scholarly journals Reno-Renal and Reno-Adrenal Reflexes in the Rat

1980 ◽  
Vol 59 (s6) ◽  
pp. 323s-325s ◽  
Author(s):  
G. Recordati ◽  
S. Genovesi ◽  
D. Cerati ◽  
R. Di Cintio
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Nervous System ◽  
Renal Artery ◽  
Sympathetic Activity ◽  
Nerve Activity ◽  
Natural Stimuli ◽  
Anaesthetized Rats ◽  
Excitatory Responses

1. Experiments were carried out to investigate whether the activation of renal chemoceptive receptors by natural stimuli might induce reflex alterations of efferent postganglionic activity to the ipsilateral kidney and preganglionic activity to the ipsilateral adrenal. 2. In anaesthetized rats with intact nervous system back-flow of urine and occlusion of the renal artery were accompanied by increments in efferent sympathetic activity both to the kidney and adrenal without concomitant changes in heart rate and blood pressure. 3. Greater excitatory responses in nerve activity to the same test stimuli were observed in rats with the spinal cord cut at C1. 4. These results indicate that the natural activation of renal chemoceptive receptors might induce reno-renal and reno-adrenal excitatory reflexes which are likely to be integrated at spinal and supraspinal levels.

Nervous System and Hypertension

1978 ◽  
Vol 55 (s4) ◽  
pp. 45s-56s ◽  
Author(s):  
J. P. Chalmers
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Nervous System ◽  
Arterial Pressure ◽  
High Blood Pressure ◽  
Sympathetic Activity ◽  
Experimental Hypertension ◽  
Primary Role ◽  
Noradrenergic Nerves ◽  
Peripheral Sympathetic Activity

1. Presynaptic regulation. The regulation of noradrenaline release by a wide variety of substances acting on presynaptic receptors suggests that local factors may play a greater role in the control of blood pressure than was previously believed and that a number of new approaches to the drug treatment of hypertension could be developed. It also raises the possibility that there might be differences in the presynaptic receptor populations of hypertensive and normotensive subjects or animals. 2. Central nerve pathways. There is a need for more precise delineation of central nerve tracts subserving a cardiovascular function and for greater use of morphological techniques to confirm the reliability of biochemical and physiological experiments in the central nervous system. Two appropriate techniques are described. 3. Models of experimental hypertension. (a) Neurogenic hypertension: interference with baroreceptor afferents can cause a permanent elevation of arterial pressure mediated by increased activity of peripheral sympathetic nerves and of descending noradrenergic nerves terminating in the spinal cord. Catecholamine nerve connections of the nucleus tractus solitarius serve mainly to modulate rather than to mediate baroreceptor reflexes. (b) DOCA—salt hypertension: increased peripheral sympathetic activity is important in both the initiation and the maintenance of this form of hypertension. The decrease in brain-stem noradrenaline turnover found in this model could play a determinant role in the development of the high blood pressure. (c) Renal hypertension: both central and peripheral nervous mechanisms contribute to the development and the early phase of ‘one-kidney’ hypertension in animals. Their role in the maintenance of this form of hypertension is still controversial. (d) Spontaneously hypertensive rats: peripheral and central mechanisms do not appear to have a major role in the maintenance of this form of hypertension. However, it seems possible that centrally evoked increases in peripheral sympathetic activity could be important in the initiation of the high blood pressure. (e) Central catecholamines and blood pressure control; central catecholaminergic nerves do not make up a single homogeneous system. For example, the activity of descending noradrenergic nerves in the spinal cord contributes to an elevation of arterial pressure, whereas the activity of catecholaminergic nerves in the dorsomedial medulla appears to have a depressor effect. 4. Human essential hypertension. (a) There is no good evidence that the nervous system plays the major primary role in the development or maintenance of essential human hypertension. (b) Effective treatment of raised blood pressure through nervous mechanisms requires an understanding of the factors that normally control the pressure and does not necessarily depend on reversing specific nervous processes responsible for producing the increase in pressure.

