Fos expression following isotonic volume expansion of the unanesthetized male rat

1998 ◽  
Vol 274 (5) ◽  
pp. R1345-R1352 ◽  
Author(s):  
R. R. Randolph ◽  
Q. Li ◽  
K. S. Curtis ◽  
M. J. Sullivan ◽  
J. T. Cunningham
Keyword(s):  
Volume Expansion ◽  
Supraoptic Nucleus ◽  
Venous Pressure ◽  
Isotonic Saline ◽  
Brain Regions ◽  
Ventrolateral Medulla ◽  
Male Rat ◽  
Double Labeling ◽  
Vasopressin Release ◽  
Fos Expression

Cardiopulmonary afferents, baroreceptor afferents, or atrial natriuretic peptide binding to circumventricular organs may mediate the central response to volume expansion, a condition common to pregnancy, exercise training, and congestive heart failure. This study used Fos immunocytochemistry to examine brain regions activated by volume expansion. Male Sprague-Dawley rats were infused with isotonic saline equal to 10% of their body weight in 10 min followed by a maintenance infusion of 0.5 ml/min for 110 min. Control animals received 2-h infusions at 0.01 ml/min. Five minutes after the start of volume expansion, central venous pressure of expanded animals was significantly greater than control animals. The volume-expanded group exhibited significantly greater Fos activation ( P < 0.05) in the area postrema, nucleus of the solitary tract, caudal ventrolateral medulla, paraventricular nucleus, supraoptic nucleus, and perinuclear zone of the supraoptic nucleus. Double labeling indicates that oxytocinergic neurons in the supraoptic nucleus are activated. Neurons in brain regions known to inhibit both sympathetic activity and vasopressin release show increased Fos expression following isotonic volume expansion.

scholarly journals Hypoxia activates nucleus tractus solitarii neurons projecting to the paraventricular nucleus of the hypothalamus

2012 ◽  
Vol 302 (10) ◽  
pp. R1219-R1232 ◽  
Author(s):  
T. Luise King ◽  
Cheryl M. Heesch ◽  
Catharine G. Clark ◽  
David D. Kline ◽  
Eileen M. Hasser
Keyword(s):  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Acute Hypoxia ◽  
Brain Regions ◽  
Nucleus Tractus Solitarii ◽  
Ventrolateral Medulla ◽  
Peripheral Chemoreceptor ◽  
Cardiorespiratory Function ◽  
Afferent Information ◽  
Fos Expression

Peripheral chemoreceptor afferent information is sent to the nucleus tractus solitarii (nTS), integrated, and relayed to other brain regions to alter cardiorespiratory function. The nTS projects to the hypothalamic paraventricular nucleus (PVN), but activation and phenotype of these projections during chemoreflex stimulation is unknown. We hypothesized that activation of PVN-projecting nTS neurons occurs primarily at high intensities of hypoxia. We assessed ventilation and cardiovascular parameters in response to increasing severities of hypoxia. Retrograde tracers were used to label nTS PVN-projecting neurons and, in some rats, rostral ventrolateral medulla (RVLM)-projecting neurons. Immunohistochemistry was performed to identify nTS cells that were activated (Fos-immunoreactive, Fos-IR), catecholaminergic, and GABAergic following hypoxia. Conscious rats underwent 3 h normoxia ( n = 4, 21% O2) or acute hypoxia (12, 10, or 8% O2; n = 5 each). Hypoxia increased ventilation and the number of Fos-IR nTS cells (21%, 13 ± 2; 12%, 58 ± 4; 10%, 166 ± 22; 8%, 186 ± 6). Fos expression after 10% O2was similar whether arterial pressure was allowed to decrease (−13 ± 1 mmHg) or was held constant. The percentage of PVN-projecting cells activated was intensity dependent, but contrary to our hypothesis, PVN-projecting nTS cells exhibiting Fos-IR were found at all hypoxic intensities. Notably, at all intensities of hypoxia, ∼75% of the activated PVN-projecting nTS neurons were catecholaminergic. Compared with RVLM-projecting cells, a greater percentage of PVN-projecting nTS cells was activated by 10% O2. Data suggest that increasing hypoxic intensity activates nTS PVN-projecting cells, especially catecholaminergic, PVN-projecting neurons. The nTS to PVN catecholaminergic pathway may be critical even at lower levels of chemoreflex activation and more important to cardiorespiratory responses than previously considered.

