scholarly journals Acute Changes in Blood Pressure Following Vascular Diseases in the Brain Stem

Stroke ◽  
1973 ◽  
Vol 4 (1) ◽  
pp. 80-84 ◽  
Author(s):  
AKIRA ITO ◽  
TERUO OMAE ◽  
SHIBANOSUKE KATSUKI
Keyword(s):  
Blood Pressure ◽  
Brain Stem ◽  
Vascular Diseases ◽  
Acute Changes ◽  
The Brain

Is the renal production of erythropoietin controlled by the brain stem?

2005 ◽  
Vol 289 (1) ◽  
pp. E82-E86 ◽  
Author(s):  
Ursula von Wussow ◽  
Janina Klaus ◽  
Horst Pagel
Keyword(s):  
Blood Pressure ◽  
Brain Stem ◽  
Structure And Function ◽  
Humoral Factors ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Sensitive Sensor ◽  
Releasing Factors ◽  
And Function ◽  
The Brain

Although the structure and function of erythropoietin (Epo) are well documented, the mechanisms of the regulation of the renal synthesis of Epo are still poorly understood. Especially, the description of the localization and function of the O2-sensitive sensor regulating the renal synthesis of Epo is insufficient. A body of evidence suggests that extrarenal O2-sensitive sensors, localized particularly in the brain stem, play an important role in this connection. To support this concept, high cerebral pressure with consecutive hypoxia of the brain stem was generated by insufflation of synthetic cerebrospinal fluid into the catheterized cisterna magna of rats. When the cerebral pressure of the rats was above the level of their mean arterial blood pressure or the high cerebral pressure persisted for a longer period (≥10 min), the Epo plasma concentration increased significantly. Bilateral nephrectomy or hypophysectomy before initiation of high intracranial pressure abolished this effect. Systemic parameters (heart rate, blood pressure, PaO2, PaCO2, arterial pH, renal blood flow, glucose concentration in blood) were not affected. Other stressors, like restricting the mobility of the rats, had no effect on Epo production. Hence, the effect of high cerebral pressure on renal synthesis of Epo seems to be specific. Increasing cerebral hydrostatic pressure leads to increased renal synthesis of Epo. Obviously, during hypoxia, cerebral O2-sensitive sensors release humoral factors, triggering the renal synthesis of Epo. The structure and function of these “Epo-releasing-factors” will have to be characterized in future experiments.

PACAP is expressed in sympathoexcitatory bulbospinal C1 neurons of the brain stem and increases sympathetic nerve activity in vivo

2008 ◽  
Vol 294 (4) ◽  
pp. R1304-R1311 ◽  
Author(s):  
Melissa M. J. Farnham ◽  
Qun Li ◽  
Ann K. Goodchild ◽  
Paul M. Pilowsky
Keyword(s):  
Blood Pressure ◽  
Brain Stem ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Intrathecal Administration ◽  
Ventrolateral Medulla ◽  
Cell Group ◽  
Nerve Activity ◽  
The Brain

Pituitary adenylate cyclase-activating polypeptide (PACAP) is an excitatory neuropeptide present in the rat brain stem. The extent of its localization within catecholaminergic groups and bulbospinal sympathoexcitatory neurons is not established. Using immunohistochemistry and in situ hybridization, we determined the extent of any colocalization with catecholaminergic and/or bulbospinal projections from the brain stem was determined. PACAP mRNA was found in tyrosine hydroxylase-immunoreactive (TH-ir) neurons in the C1-C3 cell groups. In the rostral ventrolateral medulla (RVLM), PACAP mRNA was found in 84% of the TH-ir neurons and 82% of bulbospinal TH-ir neurons. The functional significance of these PACAP mRNA positive bulbospinal neurons was tested by intrathecal administration of PACAP-38 in anaesthetized rats. Splanchnic sympathetic nerve activity doubled (110%) and heart rate rose significantly (19%), although blood pressure was unaffected. In addition, as previously reported, PACAP was found in the A1 cell group but not in the A5 cell group or in the locus coeruleus. The RVLM is the primary site responsible for the tonic and reflex control of blood pressure through the activity of bulbospinal presympathetic neurons, the majority of which contain TH. The results indicate 1) that pontomedullary neurons containing both TH and PACAP that project to the intermediolateral cell column originate from C1-C3 and not A5, and 2) intrathecal PACAP-38 causes a prolonged, sympathoexcitatory effect.

