Intracerebroventricular angiotensin II increases arterial blood pressure in rhesus monkeys by stimulation of pituitary hormones and the sympathetic nervous system

1982 ◽  
Vol 38 (4) ◽  
pp. 469-470 ◽  
Author(s):  
B. A. Schölkens ◽  
W. Jung ◽  
W. Rascher ◽  
R. Dietz ◽  
D. Ganten
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Sympathetic Nervous System ◽  
Arterial Blood Pressure ◽  
Rhesus Monkeys ◽  
Pituitary Hormones ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Stimulation Of

Frequency response characteristic of sympathetic-mediated vasomotor waves in conscious rats

1996 ◽  
Vol 271 (4) ◽  
pp. H1416-H1422 ◽  
Author(s):  
H. M. Stauss ◽  
K. C. Kregel
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Frequency Response ◽  
Arterial Blood Pressure ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Sympathetic Nervous

Power spectrum analysis of arterial blood pressure (BP) and heart rate (HR) has been used to investigate autonomic nervous system activity. Sympathetic-mediated vasomotor tone has been attributed to the BP power at frequencies between 0.05 and 0.15 Hz in humans and dogs and between 0.2 and 0.8 Hz in rats. In contrast, it has been suggested that the sympathetic nervous system is too sluggish to transmit frequencies higher than 0.017 Hz in dogs. Thus we investigated the frequency-response characteristics of the transmission of peripheral sympathetic nerve discharge to peripheral vascular resistance and arterial blood pressure in conscious rats. Eleven rats were instrumented with arterial catheters, nerve electrodes on the sympathetic splanchnic nerve, and flow probes on the superior mesenteric artery. The splanchnic nerve was cut proximal to the electrode to avoid afferent nerve stimulation. The next day the nerve was stimulated at frequencies of 0.05, 0.1, 0.2, 0.5, 1.0, and 2.0 Hz while mesenteric blood flow, BP, and HR were recorded in conscious rats. Mesenteric resistance (MR) was calculated off-line. Nerve stimulation at 0.05, 0.1, 0.2, 0.5, and 1.0 Hz significantly increased the power in MR at these respective frequencies. The greatest response was found between 0.2 and 0.5 Hz. These oscillations in MR were translated to oscillations in BP, but not in HR. Nerve stimulation on the second day, when the nerve was degenerated, did not elicit oscillations in MR or BP. We conclude that the peripheral sympathetic nervous system in rats can transmit signals at frequencies higher than those traditionally assigned to sympathetic vasomotor activity in several species, including humans, and may even overlap with the respiration-related high-frequency range.

An initial life-threatening effect of ionizing radiation: Hypotension

1990 ◽  
Vol 68 (9) ◽  
pp. 967-973
Author(s):  
P. C. Senanayake ◽  
C. M. Goddard ◽  
E. A. Yacyshyn ◽  
W. B. Hulbert ◽  
R. F. Ruth
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Ionizing Radiation ◽  
Sympathetic Nervous System ◽  
Rhesus Monkey ◽  
Arterial Blood Pressure ◽  
Arterial Blood ◽  
Life Threatening ◽  
Sympathetic Nervous ◽  
Reactor Accidents

Radiation hypotension (RH) is a severe decrease in arterial blood pressure during the 48 h after irradiation. RH is the presumed cause of three human deaths in reactor accidents and occurs after clinical irradiation. RH is described more fully in the rhesus monkey and the rabbit. This report describes prevention of RH in the rabbit by the cutting of two nerves of the sympathetic nervous system.