Determinants of atrial natriuretic factor secretion in dogs expanded with isotonic saline or colloid solutions

1991 ◽  
Vol 69 (2) ◽  
pp. 145-153
Author(s):  
Peter Cernacek ◽  
Mortimer Levy
Keyword(s):  
Bovine Serum Albumin ◽  
Serum Albumin ◽  
Blood Volume ◽  
Bovine Serum ◽  
Atrial Natriuretic Factor ◽  
Volume Expansion ◽  
Venous Pressure ◽  
Isotonic Saline ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

Though increments in blood volume and atrial pressure are thought to be the primary stimuli for ANF secretion, plasma levels of this peptide do not always behave as a simple function of volume status. To outline the relationship between the latter and cardiac ANF release, we used five different volume-expansion protocols in anesthetized dogs. A stepwise expansion of plasma volume (PV) was achieved by two consecutive infusions: 0.9% saline followed or preceded by 4 or 25% bovine serum albumin (BSA), 4 or 25% dextran (Dx), or homologous plasma. Saline expansion led to a two- to four-fold increase in arterial plasma ANF level in all five protocols. Both 4 and 25% BSA caused no or very modest increase in plasma ANF, while all other colloid expanders caused the expected ANF release. In all protocols, plasma ANF closely correlated with central venous pressure (CVP). BSA expansion was the only protocol with no correlation between PV and ANF release. Changes in serum Ca2+ could not explain this finding. During BSA expansion, the lack of atrial response was related to the absence of increment (or even fall) in CVP despite the expanded PV. Similarly, urinary Na+ excretion was correlated both with CVP and ANF level but not with PV in BSA expansion. When the dogs were depleted of histamine before BSA infusion, the atrial secretory response was restored, suggesting that this colloid was associated with augmented capillary leakiness and vascular fluid efflux. These results show that the expansion of PV leads neither to ANF release nor to Na+ excretion if it is not accompanied by an expanded central blood volume with elevated atrial pressure.Key words: atrial natriuretic factor, volume expansion, isotonic saline, bovine serum albumin, dextran, homologous plasma.

Osmotic stimulation of the supraoptic nucleus: central and peripheral vasopressin release and blood pressure

1994 ◽  
Vol 266 (3) ◽  
pp. E351-E356 ◽  
Author(s):  
M. Ludwig ◽  
T. Horn ◽  
M. F. Callahan ◽  
A. Grosche ◽  
M. Morris ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Supraoptic Nucleus ◽  
Pressor Response ◽  
Extracellular Fluid ◽  
Brain Regions ◽  
Vasopressin Release ◽  
Peptide Release ◽  
Osmotic Stimulation ◽  
Stimulation Of

Experiments were performed to determine the effect of direct osmotic stimulation of the supraoptic nucleus (SON) on central and peripheral vasopressin (AVP) release and arterial pressure. A microdialysis method was used to deliver hyperosmotic NaCl, mannitol or urea bilaterally into the SON and to sample SON extracellular fluid and blood. Simultaneous brain and blood microdialysis showed that hyperosmotic NaCl increased central and peripheral AVP release and increased mean arterial pressure (MAP). The pressor response was not blocked by intravenous injection of a V1-receptor antagonist, D(CH2)5Tyr(Me)AVP, suggesting that circulating AVP was not involved in that response. Hyperosmotic mannitol or urea caused an increase in central peptide release, but failed to affect MAP or peripheral AVP release. The results suggest that central AVP release within the SON may be due to osmoreceptor stimulation while the peripheral effects on AVP release and MAP are specific for sodium. The results also demonstrate the utility of brain and blood microdialysis for the delivery of stimuli into specific brain regions with simultaneous monitoring of central and peripheral peptide release.

scholarly journals Intracisternally Injected L-Proline Activates Hypothalamic Supraoptic, but Not Paraventricular, Vasopressin-Expressing Neurons in Conscious Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Yumi Takemoto
Keyword(s):  
Blood Pressure ◽  
Supraoptic Nucleus ◽  
Excitatory Amino Acid ◽  
Brain Regions ◽  
Double Labeling ◽  
Amino Acid Receptors ◽  
Freely Moving Rats ◽  
Artificial Cerebrospinal Fluid ◽  
Freely Moving ◽  
Labeling Approach

When injected into specific rat brain regions, the neurotransmitter candidate L-proline produces various cardiovascular changes through ionotropic excitatory amino acid receptors. The present study used an immunohistochemical double-labeling approach to determine whether intracisternally injected L-proline in freely moving rats, which increases blood pressure, activates hypothalamic vasopressin-expressing neurons and ventral medullary tyrosine-hydroxylase- (TH-) containing neurons. Following injection of L-proline, the number of activated hypothalamic neurons that coexpressed vasopressin and c-Fos was much greater in the supraoptic nucleus (SON) than in the paraventricular nucleus (PVN) of rats with increased blood pressure. The number of activated TH-containing neurons was significantly greater following L-proline treatment than following control injections of artificial cerebrospinal fluid (ACSF). These results clearly demonstrate that intracisternally injected L-proline activates hypothalamic supraoptic, but not paraventricular, vasopressin-expressing neurons and medullary TH-containing (A1/C1) neurons in freely moving rats.