Vasopressin in brain of spontaneously hypertensive rats

1982 ◽  
Vol 242 (4) ◽  
pp. H496-H499 ◽  
Author(s):  
W. Rascher ◽  
R. E. Lang ◽  
T. Unger ◽  
D. Ganten ◽  
F. Gross
Keyword(s):  
Blood Pressure ◽  
Plasma Concentration ◽  
Brain Stem ◽  
Spontaneously Hypertensive Rats ◽  
Age Groups ◽  
Plasma Osmolality ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
The Brain

In stroke-prone spontaneously hypertensive rats (SHRSP) and in normotensive Wistar-Kyoto rats (WKY), arginine vasopressin (AVP) was measured by means of a radioimmunoassay in the plasma, the pituitary gland, the hypothalamus, and the brain stem. In 6- and 14-wk-old SHRSP, the plasma concentration of AVP was lower than in age-matched WKY (P less than 0.01), whereas it was elevated at 28 wk of age (P less than 0.01). In the pituitary of 6-wk-old SHRSP, AVP was higher than in WKY (P less than 0.05), but no such difference was found in older rats. In the hypothalamus and the brain stem, AVP content was reduced in all age groups of SHRSP. Plasma osmolality was diminished in 28-wk-old SHRSP only (P less than 0.01), whereas hematocrit in all age groups was higher in SHRSP than in WKY. It is concluded that the secretion of AVP and possibly its synthesis in the hypothalamus are reduced in SHRSP. Whether the reduced AVP content in the brain stem is related to the sustained elevation of blood pressure has to be studied further.

Predominance of vagal bradycardia mechanism in the brain stem of turtles

1988 ◽  
Vol 140 (1) ◽  
pp. 405-420 ◽  
Author(s):  
J. H. Hsieh ◽  
C. M. Pan ◽  
J. S. Kuo ◽  
C. Y. Chai
Keyword(s):  
Blood Pressure ◽  
Brain Stem ◽  
Pressor Response ◽  
Inhibitory Response ◽  
Cardiac Contraction ◽  
Vagus Nerves ◽  
Arterial Blood ◽  
Vagal Bradycardia ◽  
The Brain ◽  
Stimulation Of

Cardiovascular parameters of spontaneously breathing pond turtles (Cyclemys flavomarginata) anaesthetized with chloralose (4 mg 100 g-1) and urethane (40 mg 100 g-1), were examined during exploratory electrical stimulation of the brain stem. Turtles exhibited a low mean systemic arterial blood pressure (MSAP, average 25 mmHg) and slow heart rate (average 24 beats min-1). Upon stimulation, pressor (sympathetic), depressor (sympathetic inhibition), bradycardia and hypotensive (vagal) responses were elicited from regions of the brain stem extending from the hypothalamus to the medulla, principally in the medial region. The pressor response appeared after a longer latency than did the bradycardia and hypotensive responses. It developed rather slowly, and rarely attained a magnitude double its resting value. In contrast, stimulation of many points in the brain stem produced marked slowing or even cessation of the heart beat, and thus resulted in an immediate fall of the blood pressure even to zero. This cardio-inhibitory response depended on the integrity of the vagus nerves and was particularly marked upon stimulation in the caudal medulla, the areas of the ambiguus, solitary and dorsomotor nuclei of the vagus and the midline structures. When such an area was stimulated continuously the heart stopped beating throughout the stimulation. The longest period of cardiac arrest before the appearance of escape was 35 min. With continuous stimulation of the peripheral end of the cut vagus, the earliest escape beat occurred even later (65 min). Epinephrine given intravenously produced an increase of MSAP and force of cardiac contraction, although the slope of pressor rise was shallow. Reflex bradycardia, however, was not observed. These experiments show that a very prominent vagal bradycardia can be evoked from the turtle brain stem, which may contribute to its well-known capacity for tolerating anoxia.

