Is the Area Postrema a Control Centre of Blood Pressure?

Nature ◽  
1974 ◽  
Vol 247 (5435) ◽  
pp. 58-59 ◽  
Author(s):  
PAULI YLITALO ◽  
HEIKKI KARPPANEN ◽  
MATTI K. PAASONEN
Keyword(s):  
Blood Pressure ◽  
Area Postrema ◽  
Control Centre

Autonomic mechanisms underlying area postrema stimulation-induced cardiovascular responses in rats

1991 ◽  
Vol 261 (1) ◽  
pp. R1-R8 ◽  
Author(s):  
A. V. Ferguson ◽  
P. Smith
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rate Control ◽  
Area Postrema ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Blocking Agent ◽  
Adrenergic Blockade ◽  
Neural Pathways ◽  
Heart Rate Control

Experiments were designed to examine the autonomic mechanisms underlying the decreases in blood pressure and heart rate elicited by electrical stimulation in the rat area postrema (AP). Vagotomy was found to significantly reduce the bradycardia observed in response to AP stimulation (control -123.5 +/- 23.5 beats/min; vagotomized -7 +/- 5.4 beats/min; P less than 0.001) but was without significant effect on blood pressure responses. Hexamethonium significantly reduced both heart rate (control -225.5 +/- 11.9 beats/min; hexamethonium -5.5 +/- 2.8 beats/min; P less than 0.001) and depressor (control -35.4 +/- 4.7 mmHg; hexamethonium -6.4 +/- 0.8 mmHg; P less than 0.001) responses to such stimulation, whereas combined alpha- and beta-adrenergic blockade was without effect. The muscarinic blocking agent atropine also abolished both blood pressure (control -22.0 +/- 4.3 mmHg; atropine 2.8 +/- 4.4 mmHg; P less than 0.01) and heart rate (control -187.0 +/- 41.9 beats/min; atropine 8.8 +/- 2.6 beats/min; P less than 0.01) responses to AP stimulation. These data suggest that AP stimulation influences two separate neural pathways eliciting distinct cardiovascular responses. It would appear that activation of one of these pathways results in activation of vagal efferents to the heart and thus bradycardia. A second parallel pathway influenced by AP stimulation apparently elicits depressor response through actions on cholinergic muscarinic receptors.

Adrenomedullin microinjection into the area postrema increases blood pressure

1997 ◽  
Vol 272 (6) ◽  
pp. R1698-R1703 ◽  
Author(s):  
M. A. Allen ◽  
P. M. Smith ◽  
A. V. Ferguson
Keyword(s):  
Blood Pressure ◽  
Area Postrema ◽  
Area Under The Curve ◽  
Physiological Role ◽  
Cardiovascular Responses ◽  
Hypotensive Effect ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Brain Site

Adrenomedullin (ADM) circulates in the blood at concentrations comparable to other vasoactive peptides with established roles in cardiovascular regulation. Intravenously administered ADM produces a clear hypotensive effect, whereas intracerebroventricular microinjections result in increases in blood pressure (BP). Recently, we demonstrated that ADM influences neurons of the area postrema (AP), a central nervous system site implicated in cardiovascular control. However, to address directly the physiological significance of the actions of ADM at the AP, an in vivo microinjection study was undertaken. ADM, at two concentrations (1 and 10 microM), in volumes of 50, 100, and 200 nl, was microinjected into the AP or NTS of 21 urethan-anesthetized male Sprague-Dawley rats. Microinjection of 10 microM ADM (100 nl) resulted in significant transient (2-5 min) increases in BP [120 s area under the curve (AUC): 684.3 +/- 268.6 mmHg/s (P < 0.05)], and heart rate (HR) [AUC: 12.5 +/- 4.5 beats/min (P < 0.05)]. The lower concentration of ADM (1 microM) had no effect on either BP (179.1 +/- 143.6 mmHg/s) or HR (0.8 +/- 2.6 beats/min). ADM was also microinjected into the immediately adjacent nucleus of the solitary tract, where it was found to be without effect on either BP or HR. This study demonstrates, for the first time, a physiological role for ADM acting at a specific brain site, the AP, to produce significant cardiovascular responses.