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

Influences of exogenous insulin on arterial blood pressure measurements of the rat

1989 ◽  
Vol 67 (6) ◽  
pp. 2335-2342 ◽  
Author(s):  
J. G. Edwards ◽  
C. M. Tipton
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Smooth Muscle ◽  
Sympathetic Nervous System ◽  
Arterial Blood Pressure ◽  
Insulin Infusion ◽  
Control Period ◽  
Male Rats ◽  
Arterial Blood ◽  
Sympathetic Nervous

Studies were undertaken with adult male rats to test the hypothesis that euglycemic hyperinsulinemia would alter mean arterial blood pressure (MAP) and heart rate (HR) relationships by activation of the sympathetic nervous system. Conscious rats were infused either with insulin or control vehicle (0, 0.47, 1.5, 4.7, 15.0 mU.kg-1.min-1) for 75 min before injection of hexamethonium. Compared with the control period, insulin infusion significantly increased MAP by 7.1 +/- 0.1, 12.7 +/- 2.0, and 19.7 +/- 0.3 (SE) mmHg and HR by 44 +/- 8.4, 66 +/- 10.3, and 95 +/- 6.3 beats/min, respectively, during the three highest rates of infusion. The dose-dependent increases in MAP and HR were due to increases in the activity of hexamethonium-sensitive pathways. In chemically sympathectomized rats, insulin infusion did not produce a significant increase in either MAP or HR. The influence of exogenous norepinephrine on MAP and HR was also studied after insulin infusion. Compared with the insulin-vehicle infusion, insulin infusion significantly depressed (P less than 0.05) the norepinephrine dose-response increase in MAP. In addition, isolated smooth muscle strips were studied to determine the influence of insulin on their in vitro responses to increasing doses of norepinephrine. Although insulin did not alter contractility, it significantly (P less than 0.05) decreased the sensitivity of the vascular strips to norepinephrine. Collectively, the data from these euglycemic experiments indicated that infusions of insulin caused increases in HR and MAP because of activation of the sympathetic nervous system, even though the responsiveness of the vascular smooth muscle was depressed.

Sustained sympathetic nervous system support of arterial blood pressure during repeated brief umbilical cord occlusions in near-term fetal sheep

2014 ◽  
Vol 306 (11) ◽  
pp. R787-R795 ◽  
Author(s):  
Robert Galinsky ◽  
Ellen C. Jensen ◽  
Laura Bennet ◽  
Clinton J. Mitchell ◽  
Eleanor R. Gunn ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Blood Pressure ◽  
Umbilical Cord ◽  
Prolonged Exposure ◽  
Fetal Sheep ◽  
Arterial Blood ◽  
Significant Difference ◽  
Sympathetic Nervous

Sympathetic nervous system (SNS)-mediated peripheral vasoconstriction plays a key role in initial maintenance of blood pressure during rapid-onset asphyxia in the mammalian fetus, but it is attenuated after the first few minutes. It is unclear whether the SNS response is sustained during the brief, but frequently repeated, episodes of asphyxia characteristic of labor. In the present study, 14 fetal sheep at 0.85 of gestation received either chemical sympathectomy with 6-hydroxydopamine (6-OHDA; n = 7) or sham injection (control; n = 7), followed 4–5 days later by repeated 2-min episodes of complete umbilical cord occlusion every 5 min for up to 4 h or until mean arterial blood pressure (MAP) fell to <20 mmHg for two successive occlusions. In controls, umbilical cord occlusions were associated with a rapid initial fall in fetal heart rate (FHR) and femoral blood flow (FBF), with initial hypertension, followed by progressive development of hypotension during ongoing occlusions. Sympathectomy was associated with attenuation of the initial rise in MAP during umbilical cord occlusion, and after the onset of hypotension, a markedly more rapid fall of MAP to the nadir, with a correspondingly slower fall in FBF ( P < 0.05). In contrast, MAP and FHR between successive occlusions were higher after sympathectomy ( P < 0.05). There was no significant difference in the number of occlusions before terminal hypotension (6-OHDA; 16.1 ± 2.2 vs. control; 18.7 ± 2.3). These data show that SNS activity provides ongoing support for fetal MAP during prolonged exposure to brief repeated asphyxia.

scholarly journals The Impact of α-Adrenoceptors in the Regulation of the Hypotonicity-Induced Increase in Duodenal Mucosal Permeability In Vivo

Pharmaceutics ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2096
Author(s):  
John Sedin ◽  
David Dahlgren ◽  
Markus Sjöblom ◽  
Olof Nylander
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Arterial Blood Pressure ◽  
Dependent Manner ◽  
Mucosal Permeability ◽  
Arterial Blood ◽  
Α2 Adrenoceptor ◽  
Sympathetic Nervous

