Long-term control of arterial blood pressure

1992 ◽  
Vol 72 (1) ◽  
pp. 231-300 ◽  
Author(s):  
A. W. Cowley
Keyword(s):  
Nervous System ◽  
Arterial Pressure ◽  
Volume Regulation ◽  
Neural Control ◽  
Muscle Tone ◽  
Feedback Signal ◽  
Work Related ◽  
Arterial Blood ◽  
The Moment

Two concepts for the long-term regulation of arterial pressure were considered in this review, the neural control hypothesis and the volume regulation hypothesis. The role of the nervous system and fluid volume regulation are intertwined in a way that has made it difficult to experimentally evaluate their separate contributions in the long-term regulation of arterial pressure. Nevertheless, from a substantial body of work related to the neural control of cardiovascular function, it appears that the ability of the nervous system to control arterial pressure is limited to the detection and correction of rapid short-term changes of arterial pressure. A long and exhaustive search has yet yielded no new neural mechanisms beyond the classic sinoaortic baroreceptors that can detect changes of arterial pressure. The baroreceptor mechanisms are of great importance for the moment-to-moment stabilization of arterial pressure, but because they do not possess sufficient strength and because they reset in time to the prevailing level of arterial pressure, they cannot provide a sustained negative feedback signal to provide long-term regulation of arterial pressure in face of sustained stimuli. This is not to say that the nervous system cannot affect the long-term level of arterial pressure. A distinction is made here between the many factors that can influence the long-term level of pressure and those that actually serve to detect changes of pressure and serve to maintain the level of pressure within a narrow range over the period of our adult lifetime. In this sense, there is evidence that in genetically susceptible individuals, environmental stresses can influence the long-term level of arterial pressure via the central and peripheral neural autonomic pathways. It is inappropriate, however, to view the nervous system as a long-term controller of arterial pressure because there is yet no evidence that the CNS can detect changes of arterial pressure nor changes in total body sodium and water content over sustained periods whereby it could provide an adequate long-term normalization of such error signals. In contrast, evidence has grown in support of the renal pressure-diuresis volume regulation hypothesis for the long-term control of arterial pressure over the past decade. An enhanced understanding of the mechanisms of pressure diuresis-natriuresis coupled with studies exploring how changes of vascular volume can influence vascular smooth muscle tone provide a compelling basis for this hypothesis of long-term arterial pressure regulation. This overall concept is represented and summarized in Figure 12.(ABSTRACT TRUNCATED AT 400 WORDS)

Hormonal-sympathetic interactions in long-term regulation of arterial pressure: an hypothesis

1995 ◽  
Vol 268 (6) ◽  
pp. R1343-R1358 ◽  
Author(s):  
V. L. Brooks ◽  
J. W. Osborn
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Arterial Pressure ◽  
Plasma Concentrations ◽  
Circumventricular Organs ◽  
Feedback Signal ◽  
Salt Loading ◽  
Alternate Model ◽  
The Central Nervous System

The importance of the sympathetic nervous system in short-term regulation of arterial pressure is well accepted. However, the question of whether neural systems participate in long-term control of pressure has been debated for decades and remains unresolved. The principal argument against such a control system is that arterial baroreceptors adapt to sustained changes in arterial pressure. In addition, denervation of baroreceptors has minimal to no effect on basal levels of arterial pressure chronically. This argument assumes, however, that baroreceptors provide the primary chronic feedback signal to the central nervous system. An alternate model is proposed in which circulating hormones, primarily arginine vasopressin and angiotensin II, provide a long-term afferent signal to the central nervous system via binding to specific receptors in central sites lacking a blood-brain barrier (circumventricular organs). Studies suggest that the release of the hormones and the sympathetic response to alterations in their plasma concentrations are nonadaptive but may be gated by baroreceptor input. Evidence that this "hormonal-sympathetic reflex" model may explain the long-term alterations in sympathetic activity in response to chronic salt depletion and salt loading as well as congestive heart failure is presented. Finally, the role of an impaired hormonal sympathetic reflex in hypertension, specifically salt-dependent hypertension, is discussed.

scholarly journals Sympathetic baroreflex gain in normotensive pregnant women

2015 ◽  
Vol 119 (5) ◽  
pp. 468-474 ◽  
Author(s):  
Charlotte W. Usselman ◽  
Rachel J. Skow ◽  
Brittany A. Matenchuk ◽  
Radha S. Chari ◽  
Colleen G. Julian ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Pregnant Women ◽  
Sympathetic Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Sequence Method ◽  
Normotensive Pregnancy ◽  
Dependent Mechanism