17β-Estradiol inhibits angiotensin II activation of area postrema neurons

2003 ◽  
Vol 285 (4) ◽  
pp. H1515-H1520 ◽  
Author(s):  
Jaya Pamidimukkala ◽  
Meredith Hay
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Area Postrema ◽  
Ang Ii ◽  
Circumventricular Organ ◽  
Ici 182,780 ◽  
Central Neurons ◽  
Total Inhibition ◽  
17Β Estradiol ◽  
Vasoactive Peptide

It is well established that the area postrema, as a circumventricular organ, is susceptible to modulation by circulating hormones and peptides. Furthermore, activation of the area postrema has been shown to modulate central neurons involved in the regulation of cardiovascular function and blood pressure. In particular, the vasoactive peptide angiotensin II (ANG II) has been shown to inhibit baroreflex regulation of heart rate and increase sympathetic outflow and blood pressure via activation of area postrema neurons. Estrogen is thought to protect against hypertension in both humans and animal models and has been shown in a number of systems to alter the effects of ANG II. The purpose of the present study was to determine the effects of estrogen on ANG II activation of area postrema neurons. In this study, the effects of ANG II and KCl on fura 2-measured cytosolic Ca2+ concentration ([Ca2+]i) responses in cultured area postrema neurons in the presence and absence of 12-h exposure to 100 nM 17β-estradiol (E2) were evaluated. In neurons incubated in control vehicle media, 50 nM ANG II increased [Ca2+]i by 92 ± 12%. In neurons preincubated with 100 nM E2, ANG II increased [Ca2+]i by only 68 ± 11%, for a total inhibition of the ANG II-evoked response of 24%. Coapplication of the estrogen receptor antagonist ICI-182,780 did not inhibit the effects of E2. In the same cells in which the effects of E2 on ANG II-evoked responses were tested, the effects of incubation in E on the depolarization-induced increased [Ca2+2]i due to 60 mM KCl were also tested. Incubation of the cells with 100 nM E increased the KCl-evoked [Ca2+2]i response, and this response was blocked by ICI-182,780. These results suggest that in the area postrema, estrogen may utilize multiple pathways to modulate neural activity and responses to ANG II.

Two Sites of Cardiovascular Action of Angiotensin II in the Brain of the Dog

1973 ◽  
Vol 44 (4) ◽  
pp. 417-420 ◽  
Author(s):  
P. L. Gildenberg ◽  
C. M. Ferrario ◽  
J. W. McCubbin
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Lateral Ventricle ◽  
Area Postrema ◽  
Pressor Response ◽  
Cerebral Ventricle ◽  
Vertebral Arteries ◽  
Adjacent Structures ◽  
The Brain ◽  
Lateral Cerebral Ventricle

1. Infusion of angiotensin into both vertebral arteries or into a lateral cerebral ventricle of dogs anaesthetized with morphine-chloralose elicited a centrally mediated rise in blood pressure. 2. Heat coagulation of the area postrema and immediately adjacent structures abolished the pressor response to infusion of angiotensin into the circulation of the vertebral arteries, but did not alter the pressor response when the peptide was delivered into a cerebral lateral ventricle; transection of the midbrain eliminated the latter response but not the former. 3. It is concluded that there are at least two areas in the dog's brain that respond to angiotensin by inducing a raised blood pressure.

The origin of the vomiting response: a neuroanatomical hypothesis

1990 ◽  
Vol 68 (2) ◽  
pp. 254-259 ◽  
Author(s):  
L N. C. Lawes
Keyword(s):  
Blood Pressure ◽  
Direct Evidence ◽  
Area Postrema ◽  
Pattern Generator ◽  
The Other ◽  
Behaviour Pattern ◽  
Electrolyte Balance ◽  
Pia Mater ◽  
Paraventricular Nuclei ◽  
Autonomic Pathways

The connections of area postrema include a set of nuclei with a common topographical location immediately deep to the ependyma or pia mater. These nuclei are all within two principal synapses of the area postrema and can be reached by more than one route from it. There is direct evidence that, like the area postrema, a number of these nuclei participate in vomiting. It is suggested that the paraventricular system may act as a distributed pattern generator for the several processes known to be integrated in the emetic response. It is also suggested that the other functions of the paraventricular nuclei, mainly homeostatic in mammals, have all evolved from a prototypical behaviour pattern of escape from, and subsequent avoidance of, noxious stimuli. Thus, through this system of nuclei, blood pressure, respiration, gastrointestinal motility and secretion, fluid and electrolyte balance, and the ingestion of food may all be influenced by noxious situations.Key words: vomiting, central autonomic pathways, homeostasis, escape, osmoregulation.