Angiotensin, Thirst, and Sodium Appetite

1998 ◽  
Vol 78 (3) ◽  
pp. 583-686 ◽  
Author(s):  
J. T. FITZSIMONS
Keyword(s):  
Blood Pressure ◽  
Brain Stem ◽  
Blood Pressure Control ◽  
Drinking Behavior ◽  
Pressure Control ◽  
Ang Ii ◽  
Sodium Appetite ◽  
Angiotensin Peptides ◽  
Body Fluid Homeostasis ◽  
The Brain

Fitzsimons, J. T. Angiotensin, Thirst, and Sodium Appetite. Physiol. Rev. 78: 583–686, 1998. — Angiotensin (ANG) II is a powerful and phylogenetically widespread stimulus to thirst and sodium appetite. When it is injected directly into sensitive areas of the brain, it causes an immediate increase in water intake followed by a slower increase in NaCl intake. Drinking is vigorous, highly motivated, and rapidly completed. The amounts of water taken within 15 min or so of injection can exceed what the animal would spontaneously drink in the course of its normal activities over 24 h. The increase in NaCl intake is slower in onset, more persistent, and affected by experience. Increases in circulating ANG II have similar effects on drinking, although these may be partly obscured by accompanying rises in blood pressure. The circumventricular organs, median preoptic nucleus, and tissue surrounding the anteroventral third ventricle in the lamina terminalis (AV3V region) provide the neuroanatomic focus for thirst, sodium appetite, and cardiovascular control, making extensive connections with the hypothalamus, limbic system, and brain stem. The AV3V region is well provided with angiotensinergic nerve endings and angiotensin AT1 receptors, the receptor type responsible for acute responses to ANG II, and it responds vigorously to the dipsogenic action of ANG II. The nucleus tractus solitarius and other structures in the brain stem form part of a negative-feedback system for blood volume control, responding to baroreceptor and volume receptor information from the circulation and sending ascending noradrenergic and other projections to the AV3V region. The subfornical organ, organum vasculosum of the lamina terminalis and area postrema contain ANG II-sensitive receptors that allow circulating ANG II to interact with central nervous structures involved in hypovolemic thirst and sodium appetite and blood pressure control. Angiotensin peptides generated inside the blood-brain barrier may act as conventional neurotransmitters or, in view of the many instances of anatomic separation between sites of production and receptors, they may act as paracrine agents at a distance from their point of release. An attractive speculation is that some are responsible for long-term changes in neuronal organization, especially of sodium appetite. Anatomic mismatches between sites of production and receptors are less evident in limbic and brain stem structures responsible for body fluid homeostasis and blood pressure control. Limbic structures are rich in other neuroactive peptides, some of which have powerful effects on drinking, and they and many of the classical nonpeptide neurotransmitters may interact with ANG II to augment or inhibit drinking behavior. Because ANG II immunoreactivity and binding are so widely distributed in the central nervous system, brain ANG II is unlikely to have a role as circumscribed as that of circulating ANG II. Angiotensin peptides generated from brain precursors may also be involved in functions that have little immediate effect on body fluid homeostasis and blood pressure control, such as cell differentiation, regeneration and remodeling, or learning and memory. Analysis of the mechanisms of increased drinking caused by drugs and experimental procedures that activate the renal renin-angiotensin system, and clinical conditions in which renal renin secretion is increased, have provided evidence that endogenously released renal renin can generate enough circulating ANG II to stimulate drinking. But it is also certain that other mechanisms of thirst and sodium appetite still operate when the effects of circulating ANG II are blocked or absent, although it is not known whether this is also true for angiotensin peptides formed in the brain. Whether ANG II should be regarded primarily as a hormone released in hypovolemia helping to defend the blood volume, a neurotransmitter or paracrine agent with a privileged role in the neural pathways for thirst and sodium appetite of all kinds, a neural organizer especially in sodium appetite, or all of these, remains uncertain. ANG II-induced drinking behavior serves as a model of how other complex behaviors involving neural and peptide inputs might be organized.

Localization of Central Noradrenergic Mechanisms in Cardiovascular Regulation in Rats

1974 ◽  
Vol 48 (s2) ◽  
pp. 277s-278s ◽  
Author(s):  
H. Struyker Boudier ◽  
G. Smeets ◽  
G. Brouwer ◽  
J. Van Rossum
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Brain Stem ◽  
Cardiovascular Regulation ◽  
Anterior Hypothalamus ◽  
Anaesthetized Rats ◽  
Lower Brain Stem ◽  
The Brain

1. Various drugs were injected stereotactically into the brain of anaesthetized rats. 2. Noradrenaline injected into the area of the nucleus of the tractus solitarius in the lower brain stem or into the far anterior hypothalamus/pre-optic region induced a fall in blood pressure and in heart rate related to the administered dose. 3. When injected into the anterior hypothalamus/pre-optic region, clonidine and alpha-methyl-noradrenaline induced a long-lasting decrease in blood pressure and heart rate.

