Right Atrial Stretch Induces Renal Nerve Inhibition and c-fos Expression in Parvocellular Neurones of the Paraventricular Nucleus in Rats

2002 ◽  
Vol 87 (1) ◽  
pp. 25-32 ◽  
Author(s):  
S. Pyner ◽  
J. Deering ◽  
J. H. Coote
Keyword(s):  
Paraventricular Nucleus ◽  
Right Atrial ◽  
Renal Nerve ◽  
Fos Expression ◽  
Nerve Inhibition

Renal nerve inhibition by central NaCl and ANG II is abolished by lesions of the lamina terminalis

2000 ◽  
Vol 279 (5) ◽  
pp. R1827-R1833 ◽  
Author(s):  
C. N. May ◽  
R. M. McAllen ◽  
M. J. McKinley
Keyword(s):  
Hypertonic Saline ◽  
Third Ventricle ◽  
Plasma Renin ◽  
Anterior Wall ◽  
Lamina Terminalis ◽  
Ang Ii ◽  
Renal Nerve ◽  
Intracerebroventricular Infusion ◽  
Conscious Sheep ◽  
Nerve Inhibition

The lamina terminalis is situated in the anterior wall of the third ventricle and plays a major role in fluid and electrolyte homeostasis and cardiovascular regulation. The present study examined whether the effects of intracerebroventricular infusion of hypertonic saline and ANG II on renal sympathetic nerve activity (RSNA) were mediated by the lamina terminalis. In control, conscious sheep ( n = 5), intracerebroventricular infusions of 0.6 M NaCl (1 ml/h for 20 min) and ANG II (10 nmol/h for 30 min) increased mean arterial pressure (MAP) by 6 ± 1 ( P < 0.001) and 14 ± 3 mmHg ( P < 0.001) and inhibited RSNA by 80 ± 6 ( P < 0.001) and 89 ± 7% ( P < 0.001), respectively. Both treatments reduced plasma renin concentration (PRC). Intracerebroventricular infusion of artificial cerebrospinal fluid (1 ml/h for 30 min) had no effect. In conscious sheep with lesions of the lamina terminalis ( n = 6), all of the responses to intracerebroventricular hypertonic saline and ANG II were abolished. In conclusion, the effects of intracerebroventricular hypertonic saline and ANG II on RSNA, PRC, and MAP depend on the integrity of the lamina terminalis, indicating that this site plays an essential role in coordinating the homeostatic responses to changes in brain Na+ concentration.

Volume expansion does not activate neuronal projections from the NTS or depressor VLM to the RVLM

1999 ◽  
Vol 277 (1) ◽  
pp. R39-R46 ◽  
Author(s):  
Anthony D. Shafton ◽  
Andrew Ryan ◽  
Barry McGrath ◽  
Emilio Badoer
Keyword(s):  
Volume Expansion ◽  
Nucleus Tractus Solitarius ◽  
Ventrolateral Medulla ◽  
Cell Nuclei ◽  
Renal Nerve ◽  
Monosynaptic Connection ◽  
Reflex Pathways ◽  
Nerve Inhibition ◽  
Cardiopulmonary Baroreceptors ◽  
Medullary Neurons

We investigated whether a monosynaptic connection from the nucleus tractus solitarius (NTS) or the depressor ventrolateral medulla (VLM) to the pressor region of the rostral VLM (RVLM) constituted part of the reflex pathway activated by cardiopulmonary baroreceptors. Volume expansion in the conscious rabbit, which elicits renal nerve inhibition predominantly via cardiac mechanoreceptors, was used as the stimulus. The protein Fos was used as a marker of neuronal activation. The retrogradely transported tracer rhodamine-tagged microspheres, previously injected into the pressor region of the RVLM, identified medullary neurons that projected to that region. Volume expansion significantly increased the number of Fos-positive cell nuclei in the NTS and in the depressor VLM. Neurons that projected to the RVLM were found throughout the depressor region of the VLM and in the NTS but were not activated by volume expansion. Thus, although the central reflex pathways activated by volume expansion include the NTS and the depressor region of the VLM, we could not find evidence for a monosynaptic connection between those regions and the RVLM.

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.

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