Muscle sympathetic nerve activity is increased during normotensive pregnancy while mean arterial pressure is maintained or reduced, suggesting baroreflex resetting. We hypothesized spontaneous sympathetic baroreflex gain would be reduced in normotensive pregnant women relative to nonpregnant matched controls. Integrated muscle sympathetic burst incidence and total sympathetic activity (microneurography), blood pressure (Finometer), and R-R interval (ECG) were assessed at rest in 11 pregnant women (33 ± 1 wk gestation, 31 ± 1 yr, prepregnancy BMI: 23.5 ± 0.9 kg/m2) and 11 nonpregnant controls (29 ± 1 yr; BMI: 25.2 ± 1.7 kg/m2). Pregnant women had elevated baseline sympathetic burst incidence (43 ± 2 vs. 33 ± 2 bursts/100 heart beats, P = 0.01) and total sympathetic activity (1,811 ± 148 vs. 1,140 ± 55 au, P < 0.01) relative to controls. Both mean (88 ± 3 vs. 91 ± 2 mmHg, P = 0.4) and diastolic (DBP) (72 ± 3 vs. 73 ± 2 mmHg, P = 0.7) pressures were similar between pregnant and nonpregnant women, respectively, indicating an upward resetting of the baroreflex set point with pregnancy. Baroreflex gain, calculated as the linear relationship between sympathetic burst incidence and DBP, was reduced in pregnant women relative to controls (−3.7 ± 0.5 vs. −5.4 ± 0.5 bursts·100 heart beats−1·mmHg−1, P = 0.03), as was baroreflex gain calculated with total sympathetic activity (−294 ± 24 vs. −210 ± 24 au·100 heart beats−1·mmHg−1; P = 0.03). Cardiovagal baroreflex gain (sequence method) was not different between nonpregnant controls and pregnant women (49 ± 8 vs. 36 ± 8 ms/mmHg; P = 0.2). However, sympathetic (burst incidence) and cardiovagal gains were negatively correlated in pregnant women ( R = −0.7; P = 0.02). Together, these data indicate that the influence of the sympathetic nervous system over arterial blood pressure is reduced in normotensive pregnancy, in terms of both long-term and beat-to-beat regulation of arterial pressure, likely through a baroreceptor-dependent mechanism.

Relation of arterial pressure to spontaneous variations in digital volume

1960 ◽  
Vol 15 (1) ◽  
pp. 23-24 ◽  
Author(s):  
G. E. Burch ◽  
N. DePasquale
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Pressure ◽  
Blood Vessels ◽  
Arterial Blood Pressure ◽  
Peripheral Blood ◽  
Normal Subjects ◽  
Arterial Blood ◽  
Sympathetic Nervous

Simultaneous digital plethysmographic and brachial arterial pressure recordings in 11 normal subjects at rest in bed in a comfortable atmosphere showed that the spontaneous variations in digital volume (alpha and beta deflections) were independent of variations in arterial blood pressure. This indicates that the regulation of the caliber of the peripheral blood vessels as well as the spontaneous variations in the volume of the digital vessels is not passively produced by fluctuations in arterial blood pressure, including the Traube-Hering waves, but must be controlled by different centers and pathways of the sympathetic nervous system. Submitted on July 27, 1959

scholarly journals The influence of occupational environment and professional factors on the risk of cardiovascular disease

Medicina ◽  
2006 ◽  
Vol 43 (2) ◽  
pp. 96 ◽  
Author(s):  
Vytautas Obelenis ◽  
Vilija Malinauskienė
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Circulatory System ◽  
Electrolyte Imbalance ◽  
Vascular Lesions ◽  
Cholesterol Concentration ◽  
Long Term Effects ◽  
Arterial Blood ◽  
The Central Nervous System