Vasopressin acts in the area postrema to attenuate the exercise pressor reflex in anesthetized cats

1998 ◽  
Vol 274 (6) ◽  
pp. H2116-H2122 ◽  
Author(s):  
Charles L. Stebbins ◽  
Stefani Bonigut ◽  
Lea R. Liviakis ◽  
Paul A. Munch
Keyword(s):  
Blood Pressure ◽  
Area Postrema ◽  
Cardiovascular Response ◽  
Exercise Pressor Reflex ◽  
Arterial Blood ◽  
Baroreflex Function ◽  
Static Contraction ◽  
Before And After ◽  
Pressor Reflex ◽  
Anesthetized Cat

Circulating arginine vasopressin (AVP) can enhance baroreflex function via its action in the area postrema (AP). We tested the hypothesis that AVP acts in the AP to enhance baroreflex function during static contraction and, in turn, attenuates the exercise pressor reflex. Thus mean arterial blood pressure ( n = 9) and heart rate (HR) ( n = 9) during 30 s of electrically stimulated hindlimb contraction were compared before and after bilateral microinjections of 200 nl of the AVP V1-receptor antagonist d(CH2)5Tyr(Me)-AVP (V1x) (1 ng/nl) into the AP of the anesthetized cat. This protocol was repeated in three other cats in which sinoaortic denervation (SAD) was performed before any intervention. Injection of V1xinto the AP had no effect on baseline blood pressure or HR. However, pressor and HR responses to static contraction were augmented by 44 ± 10 and 29 ± 9%, respectively. Static contraction also increased plasma AVP from 15.9 ± 2.0 to 25.5 ± 3.4 pg/ml. In the SAD cats, microinjection of V1x had no effect on contraction-induced increases in blood pressure or HR. These results suggest that baroreflex opposition of the reflex cardiovascular response to static contraction is enhanced by the action of AVP in the AP.

Overlapping distributions of receptors for atrial natriuretic peptide and angiotensin II visualized by in vitro autoradiography: morphological basis of physiological antagonism

1987 ◽  
Vol 65 (8) ◽  
pp. 1517-1521 ◽  
Author(s):  
F. A. O. Mendelsohn ◽  
A. M. Allen ◽  
S. Y. Chai ◽  
P. M. Sexton ◽  
R. Figdor
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Area Postrema ◽  
Angiotensin Ii Receptors ◽  
Electrolyte Balance ◽  
Outer Cortex ◽  
Morphological Basis ◽  
Atrial Natriuretic

Atrial natriuretic peptides exert actions on many key organs involved in blood pressure and water and electrolyte balance. Many of these actions result in a physiological antagonism of angiotensin. To investigate the morphological basis of this interaction, we have mapped the distribution of receptors for atrial natriuretic peptide and angiotensin II in a number of target organs, using 125I-labelled rat atrial natriuretic peptide (99–126) and 125I-labelled [Sar1,Ile8]angiotensin II. In the kidney both atrial natriuretic peptide and angiotensin II receptors were observed overlying glomeruli, vasa recta bundles (high densities), and the outer cortex (moderate density). In the other tissues studied, atrial natriuretic peptide and angiotensin II receptors were codistributed in the adrenal zona glomerulosa, cerebral circumventricular organs including the subfornical organ, organum vasculosum of the lamina terminalis and area postrema, and the external plexiform layer of the olfactory bulb. The concurrent distribution of specific receptors for both peptides at these sites provides the basis for atrial natriuretic peptide to exert a functional antagonism of the actions of angiotensin II on blood pressure and water and electrolyte homeostasis at multiple sites.

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