Systemic angiotensin acts at subfornical organ to facilitate activity of neurohypophysial neurons

Ferguson, A. V.; Renaud, Leo P.

doi:10.1152/ajpregu.1986.251.4.r712

Cited by 63 publications

(41 citation statements)

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“…There is an inverse correlation between oxytocin secretion from the posterior pituitary and sodium appetite. Oxytocin release in the brain seems to parallel the secretion of this hormone into the blood, and oxytocin in both systems is activated by similar stimuli, including ANG II (12,45,46,123). However, the oxytocin found and released in the CNS inhibits sodium appetite (12)(13)(14)(121)(122)(123)(124).…”

Section: Major Neurohumoral Factors Inhibiting Water And/or Sodium Inmentioning

confidence: 99%

Role of the lateral parabrachial nucleus in the control of sodium appetite

Menani

Luca

Johnson

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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.-In states of sodium deficiency many animals seek and consume salty solutions to restore body fluid homeostasis. These behaviors reflect the presence of sodium appetite that is a manifestation of a pattern of central nervous system (CNS) activity with facilitatory and inhibitory components that are affected by several neurohumoral factors. The primary focus of this review is on one structure in this central system, the lateral parabrachial nucleus (LPBN). However, before turning to a more detailed discussion of the LPBN, a brief overview of body fluid balance-related body-to-brain signaling and the identification of the primary CNS structures and humoral factors involved in the control of sodium appetite is necessary. Angiotensin II, mineralocorticoids, and extracellular osmotic changes act on forebrain areas to facilitate sodium appetite and thirst. In the hindbrain, the LPBN functions as a key integrative node with an ascending output that exerts inhibitory influences on forebrain regions. A nonspecific or general deactivation of LPBN-associated inhibition by GABA or opioid agonists produces NaCl intake in euhydrated rats without any other treatment. Selective LPBN manipulation of other neurotransmitter systems [e.g., serotonin, cholecystokinin (CCK), corticotrophin-releasing factor (CRF), glutamate, ATP, or norepinephrine] greatly enhances NaCl intake when accompanied by additional treatments that induce either thirst or sodium appetite. The LPBN interacts with key forebrain areas that include the subfornical organ and central amygdala to determine sodium intake. To summarize, a model of LPBN inhibitory actions on forebrain facilitatory components for the control of sodium appetite is presented in this review. sodium intake; angiotensin; electrolyte balance; thirst ANIMALS CONSTANTLY LOSE WATER and electrolytes to the external environment, but specific autonomic, hormonal, and behavioral mechanisms operate continuously to adjust and restore body fluid-electrolyte balance. The rate of loss from the kidneys is primarily controlled by neural and hormonal actions, but loss may also occur passively through the largely uncontrolled processes of respiration (evaporation), perspiration, transpiration, and salivation. These later modes of loss are referred to as insensible loss because they cannot be easily measured. Severe loss of both sodium and water may also occur in disorders associated with emesis and diarrhea. However, despite such ongoing challenges, the osmolarity and volume of body fluids are maintained within reasonably narrow limits, thus allowing normal metabolic and cardiovascular functions. Although renal mechanisms can slow water and sodium loss, the restoration of fluid homeostasis is only made possible by the mobilization of behaviors that result in the ingestion of water and sodium (usually NaCl). The behavioral responses of seeking out and consuming water and salty substances involve the motivational states of thirst and salt appetite. Salt appetite is also frequently referred to as sodium appetit...

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Section: Major Neurohumoral Factors Inhibiting Water And/or Sodium Inmentioning

confidence: 99%

Role of the lateral parabrachial nucleus in the control of sodium appetite

Menani

Luca

Johnson

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Although there is considerable evidence for generation of ANG II within the central nervous system by enzymatic pathways similar to those of the peripheral renin-angiotensin system, blood-borne ANG II also appears to modulate neuronal activity in specialized brain regions. Some neurons in the area postrema and subfornical organ, which have a minimal blood-brain barrier, are influenced by increased levels of circulating ANG II (36,47,74).…”

Section: Ang In the Nts: Integrative Role And Cellular Actionsmentioning

confidence: 99%

Angiotensin potentiates excitatory sensory synaptic transmission to medial solitary tract nucleus neurons