P4388Acute detrimental effects of e-cigarette and tobacco cigarette smoking on blood pressure and sympathetic nerve activity in healthy subjects

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
K Dimitriadis ◽  
C Tsioufis ◽  
K Kontantinou ◽  
I Liatakis ◽  
E Andrikou ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Cigarette Smoking ◽  
Sympathetic Nerve ◽  
Healthy Subjects ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Tobacco Cigarette ◽  
Sympathetic Nervous

Abstract Background/Introduction Tobacco cigarette smoking is related with atherosclerosis progression, blood pressure increase and changes in sympathetic nerve activity. However, there are scarce data on the impact of e-cigarettes that have been proposed as less harmful alternatives on the cardiovascular system and sympathetic drive. Purpose This study aimed to assess the acute effects of tobacco cigarettes, e-cigarettes and sham smoking on blood pressure and sympathetic nervous system in healthy subjects. Methods We studied 10 normotensive male habitual smokers (mean age 33 years, body mass index: 24.1 kg/m2, office blood pressure=117/72 mmHg) free of cardiovascular disease. The study design was randomized and placebo controlled with 3 experimental sessions (sham smoking, tobacco cigarette smoking, and e-cigarette smoking) in random order, each session on a separate day. Subjects smoked 2 tobacco cigarettes containing 1.1 mg nicotine or simulate smoking (sham smoking) with the 2 cigarettes separated by 5 minutes, while 45 minutes after finishing the second cigarette, subjects smoked a third cigarette or sham cigarette. Additionally, participants smoked e-cigarettes for a period of 5 and 30 minutes. In all occasions, sympathetic drive was assessed by muscle sympathetic nerve activity (MSNA) (baroreflex-dependent) and skin sympathetic nerve activity (SSNA) (baroreflex-independent) based on established methodology (microneurography). Results After the first, second and third tobacco cigarette smoking there was markedly and significantly increase in mean arterial pressure (by 11.2±1.4%, 12.3±1.3% and 13.1±1.4%, respectively, p<0.05 for all) and heart rate (by 25.1±3.7%, 26.3±2.7% and 25.9±3.7%, respectively, p<0.05 for all). Similarly e-cigarette smoking at 5 and 30 minutes was accompanied by augmentation of mean arterial pressure (by 10.9±1.2% and 12.8±1.4%, respectively, p<0.05 for both) and heart rate (by 22.5±3.3% and 23.9±3.8%, respectively, p<0.05 for both). Regarding the effect on sympathetic nervous system, the first, second and third tobacco cigarette smoking was accompanied by lower MSNA (by 28.1±4.4%, 29.6±5.3% and 30.1±5.2%, respectively, p<0.05 for all), whereas SSNA was increased (by 98.2±19.4%, 100.2±22.7% and 101.5±21.6%, respectively, p<0.05 for all). Additionally, e-cigarette smoking at 5 and 30 minutes caused a decrease in MSNA (by 26.9±3.6%, and 28.3±5.1%, respectively, p<0.05 for both), and an augmentation in SSNA (by 97.9±20.1% and 100.9±20.6%, respectively, p<0.05 for both). Sham smoking was devoid of any effects on blood pressure, MSNA and SSNA. Conclusions E-cigarette smoking acutely increases blood pressure and has a detrimental effect on sympathetic nerve activity regulation similar to tobacco smoking in healthy subjects. Our findings underscore the negative impact of e-cigarettes on cardiovascular and autonomic nervous system and could aid further recommendation in their use.

Plasma noradrenaline in Goldblatt models of renovascular hypertension in the rat, before and after surgical reversal

1986 ◽  
Vol 71 (2) ◽  
pp. 199-204 ◽  
Author(s):  
S. M. Walker ◽  
R. F. Bing ◽  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Early Phase ◽  
Sympathetic Activity ◽  
Chronic Phase ◽  
Plasma Noradrenaline ◽  
Before And After ◽  
Sympathetic Nervous ◽  
2K1c Hypertension

