scholarly journals The Chemoattraction of Immune Cells into the Hypothalamic Paraventricular Nucleus Elicits Sympathetically‐Mediated Blood Pressure Elevations in Hypertension

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Khalid Elsaafien ◽  
Willian Seji Korim ◽  
Clive Newton May ◽  
Song Tieng Yao
Keyword(s):  
Blood Pressure ◽  
Paraventricular Nucleus ◽  
Immune Cells ◽  
Hypothalamic Paraventricular Nucleus

THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS AND BLOOD PRESSURE CONTROL

1997 ◽  
Vol 11 (S1) ◽  
pp. 26s-30s ◽  
Author(s):  
J H Coote ◽  
J Gardner ◽  
S Gladwell ◽  
E Sermasi ◽  
R Ranson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Control ◽  
Paraventricular Nucleus ◽  
Pressure Control ◽  
Hypothalamic Paraventricular Nucleus

Hypothalamic paraventricular nucleus is critical for renal vasoconstriction elicited by elevations in body temperature

2008 ◽  
Vol 294 (2) ◽  
pp. F309-F315 ◽  
Author(s):  
Joo Lee Cham ◽  
Emilio Badoer
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Core Temperature ◽  
Paraventricular Nucleus ◽  
Hypothalamic Paraventricular Nucleus ◽  
Body Core Temperature ◽  
Control Group ◽  
Body Core

Redistribution of blood from the viscera to the peripheral vasculature is the major cardiovascular response designed to restore thermoregulatory homeostasis after an elevation in body core temperature. In this study, we investigated the role of the hypothalamic paraventricular nucleus (PVN) in the reflex decrease in renal blood flow that is induced by hyperthermia, as this brain region is known to play a key role in renal function and may contribute to the central pathways underlying thermoregulatory responses. In anesthetized rats, blood pressure, heart rate, renal blood flow, and tail skin temperature were recorded in response to elevating body core temperature. In the control group, saline was microinjected bilaterally into the PVN; in the second group, muscimol (1 nmol in 100 nl per side) was microinjected to inhibit neuronal activity in the PVN; and in a third group, muscimol was microinjected outside the PVN. Compared with control, microinjection of muscimol into the PVN did not significantly affect the blood pressure or heart rate responses. However, the normal reflex reduction in renal blood flow observed in response to hyperthermia in the control group (∼70% from a resting level of 11.5 ml/min) was abolished by the microinjection of muscimol into the PVN (maximum reduction of 8% from a resting of 9.1 ml/min). This effect was specific to the PVN since microinjection of muscimol outside the PVN did not prevent the normal renal blood flow response. The data suggest that the PVN plays an essential role in the reflex decrease in renal blood flow elicited by hyperthermia.

scholarly journals Elevated bone marrow sympathetic drive precedes systemic inflammation in angiotensin II hypertension

2019 ◽  
Vol 317 (2) ◽  
pp. H279-H289 ◽  
Author(s):  
Niousha Ahmari ◽  
Monica M. Santisteban ◽  
Douglas R. Miller ◽  
Natalie M. Geis ◽  
Riley Larkin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Bone Marrow ◽  
T Cells ◽  
Immune System ◽  
Angiotensin Ii ◽  
Paraventricular Nucleus ◽  
Immune Cells ◽  
Rodent Models ◽  
Ang Ii ◽  
Pressure Infiltration