The duodenal mucosa is regularly exposed to a low osmolality, and recent experiments suggest that hypotonicity increases mucosal permeability in an osmolality-dependent manner. The aim was to examine whether the sympathetic nervous system, via action on α-adrenoceptors, affects the hypotonicity-induced increase in duodenal mucosal permeability. The duodenum of anaesthetised rats was perfused in vivo with a 50 mM NaCl solution in the presence of adrenergic α-adrenoceptor drugs. Studied were the effects on mucosal permeability (blood-to-lumen clearance of 51Cr-EDTA), arterial blood pressure, luminal alkalinisation, transepithelial fluid flux, and motility. Hypotonicity induced a six-fold increase in mucosal permeability, a response that was reversible and repeatable. The α2-adrenoceptor agonist clonidine abolished the hypotonicity-induced increase in mucosal permeability, reduced arterial blood pressure, inhibited duodenal motility, and decreased luminal alkalinisation. The α2-adrenoceptor antagonists, yohimbine and idazoxan, prevented the inhibitory effect of clonidine on the hypotonicity-induced increase in mucosal permeability. The α1-agonist phenylephrine or the α1-antagonist prazosin elicited their predicted effect on blood pressure but did not affect the hypotonicity-induced increase in mucosal permeability. None of the α1- or α2-adrenoceptor drugs changed the hypotonicity-induced net fluid absorption. In conclusion, stimulation of the adrenergic α2-adrenoceptor prevents the hypotonicity-induced increase in mucosal permeability, suggesting that the sympathetic nervous system has the capability to regulate duodenal mucosal permeability.

Interactions between ANG II, sympathetic nervous system, and baroreceptor reflexes in regulation of blood pressure

1992 ◽  
Vol 262 (6) ◽  
pp. E763-E778 ◽  
Author(s):  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Blood Pressure Control ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Ang Ii ◽  
Arterial Blood ◽  
Baroreceptor Reflexes ◽  
Sympathetic Nervous

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.

The sympathetic muscle metaboreflex is not different in the third trimester in normotensive pregnant women.

2020 ◽  
Author(s):  
Rachel J. Skow ◽  
Andrew R. Steele ◽  
Graham M. Fraser ◽  
Margie H. Davenport ◽  
Craig D. Steinback
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Pregnant Women ◽  
Isometric Handgrip ◽  
Third Trimester ◽  
Muscle Metaboreflex ◽  
The Third ◽  
Arterial Blood ◽  
Sympathetic Nervous

Isometric handgrip (IHG) is used to assess sympathetic nervous system responses to exercise and may be useful at predicting hypertension in both pregnant and non-pregnant populations. We have previously observed altered sympathetic nervous system control of blood pressure in late pregnancy. Therefore, we measured muscle sympathetic nerve activity (MSNA) and blood pressure during muscle metaboreflex activation (IHG) in normotensive pregnant women in the third trimester compared to healthy non-pregnant women. Nineteen pregnant (32±3wks gestation) and fourteen non-pregnant women were matched for age, non/pre-pregnant BMI, and parity. MSNA (microneurography), heart rate (ECG), and arterial blood pressure (Finometer) were continuously recorded during ten minutes of rest, and then during two-minutes of IHG at 30% of maximal voluntary contraction, and two-minutes of post-exercise circulatory occlusion (PECO). Baseline SNA was elevated in pregnant (41±11 bursts/min) compared to non-pregnant women (27 ± 9 bursts/minute; p=0.005); however, the sympathetic baroreflex gain and neurovascular transduction were not different between groups (p=0.62 and p=0.32, respectively). During IHG and PECO there was no significant differences in the pressor response (∆MAP) during IHG and PECO was not different between groups (p=0.25, main effect of group) nor the sympathetic response (interaction effect: p=0.16, 0.25, and 0.27 for burst frequency, burst incidence, and total SNA respectively). These data suggest that pregnant women who have maintained sympathetic baroreflex and neurovascular transduction also have similar sympathetic and pressor responses during exercise.

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