Cardiovascular actions of microinjections of angiotensin II in the brain stem of rats

1984 ◽  
Vol 246 (5) ◽  
pp. R811-R816 ◽  
Author(s):  
R. Casto ◽  
M. I. Phillips
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Brain Stem ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Ang Ii ◽  
The Brain

The blood pressure and heart rate responses to microinjection of angiotensin II (ANG II) into the brain stem of urethan-anesthetized rats were studied. Microinjection of ANG II into the area postrema (AP) resulted in significant elevation of blood pressure and significant reduction of heart rate. Microinjection into the region of the nucleus tractus solitarius (NTS) yielded a significant dose-dependent elevation in blood pressure and consistent increases in heart rate. The response to microinjection of ANG II into the region of the NTS was not due to leakage into the peripheral circulation, since intravenous administration of the ANG II antagonist, saralasin, did not attenuate the response. In fact, the cardiovascular response was increased after peripheral ANG II blockade, and the heart rate, which was consistently but not significantly elevated by NTS injection alone, was significantly elevated after saralasin pretreatment. Thermal ablation of the AP did not change the heart rate or the pressor response to microinjection of ANG II into the region of the NTS, indicating that the response was not mediated through the AP.

Changes in extracellular potassium concentration in cortex and brain stem during the acute phase of experimental closed head injury

1981 ◽  
Vol 55 (5) ◽  
pp. 708-717 ◽  
Author(s):  
Hiroshi Takahashi ◽  
Shinya Manaka ◽  
Keiji Sano
Keyword(s):  
Blood Pressure ◽  
Brain Stem ◽  
Low Voltage ◽  
Potassium Concentration ◽  
Control Level ◽  
Extracellular Potassium ◽  
Content Type ◽  
The Impact ◽  
The Brain ◽  
Fine Print

✓ A high potassium concentration ([K+]o) in brain tissue impedes neuronal activity, as observed in spreading cortical depression. Experimental studies were performed on mice and rats to determine the role of changes of [K+]o in cerebral concussion. In the first experiment, a 600 gm-cm impact was delivered to the vertex of the mouse skull. This impact induced arrest of spontaneous movement for 465 ± 55.9 seconds (mean ± SD), accompanied by apnea, bradycardia, and low-voltage electroencephalographic recordings (EEG). The injury was also frequently followed immediately by epilepsy. This impact induced an increase of cortical [K+]o from the control level of 4.1 ± 1.8 mM to 20–30 mM, with gradual recovery within 30 minutes to the control level. In the second experiment, an impact of 9000 gm-cm was delivered to the midline parieto-occipital area of the rat and produced concussion-like phenomena similar to those elicited in mice. This level of trauma induced a significant increase of cortical [K+]o from the control level of 4.2 ± 0.8 mM to 20–50 mM in all of the rats, and also a significant increase of brain-stem [K+]o from 3.9 ± 0.6 to 20–30 mM in 73% of the rats. In these latter rats, the impact also induced apnea and a transient elevation of blood pressure, and resulted in low-voltage EEG recordings. In 23% of the rats in which [K+]o changes in the brain stem were not significant, the impact caused a transient reduction of blood pressure. The present study disclosed that an increase of [K+]o in the cerebral cortex and also in the brain stem is an important element in the phenomenon of concussion.

Brain stem augmentation of cardiovascular activity

1960 ◽  
Vol 198 (2) ◽  
pp. 421-423 ◽  
Author(s):  
Richard L. Glasser
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Brain Stem ◽  
Cardiovascular Activity ◽  
Rostral Portion ◽  
The Brain ◽  
Pontomedullary Junction

Midpontile ischemic decerebration in vagotomized mesencephalic cats produced marked tachycardia and hypertension. Subsequent transection of the brain stem at or above the midpontile level did not affect the cardiovascular hyperactivity. Transection at the pontomedullary junction abolished the brain stem augmentation of heart rate and blood pressure. The results suggest the existence of a cardiovascular augmenter area in the caudal half of the pons and a cardiovascular depressor area in a more rostral portion of the brain stem.

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