scholarly journals Dehydration followed by sham rehydration contributes to reduced neuronal activation in vasopressinergic supraoptic neurons after water deprivation

2010 ◽  
Vol 299 (5) ◽  
pp. R1232-R1240 ◽  
Author(s):  
W. David Knight ◽  
Lisa L. Ji ◽  
Joel T. Little ◽  
J. Thomas Cunningham
Keyword(s):  
Supraoptic Nucleus ◽  
Water Deprivation ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Inhibitory Interneurons ◽  
Lamina Terminalis ◽  
Fos Expression ◽  
Supraoptic Neurons ◽  
Hypothalamic Activation

This experiment tested the role of oropharyngeal and gastric afferents on hypothalamic activation in dehydrated rats instrumented with gastric fistulas and allowed to drink water or isotonic saline compared with euhydrated controls (CON). Rats were water-deprived for 48 h (48 WD) or 46 h WD with 2 h rehydration with water (46+W) or isotonic saline (46+S). 46+W and 46+S rats were given water with fistulas open (46+WO/46+SO, sham) or closed (46+WC/46+SC). Compared with CON, water deprivation increased and water rehydration decreased plasma osmolality, while sham rehydration had no effect. Water deprivation increased c-Fos staining in the lamina terminalis. However, none of the sham or rehydration treatments normalized c-Fos staining in the lamina terminalis. Analysis of AVP and c-Fos-positive neurons in the supraoptic nucleus (SON) revealed reduced colocalization in 46+WO and 46+SC rats compared with 48 WD and 46+SO rats. However, 46+WO and 46+SC rats had higher c-Fos staining in the SON than 46+WC or CON rats. Examination of c-Fos in the perinuclear zone (PNZ) revealed that sham and rehydrated rats had increased c-Fos staining to CON, while 48 WD and 46+SO rats had little or no c-Fos staining in this region. Thus, preabsorptive reflexes contribute to the regulation of AVP neurons in a manner independent of c-Fos expression in the lamina terminalis. Further, this reflex pathway may include inhibitory interneurons in the PNZ region surrounding the SON.

Acute volume expansion decreases adrenocortical sensitivity to ACTH and angiotensin II

1985 ◽  
Vol 249 (5) ◽  
pp. R611-R616
Author(s):  
H. Raff ◽  
J. Shinsako ◽  
C. E. Wade ◽  
L. C. Keil ◽  
M. F. Dallman
Keyword(s):  
Volume Expansion ◽  
Venous Pressure ◽  
Isotonic Saline ◽  
Plasma Renin ◽  
Plasma Sodium ◽  
Ang Ii ◽  
Central Venous ◽  
Per Se ◽  
Change In Mean ◽  
Corticosteroid Response

This study examined the plasma aldosterone and corticosteroid responses to a 60-min infusion of adrenocorticotropin (ACTH) or angiotensin (ANG) II started immediately after an acute isotonic saline volume expansion (0.5 ml . kg-1 . min-1 for 30 min). Five conscious dogs of either sex with exteriorized carotid loops were used in this repeated-design study. Volume expansion per se caused a 10% decrease in hematocrit, a 12.5% decrease in plasma protein, and a 2.7-mmHg increase in central venous pressure with no change in mean arterial pressure, heart rate, or plasma sodium. Volume expansion per se also resulted in significant reductions in vasopressin, plasma renin activity, ACTH, aldosterone, and corticosteroid levels. The aldosterone responses to ACTH and ANG II were significantly inhibited (46-71%) by acute volume expansion. The corticosteroid response to ACTH was 19-29% inhibited by volume expansion. We conclude that acute volume expansion significantly inhibits the adrenocortical sensitivity to its tropic hormones probably via alterations of synergistic factors.