The article reviews the recent scientific literature and the authors’ studies on this topic. Occupational conditions and psychological factors have been shown to play an important role in the etiopathogenesis of cardiovascular diseases. Their effect is often indirect, through damage to the central nervous, respiratory, and neuroendocrine systems. Hot climate in the workplace and intense infrared radiation cause the water and electrolyte imbalance and chronic hyperthermia and manifests as neurovegetative dystonia. The long-term effects of low temperatures condition ischemic lesions in circulatory system, trophic organ destruction. The influence of ultrahigh-frequency electromagnetic radiation on the cardiovascular system is directly related to the central nervous system and neurohumoral lesions. “Microwave disease” often manifests as polymorphic dystonia. Exposure to occupational vibration causes “white finger” syndrome or Raynaud’s phenomenon together with cerebral vascular lesions. Recent studies have confirmed that noise as a chronic stressor causes the imbalance in the central and vegetative nervous systems and changes in homeostasis. Noise increases catecholamine and cholesterol concentration in blood, has an effect on plasma lipoprotein levels, increases heart rate, arterial blood pressure, and risk of myocardial infarction. Psychophysiological changes caused by long-term stress influence constant pathological changes in the central nervous system, endocrine and cardiovascular systems. The long-term effect of psychogenic stressors is very important in the etiopathogenesis of psychosomatic diseases.

scholarly journals Current computational models do not reveal the importance of the nervous system in long-term control of arterial pressure

2009 ◽  
Vol 94 (4) ◽  
pp. 389-396 ◽  
Author(s):  
John W. Osborn ◽  
Viktoria A. Averina ◽  
Gregory D. Fink
Keyword(s):  
Nervous System ◽  
Arterial Pressure ◽  
Computational Models

Renin-angiotensin mechanisms in oral contraceptive hypertension in conscious rats

1985 ◽  
Vol 248 (5) ◽  
pp. H695-H699 ◽  
Author(s):  
W. L. Fowler ◽  
J. A. Johnson ◽  
K. D. Kurz ◽  
C. G. Payne
Keyword(s):  
Oral Contraceptive ◽  
Arterial Pressure ◽  
Jugular Vein ◽  
Plasma Renin ◽  
Term Treatment ◽  
Ang Ii ◽  
Renin Substrate ◽  
Arterial Blood ◽  
Long Term Treatment

Rats were placed on powdered chow containing either no additives (controls), mestranol (a synthetic estrogen), norethynodrel (a synthetic progestin), or both mestranol and norethynodrel. After 6 mo on these diets, catheters were placed in the carotid artery and jugular vein of each rat. An arterial blood sample was obtained for plasma renin activity (PRA), plasma renin concentration (PRC), and plasma renin substrate concentration (PRS). Mean arterial pressure was measured in each rat. The angiotensin II (ANG II) antagonist, [Sar1-Ile8]ANG II, was infused intravenously for 30 min while blood pressure was recorded. Rats treated with mestranol and/or norethynodrel had PRA and PRC values that were not different from the control rats; however, mestranol-treated rats and rats treated with mestranol plus norethynodrel had PRS values that were substantially (P less than 0.01) higher than the controls. Arterial pressures in rats treated with mestranol and with mestranol plus norethynodrel were significantly (P less than 0.01) elevated when compared with the controls and with the rats treated with norethynodrel alone. Infusion of the ANG II antagonist failed to alter arterial pressure in any of the groups of rats. These results indicated that, in the steroid combination found in the oral contraceptive Enovid, it is the estrogenic component that results in hypertension in this rat model. Also this study found no evidence that ANG II plays a role in maintaining the elevated arterial pressure following long-term treatment with mestranol in rats.

Graphic format for teaching long-term control of systemic arterial pressure.

1996 ◽  
Vol 270 (6) ◽  
pp. S40
Author(s):  
J J Faber
Keyword(s):  
Cardiac Output ◽  
Steady State ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Filling Pressure ◽  
Arterial Blood ◽  
Ventricular Filling Pressure ◽  
Ventricular Filling

Circulatory homeostasis is a difficult notion. The graphic format presented here facilitates the teaching of long-term control of systemic arterial blood pressure and cardiac output. It is based on the view that the following four "function curves" cooperate in long-term regulation: the relation between blood volume and ventricular filling pressure, the relation between ventricular filling pressure and cardiac output, the relation between cardiac output and peripheral resistance, and the relation between arterial pressure and natriuresis. Positioning the function curves in the format presented here clarifies their cooperativity. The distinction between a nonsteady state and a steady state deserves emphasis. Long-term pathophysiology of the circulation is most easily taught on the basis of the assumption that, generally, there will be a steady state. The format clarifies why some known physiological relations are almost impossible to demonstrate in the intact organism, and it discourages explanations of pathophysiology that are not firmly based on physiology.

Sign in / Sign up

Export Citation Format

Share Document