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.

Effect of different types of stressors on peptide messenger ribonucleic acids in the hypothalamic paraventricular nucleus

1993 ◽  
Vol 128 (6) ◽  
pp. 485-492 ◽  
Author(s):  
Sandra Ceccatelli ◽  
Catello Orazzo
Keyword(s):  
Paraventricular Nucleus ◽  
Immobilization Stress ◽  
Thyrotropin Releasing Hormone ◽  
Hypothalamic Paraventricular Nucleus ◽  
Male Rats ◽  
Mrna Levels ◽  
Corticotropin Releasing Hormone ◽  
Ribonucleic Acids ◽  
Releasing Hormone ◽  
Different Types

Using in situ hybridization we have studied the effects of different types of stressors, such as ether, immobilization, cold and swimming, on the expression of several peptide messenger ribonucleic acids (mRNAs) in the hypothalamic paraventricular nucleus of adult male rats. Paraventricular nucleus sections were hybridized using synthetic oligonucleotide probes complementary to mRNA for corticotropin-releasing hormone, neurotensin, enkephalin and thyrotropin-releasing hormone. A clear upregulation of neurotensin mRNA was seen after ether and, to a lesser extent, after immobilization stress, whereas after the two other stressors neurotensin mRNA was undetectable, as in control rats. An increase in enkephalin mRNA was observed in a selective region of the dorsal part of the medioparvocellular subdivision of the paraventricular nucleus only after ether and immobilization stress. No significant changes were seen in corticotropin-releasing hormone and thyrotropin-releasing hormone mRNA levels in any of the experimental paradigms. The present results show selective changes for various peptide mRNAs in the paraventricular nucleus after various types of stress. Significant effects could be demonstrated only on neurotensin and enkephalin mRNA after ether and immobilization stress. This suggests that adaptive changes in the rate of synthesis, processing and transport of the peptide may develop over a longer period of time.

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.

Hypothalamic paraventricular nucleus lesions do not prevent anorectic effect of exercise in male rats

1990 ◽  
Vol 259 (3) ◽  
pp. R579-R584 ◽  
Author(s):  
S. Rivest ◽  
D. Richard
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Paraventricular Nucleus ◽  
Wistar Rats ◽  
Energy Gain ◽  
Hypothalamic Paraventricular Nucleus ◽  
Male Rats ◽  
Hypothalamic Nucleus ◽  
Serum Corticosterone ◽  
Male Wistar Rats

The effects of a hypothalamic paraventricular nucleus (PVN) lesion on energy balance were investigated in exercise-trained rats. Male Wistar rats weighing initially 250 g were divided into four groups. Two groups of rats underwent a bilateral PVN lesion, whereas the two remaining groups were sham operated. The PVN lesions were done electrolytically. One group from each surgical treatment was exercised, while the other group was kept in sedentary conditions. Rats were exercised on a rodent motor-driven treadmill at moderate intensity, 1 h/day for 21 consecutive days. Food intake and body weight were measured each day during the study. At the end of the treatment period, rats were killed, and carcasses were analyzed for their energy content. Serum corticosterone was measured by a competitive protein-binding assay. Energy gain and energy intake were lower in exercised rats than in sedentary controls, regardless of whether they were sham or PVN lesioned. Concurrently, there was no difference in the energy gain between PVN-lesioned and sham-operated rats, despite the fact that PVN-lesioned rats ended the experiment with a larger body weight than the sham-lesioned animals. Serum corticosterone levels were lower in PVN-lesioned rats than in sham-lesioned rats. In conclusion, the present results indicate that the PVN, the hypothalamic nucleus predominantly controlling the pituitary-adrenal axis activity, is not a prominent structure in the regulation of energy balance in exercised male Wistar rats.

Impairment of mitochondrial respiratory chain enzyme activities in tetralogy of fallot

2007 ◽  
Vol 377 (1-2) ◽  
pp. 138-143 ◽  
Author(s):  
Santosh B. Shinde ◽  
Vipul C. Save ◽  
Neela D. Patil ◽  
Kaushala P. Mishra ◽  
Anil G. Tendolkar
Keyword(s):  
Tetralogy Of Fallot ◽  
Respiratory Chain ◽  
Enzyme Activities ◽  
Mitochondrial Respiratory Chain ◽  
Respiratory Chain Enzyme ◽  
Mitochondrial Respiratory

scholarly journals Nitric oxide synthase, ADMA, SDMA, and nitric oxide activity in the paraventricular nucleus throughout the etiology of renal wrap hypertension

2012 ◽  
Vol 302 (11) ◽  
pp. H2276-H2284 ◽  
Author(s):  
Carrie A. Northcott ◽  
Scott Billecke ◽  
Teresa Craig ◽  
Carmen Hinojosa-Laborde ◽  
Kaushik P. Patel ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Paraventricular Nucleus ◽  
No Synthase ◽  
Elevated Blood ◽  
Inhibitory Effects ◽  
Symmetric Dimethylarginine ◽  
Inhibitory Neurotransmitters ◽  
Nos Inhibitor ◽  
Oxide Synthase

Within the paraventricular nucleus (PVN), there is a balance between the excitatory and inhibitory neurotransmitters that regulate blood pressure; in hypertension, the balance shifts to enhanced excitation. Nitric oxide (NO) is an atypical neurotransmitter that elicits inhibitory effects on cardiovascular function. We hypothesized that reduced PVN NO led to elevations in blood pressure during both the onset and sustained phases of hypertension due to decreased NO synthase (NOS) and increased asymmetrical dimethylarginine (ADMA; an endogenous NOS inhibitor) and symmetric dimethylarginine (SDMA). Elevated blood pressure, in response to PVN bilateral microinjections of a NO inhibitor, nitro-l-arginine methyl ester, was blunted in renal wrapped rats during the onset of hypertension ( day 7) and sustained renal wrap hypertension ( day 28) compared with sham-operated rats. Adenoviruses (Ad) encoding endothelial NOS (eNOS) or LacZ microinjected into the PVN [1 × 109 plaque-forming units, bilateral (200 nl/site)] reduced mean arterial pressure compared with control ( Day 7, Ad LacZ wrap: 144 ± 7 mmHg and Ad eNOS wrap: 117 ± 5 mmHg, P ≤ 0.05) throughout the study ( Day 28, Ad LacZ wrap: 123 ± 1 mmHg and Ad eNOS wrap: 108 ± 4 mmHg, P ≤ 0.05). Western blot analyses of PVN NOS revealed significantly lower PVN neuronal NOS during the onset of hypertension but not in sustained hypertension. Reduced SDMA was found in the PVN during the onset of hypertension; however, no change in ADMA was observed. In conclusion, functional indexes of NO activity indicated an overall downregulation of NO in renal wrap hypertension, but the mechanism by which this occurs likely differs throughout the development of hypertension.

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