, and while DHT increased MAP in WT controls, DHT failed to further increase MAP in MC4R null rats. These data suggest that increases in MAP with chronic hyperandrogenemia in female rats are due, in part, to activation of the sympathetic nervous system, renal nerves, and MC4R and may provide novel insights into the mechanisms responsible for hypertension in women with hyperandrogenemia such as PCOS.


1984 ◽  
Vol 2 (4) ◽  
pp. 349-359 ◽  
Author(s):  
Richard E. Katholi ◽  
Patrick L. Whitlow ◽  
Gilbert R. Hageman ◽  
Thomas W. Woods

2021 ◽  
Vol 55 (2) ◽  
pp. 63-68
Author(s):  
A.V. Demin ◽  
◽  
A.V. Suvorov ◽  
O.I. Orlov ◽  
◽  
...  

Hemodynamics was studied in essentially healthy resting 8 male subjects exposed to an experimental hypomagnetic environment (HME). The cardio-respiratory system functioning was evaluated by 8-hour continuous monitoring of heart rate (HR), blood pressure (BP) fluctuations during every cardiac cycle, Kerdo autonomic index (KAI) and blood oxygenation (SpO2) in the Earth's natural magnetic field and a field attenuated in approximately 1,000 times. Comparative analysis of the measurements made in the control and HME tests elicited different trends. Thus, the HR average reduction amounted to 4 bpm; BP dropped significantly, i.e. diastolic BP by 11 mmHg and systolic BP, 16 mmHg on average. In HME, KAI rose commonly 20 %. Hemoglobin saturation did not change. The paper contains graphic interpretations of the KAI dependence on duration of the HME exposure. Mathematical modeling suggests a physiological interpretation of these results. More often than not sitting at rest in HME reduced substantially the modulating effect of parasympathetic regulation on the cardiovascular system in comparison with the control test in the normal geomagnetic field.


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