1. Plasma noradrenaline (NA), blood pressure (BP) and heart rate (HR) were measured simultaneously in conscious rats under basal conditions in the early phase (4–6 weeks) of one-kidney, one-clip hypertension (1K1C), in the early (4–6 weeks) and chronic (> 16 weeks) phases of the two-kidney, one-clip model (2K1C) and in age-matched loose clip control animals before and 2 days after unclipping. 2. The elevated BP in all three hypertensive groups fell to normal after unclipping, whereas removal of the constricting clip in loose clip controls had no effect on BP. 3. Plasma NA was elevated in 1K1C hypertension (P < 0.05) and fell slightly but non-significantly on unclipping. However, in the early phase of 2K1C hypertension plasma NA was unaltered before and rose significantly (P < 0.05) after unclipping. Plasma NA did not change with unclipping in the chronic phase of 2K1C hypertension and was not different from controls. Unclipping loose clip control animals produced no change in plasma NA. 4. Changes in HR on unclipping followed a similar pattern to changes in plasma NA: changes in the two variables were significantly correlated in all three models (1K1C: r = 0.61, P < 0.005; early 2K1C: r = 0.45, P < 0.05; chronic 2K1C: r = 0.62, P < 0.01). However, BP was only correlated with plasma NA in 1K1C hypertension (r = 0.49, P < 0.02) and not in either phase of the 2K1C model. There was also a highly significant correlation between HR and plasma NA in 1K1C hypertension (r = 0.71, P < 0.001). The pattern of the changes in plasma NA and HR that occurred with reversal of 1K1C hypertension was significantly different from those in the early phase 2K1C model (P < 0.05). 5. These data suggest that there is sympathetic nervous system (SNS) activation in the early phase of 1K1C hypertension, but provide no evidence for increased sympathetic activity in either the early or chronic phases of the 2K1C model. Neither do they support the hypothesis that the fall in BP with unclipping in this model is mediated by reduced SNS activity.

Does the spinal cord generate functionally significant sympathetic activity in the awake rat?

1994 ◽  
Vol 266 (4) ◽  
pp. R1102-R1110
Author(s):  
K. A. Trostel ◽  
J. W. Osborn
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Cervical Spinal Cord ◽  
Adrenergic Blockade ◽  
Nerve Activity ◽  
Nonspecific Effects ◽  
Awake Rat ◽  
Adrenergic Antagonists

Previous studies reach conflicting conclusions regarding the presence of physiologically significant sympathetic nerve activity (SNA) in conscious rats with transection of the cervical spinal cord (CST). The objective of the current study was to determine whether either spinally generated SNA or nonspecific effects of antagonists are responsible for the natriuresis and decreased heart rate that accompany adrenergic blockade in CST rats. To test the first possibility, adrenergic antagonists (phentolamine and propranolol) were administered to three groups of CST rats: 1) renal denervated, 2) adrenalectomized or sham-adrenalectomized, and 3) rats who received the ganglionic blocker hexamethonium. Neither renal denervation, adrenalectomy, nor ganglionic blockade prevented either the three- to fivefold increase in sodium excretion or the 25-50 beats/min decrease in heart rate previously reported. We then administered combinations of different adrenergic antagonists to CST rats to test for nonspecific effects of the drugs. Whereas idazoxan+propranolol reproduced the natriuresis seen with phentolamine+propranolol, prazosin+yohimbine+propranolol did not. We conclude that there is no evidence for functionally significant spinally generated SNA in conscious CST rats and that the natriuresis observed with phentolamine administration is due to imidazoline binding.

Racemic Ketamine Decreases Muscle Sympathetic Activity but Maintains the Neural Response to Hypotensive Challenges in Humans

2000 ◽  
Vol 92 (1) ◽  
pp. 94-94 ◽  
Author(s):  
Peter Kienbaum ◽  
Thorsten Heuter ◽  
Martin C. Michel ◽  
Jürgen Peters
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sodium Nitroprusside ◽  
Sympathetic Activity ◽  
Sympathetic Nerve Activity ◽  
Plasma Concentrations ◽  
Nerve Activity ◽  
Arterial Blood ◽  
Ketamine Anesthesia ◽  
Racemic Ketamine