Barnes

DeWeese

Andresen

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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Barnes, Karen L., Dannette M. DeWeese, and Michael C. Andresen. Angiotensin potentiates excitatory sensory synaptic transmission to medial solitary tract nucleus neurons. Am J Physiol Regul Integr Comp Physiol 284: R1340-R1353, 2003. First published January 16, 2003 10.1152/ajpregu.00505.2002-Femtomole doses of angiotensin (ANG) II microinjected into nucleus tractus solitarii (nTS) decrease blood pressure and heart rate, mimicking activation of the baroreflex, whereas higher doses depress this reflex. ANG II might generate cardioinhibitory responses by augmenting cardiovascular afferent synaptic transmission onto nTS neurons. Intracellular recordings were obtained from 99 dorsal medial nTS region neurons in rat medulla horizontal slices to investigate whether ANG II modulated short-latency excitatory postsynaptic potentials . ANG II appeared to selectively augment presynaptic sensory transmission in one class of nTS neurons but had only postsynaptic effects on another group of cells. Thus ANG II is likely to modulate cardiovascular function by more than one nTS neuronal pathway. cardiovascular regulation; L-glutamate; substance P, non-Nmethyl-D-aspartate receptor THE NUCLEUS TRACTUS SOLITARII (nTS) in the dorsal medulla comprises rostrocaudally oriented columns of diverse neurons and fiber tracts that lie lateral to the walls of the fourth cerebral ventricle and join above the central canal caudal to the obex (4, 73). This complex structure, with bidirectional connections to medullary and forebrain nuclei that subserve autonomic functions, plays a major role in the regulation and integration of visceral systems, including normal and impaired cardiovascular mechanisms (60,61,82). Anatomic studies (25,26,43,52,85) and in vivo recordings (91) verify that a substantial proportion of the arterial baroreceptor sensory fibers that originate from receptors in the aortic arch and carotid sinus regions course through the solitary tract (TS) into the nTS and make their first synapse on neurons in the dorsal medial region of the nucleus. Neurons in this region also receive synaptic inputs from other viscera and brain autonomic nuclei via the TS (79). The nTS is a primary central site at which angiotensin (ANG) II influences cardiovascular function. Within the brain, the anatomic distributions of ANG II and its receptors and their mRNAs correlate reasonably well with the probable functions of the peptide (2, 57). However, the cellular mechanisms responsible for the cardiovascular effects of ANG II mediated by the nTS remain unclear.Microinjection of femtomole doses of ANG II into the dorsal medial region of the nTS produces a transient fall in blood pressure and heart rate very similar to the response to activation of the cardiovascular baroreflex in anesthetized rats (41,71,78) and evokes a comparable bradycardia in an in vitro beating heart-brain stem rat preparation (75). Paradoxically, however, higher doses evoke pressor responses, creating dose-response relationships that are biphasic. ANG II injection into the nTS al...

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“…It is sensitive to stimulation by angiotensin II (ANG) and vasopressin and is intrinsically osmosensitive. The SFO influences cardiovascular function through projections to the hypothalamus and other autonomic control centers (Lind et al, 1982;Ferguson and Renaud, 1986).…”

Section: Introductionmentioning

confidence: 99%

Prokineticin 2 Modulates the Excitability of Subfornical Organ Neurons

Cottrell

Zhou²,

Ferguson³

2004

J. Neurosci.

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The recent discovery of prokineticin 2 (PK2) expression in the suprachiasmatic nucleus and its receptors in critical autonomic control centers of the brain, including the subfornical organ (SFO), suggests the intriguing possibility that PK2 regulates the excitability of SFO neurons and thus influences autonomic function. Using current-clamp techniques to record from dissociated SFO neurons, we examined the effects of PK2 on the excitability of these cells. PK2 (20 nM) induced depolarizations in 40% of SFO neurons (n ϭ 45; mean, 7.5 Ϯ 1.7 mV), an effect that was reversible, PK2-specific, and concentration dependent. The depolarization was accompanied by an increase in action potential frequency from 0.4 Ϯ 0.1 to 1.4 Ϯ 0.5 Hz in responding cells (n ϭ 10). This excitatory effect appears to be, in part, attributable to a PK2-induced decrease in the delayed rectifier potassium current (I K ). In 10 SFO neurons recorded using perforated patch voltage-clamp techniques, six demonstrated a reversible decrease in I K (mean decrease, 26.7 Ϯ 6.4%) in response to 20 nM PK2, whereas artificial CSF alone was without an effect on these currents. These data are the first to show excitatory effects of PK2 on neurons and, in addition, demonstrate that this peptide modulates voltage-activated K ϩ channels. The activation of SFO neurons by PK2 illustrates a mechanism through which this peptide may exert circadian control of autonomic functions.

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Systemic angiotensin acts at subfornical organ to facilitate activity of neurohypophysial neurons

Cited by 63 publications

References 0 publications

Role of the lateral parabrachial nucleus in the control of sodium appetite

Role of the lateral parabrachial nucleus in the control of sodium appetite

Angiotensin potentiates excitatory sensory synaptic transmission to medial solitary tract nucleus neurons

Prokineticin 2 Modulates the Excitability of Subfornical Organ Neurons

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