Autonomic control of blood pressure in mice: basic physiology and effects of genetic modification

2002 ◽  
Vol 282 (6) ◽  
pp. R1545-R1564 ◽  
Author(s):  
Ben J. A. Janssen ◽  
Jos F. M. Smits

Control of blood pressure and of blood flow is essential for maintenance of homeostasis. The hemodynamic state is adjusted by intrinsic, neural, and hormonal mechanisms to optimize adaptation to internal and environmental challenges. In the last decade, many studies showed that modification of the mouse genome may alter the capacity of cardiovascular control systems to respond to homeostatic challenges or even bring about a permanent pathophysiological state. This review discusses the progress that has been made in understanding of autonomic cardiovascular control mechanisms from studies in genetically modified mice. First, from a physiological perspective, we describe how basic hemodynamic function can be measured in conscious conditions in mice. Second, we focus on the integrative role of autonomic nerves in control of blood pressure in the mouse, and finally, we depict the opportunities and insights provided by genetic modification in this area.

1978 ◽  
Vol 234 (2) ◽  
pp. H152-H156
Author(s):  
G. S. Geis ◽  
G. Barratt ◽  
R. D. Wurster

Resting cardiovascular parameters and the responses to bilateral carotid occlusions (BCO) were monitored in pentobarbital-anesthetized and conscious dogs before and after placing lesions in the dorsolateral funiculi at C7-C8 and after spinal transections at C7. Pre- and postlesion blood pressure (BP) and heart rate (HR) responses to exercise were also monitored. The lesions significantly attenuated the responses to BCO and decreased resting BP in anesthetized dogs. Yet neither resting HR in anesthetized or conscious dogs nor the resting BP in conscious dogs was affected by the lesions. Subsequent spinal transections significantly decreased resting HR and BP and the responses to BCO but did not affect the BP response to BCO in anesthetized dogs as compared with corresponding postlesion parameters. BP responses to exercise were significantly attenuated by the lesions, but HR responses were not affected. Since stimulation and BP studies indicated that the descending pressor pathway had been ablated, the data suggest that the pathway mediates BP and HR responses to BCO in pentobarbital-anesthetized and conscious dogs. It does not maintain resting HR in anesthetized or conscious animals, and the resting BP in conscious dogs. This pathway is important for BP responses to exercise but is not necessary for HR responses. Finally, other spinal pathways are involved in cardiovascular control.


2012 ◽  
Vol 30 ◽  
pp. e300
Author(s):  
Daniela Ravizzoni Dartora ◽  
Karina Rabello Casali ◽  
Mariane Bertagnolli ◽  
Maria Claudia Irigoyen ◽  
Robson Santos

2017 ◽  
Vol 312 (4) ◽  
pp. R575-R584 ◽  
Author(s):  
John L. Dobson ◽  
Mary Beth Yarbrough ◽  
Jose Perez ◽  
Kelsey Evans ◽  
Thomas Buckley

Recent evidence suggests that concussions may disrupt autonomic cardiovascular control. This study investigated the initial effects of concussion on cardiovascular function using three autonomic reflex tests. Twenty-three recreational athletes (12 women, 11 men) were divided into concussed ( n = 12) and control ( n = 11) groups. Concussed participants performed forced breathing, standing, and Valsalva autonomic tests four times: 1) within 48 h of injury; 2) 24 h later; 3) 1 wk after injury; and 4) 2 wk after injury. The controls performed the same tests on the same schedule. Differences in heart rate (HR), systolic blood pressure (SBP), and diastolic blood pressure (DBP) responses to the tests were continuously measured using finger photoplethysmography and were analyzed using repeated-measures multivariate ANOVAs and ANOVAs. Within 48 h of injury, the concussed group had significantly greater resting SBP ( t21= 2.44, P = 0.02, d = 1.03), HR ( t21= 2.33, P = 0.03, d = 1.01), and SBP responses to standing ( t21= 2.98, P = 0.01, d = 1.24), and 90% SBP normalization times ( t21= 2.64, P = 0.02, d = 1.10) after the Valsalva, but those group differences subsided 24 h later. There was also a significant interaction with the HR responses to forced breathing ( F3,60= 4.13, P = 0.01, ηp2= 0.17), indicating the concussed responses declined relative to the control’s over time. The results demonstrate that concussion disrupted autonomic cardiovascular control, and that autonomic reflex tests are practical means by which to evaluate that dysfunction.


2003 ◽  
Vol 105 (5) ◽  
pp. 545-547 ◽  
Author(s):  
Gianfranco PARATI

Blood pressure variability is the result of a complex interaction between external stimulation and several cardiovascular control mechanisms and is enhanced in all those conditions characterized by an impaired autonomic regulation of circulation. In particular, blood pressure variability is enhanced in hypertension over 24 h and may independently contribute to the cardiovascular complications of this condition. The paper by Mussalo and co-workers in this issue of Clinical Science offers additional information in this field by suggesting that different forms of hypertension are characterized by different patterns of blood pressure variability, and that these differences may reflect variations in the underlying autonomic regulation of the heart and blood vessels.