Intravascular receptors and renal responses of monkey to volume expansion

1983 ◽  
Vol 244 (1) ◽  
pp. H55-H59 ◽  
Author(s):  
T. V. Peterson ◽  
F. T. Felts ◽  
N. L. Chase
Keyword(s):  
Volume Expansion ◽  
Macaca Fascicularis ◽  
Venous Pressure ◽  
Isotonic Saline ◽  
Neural Pathways ◽  
Central Venous ◽  
Dorsal Rhizotomy ◽  
Salt And Water Balance ◽  
The Times ◽  
Renal Responses

Experiments were performed in anesthetized Macaca fascicularis monkeys to determine the effects of combined thoracic dorsal rhizotomy (C8-T7) and vagotomy-sinoaortic denervation on the renal responses to acute intravascular volume expansion. Expansion of the estimated blood volume by 15% with 6% dextran in isotonic saline produced attenuated diuretic and natriuretic responses in the denervated animals when compared with sham-operated controls. The times to peak diuresis and natriuresis after volume expansion also were significantly earlier in the denervated group. Although central venous pressure increased similarly in both groups, mean arterial pressure increased to a greater extent after volume expansion in the denervated group. As opposed to the previously reported failure of either denervation alone to attenuate the renal responses to hypervolemia in the monkey, our results suggest that these neural pathways may play a role in maintaining salt and water balance in this species. However, because of the possibility of functionally redundant afferent mechanisms, blunted renal responses to volume expansion in the primate can only be demonstrated after an extensive denervation.

Intravenous angiotensin induces brain c-fos expression and vasopressin release in the near-term ovine fetus

2003 ◽  
Vol 285 (6) ◽  
pp. E1216-E1222 ◽  
Author(s):  
Lijun Shi ◽  
Fang Hu ◽  
Paul Morrissey ◽  
Jiaming Yao ◽  
Zhice Xu
Keyword(s):  
Intravenous Infusion ◽  
Fetal Brain ◽  
Circumventricular Organs ◽  
Ang Ii ◽  
Double Labeling ◽  
Vasopressin Release ◽  
Fetal Plasma ◽  
Ovine Fetus ◽  
Fos Expression ◽  
Near Term

The effect of intravenous angiotensin II (ANG II) on fetal brain c- fos expression and arginine vasopressin (AVP) release was studied in the near-term ovine fetus. Fetuses with chronically implanted catheters received an intravenous infusion of ANG II or saline. Fetal plasma AVP concentrations were significantly increased after the peripheral administration of ANG II, with peak levels (3-fold) at 30 min after the intravenous infusion. There was no change in fetal plasma osmolality, sodium, and hematocrit levels between the control and experimental groups or between the periods before and after the infusion of ANG II. Intravenous ANG II administration induced Fos immunoreactivity (Fos-IR) in the circumventricular organs and the median preoptic nucleus of the fetal brain. Fos-IR was also demonstrated in the fetal supraoptic nuclei (SON). Double labeling demonstrated that the AVP-containing neurons in the SON were expressing c- fos in response to intravenous ANG II. These results indicate that the peripheral ANG II in the fetus may play a significant role in stimulating the central hypothalamic-neurohypophysial system during late gestation. It supports the hypothesis that circulating ANG II may act at the fetal AVP neurons in the hypothalamus in body fluid balance via the circumventricular organs, which are situated outside the blood-brain barrier, and the central neural pathway between these two brain structures has been relatively established in utero, at least at near-term.

Fetal whole-body interstitial compliance, vascular compliance, and capillary filtration coefficient

1984 ◽  
Vol 247 (5) ◽  
pp. R800-R805 ◽  
Author(s):  
R. A. Brace ◽  
P. S. Gold
Keyword(s):  
Venous Pressure ◽  
Isotonic Saline ◽  
Optimization Techniques ◽  
Filtration Coefficient ◽  
Whole Body ◽  
Fetal Sheep ◽  
Mean Values ◽  
Capillary Filtration ◽  
Vascular Compliance ◽  
Capillary Filtration Coefficient

Fluid movements across the capillary wall were studied in chronically catheterized, near-term fetal sheep. We hemorrhaged 15 fetuses and infused isotonic saline in seven fetuses. The average experimental changes in arterial pressure, venous pressure, and blood volume were then analyzed by using mathematical modeling and parameter optimization techniques to estimate mean values for the average whole-body interstitial and vascular compliances of the fetus and for the average whole-body fetal capillary filtration coefficient. After fetal hemorrhage, interstitial compliance averaged 45 ml X mmHg-1 X kg-1 of fetal weight and vascular compliance averaged 3.0 ml X mmHg-1 X kg-1, whereas the capillary filtration coefficient averaged 0.4 ml X min-1 X mmHg-1 X kg-1. For intravenous saline infusions, interstitial compliance averaged 45 ml X mmHg-1 X kg-1, and vascular compliance averaged 3.5 ml X mmHg-1 X kg-1, whereas the capillary filtration coefficient averaged 0.8 ml X min-1 X mmHg-1 X kg-1. These data suggest that the fetus has a high whole-body interstitial compliance and a high capillary filtration coefficient compared with the adult. In addition, it appears that the fetus has the ability to decrease its vascular compliance and capillary surface area after a fetal hemorrhage.

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