Increased sympathetic nervous system activity is a hallmark of hypertension (HTN), and it is implicated in altered immune system responses in its pathophysiology. However, the precise mechanisms of neural-immune interaction in HTN remain elusive. We have previously shown an association between elevated sympathetic drive to the bone marrow (BM) and activated BM immune cells in rodent models of HTN. Moreover, microglial-dependent neuroinflammation is also seen in rodent models of HTN. However, the cause-effect relationship between central and systemic inflammatory responses and the sympathetic drive remains unknown. These observations led us to hypothesize that increase in the femoral BM sympathetic nerve activity (fSNA) initiates a cascade of events leading to increase in blood pressure (BP). Here, we investigated the temporal relationship between the BM sympathetic drive, activation of the central and peripheral immune system, and increase in BP in the events leading to established HTN. The present study demonstrates that central infusion of angiotensin II (ANG II) induces early microglial activation in the paraventricular nucleus of hypothalamus, which preceded increase in the fSNA. In turn, activation of fSNA correlated with the timing of increased production and release of CD4+.IL17+ T cells and other proinflammatory cells into circulation and elevation in BP, whereas infiltration of CD4+ cells to the paraventricular nucleus marked establishment of ANG II HTN. This study identifies cellular and molecular mechanisms involved in neural-immune interactions in early and established stages of rodent ANG II HTN. NEW & NOTEWORTHY Early microglia activation in paraventricular nucleus precedes sympathetic activation of the bone marrow. This leads to increased bone marrow immune cells and their release into circulation and an increase in blood pressure. Infiltration of CD4+ T cells into paraventricular nucleus paraventricular nucleus marks late hypertension.

Median preoptic neurons projecting to the hypothalamic paraventricular nucleus are sensitive to blood pressure changes

1993 ◽  
Vol 605 (2) ◽  
pp. 338-341 ◽  
Author(s):  
Junichi Tanaka ◽  
Masahiko Nomura ◽  
Katsuhide Kariya ◽  
Jun-ichi Nishimura ◽  
Fukuko Kimura
Keyword(s):  
Blood Pressure ◽  
Paraventricular Nucleus ◽  
Hypothalamic Paraventricular Nucleus ◽  
Pressure Changes

scholarly journals Effects of Nrf1 in Hypothalamic Paraventricular Nucleus on Regulating the Blood Pressure During Hypertension

2021 ◽  
Vol 15 ◽  
Author(s):  
Xiao-Jing Yu ◽  
Tong Xiao ◽  
Xiao-Jing Liu ◽  
Ying Li ◽  
Jie Qi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Respiratory Chain ◽  
Neuronal Activity ◽  
Paraventricular Nucleus ◽  
Critical Role ◽  
Mitochondrial Respiratory Chain ◽  
Hypothalamic Paraventricular Nucleus ◽  
Male Rats ◽  
Respiratory Chain Enzyme ◽  
Inhibitory Neurotransmitters

The incidence rate and mortality of hypertension increase every year. Hypothalamic paraventricular nucleus (PVN) plays a critical role on the pathophysiology of hypertension. It has been demonstrated that the imbalance of neurotransmitters including norepinephrine (NE), glutamate (Glu) and γ-aminobutyric acid (GABA) are closely related to sympathetic overactivity and pathogenesis of hypertension. N-methyl-D-aspartate receptor (NMDAR), consisting of GluN1 and GluN2 subunits, is considered to be a glutamate-gated ion channel, which binds to Glu, and activates neuronal activity. Studies have found that the synthesis of respiratory chain enzyme complex was affected and mitochondrial function was impaired in spontaneously hypertensive rats (SHR), further indicating that mitochondria is associated with hypertension. Nuclear respiratory factor 1 (Nrf1) is a transcription factor that modulates mitochondrial respiratory chain and is related to GluN1, GluN2A, and GluN2B promoters. However, the brain mechanisms underlying PVN Nrf1 modulating sympathoexcitation and blood pressure during the development of hypertension remains unclear. In this study, an adeno-associated virus (AAV) vector carrying the shRNA targeting rat Nrf1 gene (shNrf1) was injected into bilateral PVN of male rats underwent two kidneys and one clip to explore the role of Nrf1 in mediating the development of hypertension and sympathoexcitation. Administration of shNrf1 knocked down the expression of Nrf1 and reduced the expression of excitatory neurotransmitters, increased the expression of inhibitory neurotransmitters, and reduced the production of reactive oxygen species (ROS), and attenuated sympathoexcitation and hypertension. The results indicate that knocking down Nrf1 suppresses sympathoexcitation in hypertension by reducing PVN transcription of NMDAR subunits (GluN1, GluN2A, and GluN2B), rebalancing PVN excitatory and inhibitory neurotransmitters, inhibiting PVN neuronal activity and oxidative stress, and attenuating sympathetic activity.

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