Background Cardiovascular stimulation and increased catecholamine plasma concentrations during ketamine anesthesia have been attributed to increased central sympathetic activity as well as catecholamine reuptake inhibition in various experimental models. However, direct recordings of efferent sympathetic nerve activity have not been performed in humans. The authors tested the hypothesis that racemic ketamine increases efferent muscle sympathetic activity (MSA) and maintains the muscle sympathetic response to hypotensive challenges. Methods Muscle sympathetic activity was recorded by microneurography in the peroneal nerve of six healthy subjects before and during anesthesia with racemic ketamine (2 mg/kg intravenously plus 30 microg x kg(-1) x min(-1)). Catecholamine plasma concentrations, heart rate, and blood pressure were also determined. Muscle sympathetic neural responses to a hypotensive challenge were assessed by injection of sodium nitroprusside (2-10 microg/kg) before and during ketamine anesthesia. In the final step, increased arterial pressure observed during ketamine anesthesia was adjusted to preanesthetic baseline by sodium nitroprusside infusion (1-6 microg x kg(-1) x min(-1)). Results Ketamine significantly decreased MSA burst frequency (mean +/- SD, 18 +/- 9 bursts/min to 9 +/- 8 bursts/min) and burst incidence (26 +/- 11 bursts/100 heart beats to 9 +/- 6 bursts/100 heart beats). However, when increased mean arterial pressure (85 +/- 8 mmHg to 121 +/- 20 mmHg) was normalized to the awake baseline by sodium nitroprusside, MSA recovered (25 +/- 18 bursts/min; 23 +/- 14 bursts/100 heart beats). During ketamine anesthesia, both epinephrine (15 +/- 10 pg/ml to 256 +/- 193 pg/ml) and norepinephrine (250 +/- 105 pg/ml to 570 +/- 270 pg/ml) plasma concentrations significantly increased, as did heart rate (67 +/- 13 beats/min to 113 +/- 15 beats/min). Hypotensive challenges similarly increased MSA both in the awake state and during ketamine anesthesia. Conclusions During increased arterial blood pressure associated with ketamine, sympathetic discharge to muscle blood vessels decreases at the same time that plasma concentrations of norepinephrine increase. When this increase in arterial blood pressure is reversed, MSA during ketamine is not changed from preketamine baseline recordings. Finally, hypotensive challenges still evoke an unchanged sympathetic reflex response. Thus, our results do not support the assumption that ketamine anesthesia increases sympathetic nerve activity in a generalized fashion.

scholarly journals Post-Exertional Malaise May Be Related to Central Blood Pressure, Sympathetic Activity and Mental Fatigue in Chronic Fatigue Syndrome Patients

2021 ◽  
Vol 10 (11) ◽  
pp. 2327
Author(s):  
Sławomir Kujawski ◽  
Joanna Słomko ◽  
Lynette Hodges ◽  
Derek F. H. Pheby ◽  
Modra Murovska ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Chronic Fatigue Syndrome ◽  
Systolic Blood Pressure ◽  
Sympathetic Activity ◽  
Chronic Fatigue ◽  
Mental Fatigue ◽  
Fatigue Syndrome ◽  
Central Systolic Blood Pressure

Post-exertional malaise (PEM) is regarded as the hallmark symptom in chronic fatigue syndrome (CFS). The aim of the current study is to explore differences in CFS patients with and without PEM in indicators of aortic stiffness, autonomic nervous system function, and severity of fatigue. One-hundred and one patients met the Fukuda criteria. A Chronic Fatigue Questionnaire (CFQ) and Fatigue Impact Scale (FIS) were used to assess the level of mental and physical fatigue. Aortic systolic blood pressure (sBPaortic) and the autonomic nervous system were measured with the arteriograph and Task Force Monitor, respectively. Eighty-two patients suffered prolonged PEM according to the Fukuda criteria, while 19 did not. Patients with PEM had higher FIS scores (p = 0.02), lower central systolic blood pressure (p = 0.02) and higher mental fatigue (p = 0.03). For a one-point increase in the mental fatigue component of the CFQ scale, the risk of PEM increases by 34%. For an sBPaortic increase of 1 mmHg, the risk of PEM decreases by 5%. For a one unit increase in sympathovagal balance, the risk of PEM increases by 330%. Higher mental fatigue and sympathetic activity in rest are related to an increased risk of PEM, while higher central systolic blood pressure is related to a reduced risk of PEM. However, none of the between group differences were significant after FDR correction, and therefore conclusions should be treated with caution and replicated in further studies.

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