Amino Acids ◽  
2012 ◽  
Vol 43 (1) ◽  
pp. 97-109 ◽  
Author(s):  
Katsuya Nagai ◽  
Mamoru Tanida ◽  
Akira Niijima ◽  
Nobuo Tsuruoka ◽  
Yoshinobu Kiso ◽  
...  

1988 ◽  
Vol 255 (5) ◽  
pp. R855-R860 ◽  
Author(s):  
A. V. Ferguson ◽  
P. Marcus

The studies described here have utilized electrical stimulation techniques to examine the effects of activation of neural elements within the area postrema (AP) on cardiovascular control mechanisms. A total of 45 urethananesthetized male Sprague-Dawley rats were used in these experiments. Low-frequency electrical stimulation (10 Hz, 200 microA) in the AP resulted in rapid onset (less than 2 s), short-lasting (less than 5 s after end of stimulation) decreases in mean arterial blood pressure (-34.8 +/- 2.7 mmHg, n = 17 rats). In contrast, similar stimulation in the adjacent nucleus tractus solitarius (NTS) caused similarly timed increases in blood pressure (+43.1 +/- 6.7 mmHg, n = 5 rats). Activation of neural elements within the AP was found to significantly (Student's t test, P less than 0.01) reduce heart rate, an effect that was also specific to the AP site as similar stimulation in the NTS was without effect. These data support an important role for AP in cardiovascular control mechanisms. They demonstrate that stimulation in AP results in rapid reversible decreases in mean arterial blood pressure and heart rate. Such findings further emphasise the potential roles of this circumventricular structure in autonomic control mechanisms.


2020 ◽  
Vol 47 (4) ◽  
pp. 5-10
Author(s):  
R. Nikolova ◽  
S. Danev ◽  
T. Kundurjiev ◽  
N. Madjarov

AbstractCardiovascular diseases (CVD) are among the most significant and common chronic non-communicable diseases in Bulgaria. Screening, identification and registration of pathophysiological mechanisms and psychological and occupational factors related to CVD should be implemented in the diagnostic work-up. Job analysis contributes to the implementation of screening and identification of the most significant psychological and professional factors related to the work activity.Aim: The aim of our study is to examine the pathophysiological mechanisms of autonomic cardiovascular control and psychological and occupational factors determining the risk of CVD.Materials and methods: The following groups of individuals were examined: 83 physicians, 54 nurses, 23 employees and 40 militaries. The autonomic cardiovascular control was studied through the time-and frequency-domain based measures of the Analysis of Heart Rate Variability (HRV).Results: The results of the ANOVA test showed that there was a statistically significant difference in the time-domain and frequency-domain based HRV measures between the compared groups: X [F (4; 225) = 4.455, p = 0.001]; SDNN [F (4; 225) = 3.876, p = 0.005]; SDNN5 [F (4; 225) = 3.083, p = 0.01]; pNN50 [F (4; 225) = 8.303, p < 0.001]; rMSSD [F (4; 225) = 8.711, p < 0.001]; SDSD [F (4; 225) = 8.323, p < 0.001; VLF [F (4; 225) = 1.204, p = 0.31]; LF [F (4; 225) = 3.874, p = 0.005]; HF [F (4; 225) = 7.790, p < 0.001] and LF/HF [F (4; 225) = 8.601, p < 0.001]. The results of our study revealed that occupational stress and cognitive workload in physicians, nurses, and employees induced a process of reciprocally combined inhibition of the parasympathetic branch of the autonomic nervous system (ANS) (SDNN, SDNN5, pNN50, rMSSD, and HF) and activation of the sympathetic branch of ANS (LF), while in military personnel they cause a process of co-activation of the parasympathetic and sympathetic branches of the ANS (rMSSD, SDNN, SDNN5, pNN50 and LF/HF).Conclusion: Stress-induced dysfunctional autonomic cardiovascular regulation, patho-physiological control mechanisms, psychological and occupational factors determine the risk of CVD. Their identification could contribute to the diagnostics and prevention of CVD.


2005 ◽  
Vol 109 (5) ◽  
pp. 431-437 ◽  
Author(s):  
Nancy L. Kanagy

Cardiovascular regulation by the sympathetic nervous system is mediated by activation of one or more of the nine known subtypes of the adrenergic receptor family; α1A-, α1B-, α1D-, α2A-, α2B-, α2C-, β1-, β2- and β3-ARs (adrenoceptors). The role of the α2-AR family has long been known to include presynaptic inhibition of neurotransmitter release, diminished sympathetic efferent traffic, vasodilation and vasoconstriction. This complex response is mediated by one of three subtypes which all uniquely affect blood pressure and blood flow. All three subtypes are present in the brain, kidney, heart and vasculature. However, each differentially influences blood pressure and sympathetic transmission. Activation of α2A-ARs in cardiovascular control centres of the brain lowers blood pressure and decreases plasma noradrenaline (norepinephrine), activation of peripheral α2B-ARs causes sodium retention and vasoconstriction, whereas activation of peripheral α2C-ARs causes cold-induced vasoconstriction. In addition, non-selective agonists elicit endothelium-dependent vasodilation and presynaptic inhibition of noradrenaline release. The evidence that each of these receptor subtypes uniquely participates in cardiovascular control is discussed in this review.


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