scholarly journals Elevated brain‐derived neurotrophic factor (BDNF) levels in the paraventricular nucleus (PVN) increase blood pressure, heart rate and indices of sympathetic activity

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Benedek Erdos ◽  
Iara Backes ◽  
Michael L McCowen ◽  
Deborah A Scheuer
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Paraventricular Nucleus ◽  
Neurotrophic Factor ◽  
Sympathetic Activity ◽  
Brain Derived Neurotrophic Factor ◽  
Increase Blood Pressure

scholarly journals Inhibition of BDNF signaling in the paraventricular nucleus of the hypothalamus lowers acute stress-induced pressor responses

2018 ◽  
Vol 120 (2) ◽  
pp. 633-643 ◽  
Author(s):  
Chris L. Schaich ◽  
Theresa L. Wellman ◽  
Zachary Einwag ◽  
Richard A. Dutko ◽  
Benedek Erdos
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Body Weight ◽  
Food Intake ◽  
Paraventricular Nucleus ◽  
Neurotrophic Factor ◽  
Restraint Stress ◽  
Acute Stress ◽  
Cardiovascular Responses ◽  
High Affinity

Brain-derived neurotrophic factor (BDNF) expression increases in the paraventricular nucleus of the hypothalamus (PVN) during stress, and our recent studies indicate that BDNF induces sympathoexcitatory and hypertensive responses when injected acutely or overexpressed chronically in the PVN. However, it remained to be investigated whether BDNF is involved in the mediation of stress-induced cardiovascular responses. Here we tested the hypothesis that inhibition of the high-affinity BDNF receptor TrkB in the PVN diminishes acute stress-induced cardiovascular responses. Male Sprague-Dawley rats were equipped with radiotelemetric transmitters for blood pressure measurement. BDNF-TrkB signaling was selectively inhibited by viral vector-mediated bilateral PVN overexpression of a dominant-negative truncated TrkB receptor (TrkB.T1, n = 7), while control animals ( n = 7) received green fluorescent protein (GFP)-expressing vector injections. Rats were subjected to acute water and restraint stress 3–4 wk after vector injections. We found that body weight, food intake, baseline mean arterial pressure (MAP), and heart rate were unaffected by TrkB.T1 overexpression. However, peak MAP increases were significantly reduced in the TrkB.T1 group compared with GFP both during water stress (GFP: 39 ± 2 mmHg, TrkB.T1: 27 ± 4 mmHg; P < 0.05) and restraint stress (GFP: 41 ± 3 mmHg, TrkB.T1: 34 ± 2 mmHg; P < 0.05). Average MAP elevations during the poststress period were also significantly reduced after both water and restraint stress in the TrkB.T1 group compared with GFP. In contrast, heart rate elevations to both stressors remained unaffected by TrkB.T1 overexpression. Our results demonstrate that activation of BDNF high-affinity TrkB receptors within the PVN is a major contributor to acute stress-induced blood pressure elevations. NEW & NOTEWORTHY We have shown that inhibition of the high-affinity brain-derived neurotrophic factor receptor TrkB in the paraventricular nucleus of the hypothalamus significantly reduces blood pressure elevations to acute stress without having a significant impact on resting blood pressure, body weight, and food intake.

scholarly journals Corticotropin-releasing hormone projections from the paraventricular nucleus of the hypothalamus to the nucleus of the solitary tract increase blood pressure

2019 ◽  
Vol 121 (2) ◽  
pp. 602-608 ◽  
Author(s):  
Lei A. Wang ◽  
Dianna H. Nguyen ◽  
Steve W. Mifflin
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Paraventricular Nucleus ◽  
Cardiovascular Responses ◽  
Solitary Tract ◽  
Increase Blood Pressure ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Optogenetic Stimulation ◽  
Stimulation Of

Activation of corticotropin-releasing hormone (CRH) type 2 receptors (CRHR2) in the nucleus of the solitary tract (NTS) contributes to the development of hypertension, but the source of CRH inputs to the NTS that increases blood pressure remains unknown. This study tested the hypothesis that activation of CRH-containing projections from the paraventricular nucleus of the hypothalamus (PVN) to the NTS increase blood pressure. We expressed channelrhodopsin 2 (ChR2), a light-sensitive ion channel, into CRH-containing neurons in the PVN. This was achieved by injecting Cre-inducible virus expressing ChR2 into the PVN of CRH-Cre mice. CRH-Cre mice are genetically modified mice expressing Cre recombinase only in neurons producing CRH. We found that optogenetic stimulation of CRH-containing somas in the PVN or CRH-containing fibers in the NTS originating from the PVN significantly increased blood pressure and heart rate. Microinjection of K-41498 (CRHR2 antagonist) into the NTS attenuated the pressor and tachycardiac responses induced by optogenetic stimulation of CRH-containing somas in the PVN. In vitro loose-patch recordings revealed that optogenetic stimulation of CRH-containing fibers in the NTS originating from the PVN significantly increased the discharge frequency of NTS neurons. This effect was attenuated by pretreatment of K-41498 and was abolished by pretreatment of kynurenic acid (nonselective glutamate receptor antagonist). These results suggest that activation of PVN-NTS CRH-containing projections increases blood pressure and heart rate. The cardiovascular responses may be mediated at least in part by the corelease of CRH and glutamate from NTS CRH-containing axons originating from the PVN. NEW & NOTEWORTHY Optogenetic stimulation of paraventricular nucleus of the hypothalamus (PVN) corticotropin-releasing hormone (CRH)-containing somas or nucleus of the solitary tract (NTS) CRH-containing fibers originating from the PVN increased blood pressure and heart rate. Corelease of CRH and glutamate from NTS CRH-containing axons originating from the PVN may contribute to the pressor and tachycardiac responses elicited by optogenetic stimulation of PVN CRH-containing somas.

scholarly journals Intermedin in Paraventricular Nucleus Attenuates Sympathetic Activity and Blood Pressure via Nitric Oxide in Hypertensive Rats

Hypertension ◽  
2014 ◽  
Vol 63 (2) ◽  
pp. 330-337 ◽  
Author(s):  
Ye-Bo Zhou ◽  
Hai-Jian Sun ◽  
Dan Chen ◽  
Tong-Yan Liu ◽  
Ying Han ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Paraventricular Nucleus ◽  
Sympathetic Activity ◽  
Hypertensive Rats

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.

Hypolipidemic drugs, blood pressure, heart rate, heart rate variability and sympathetic activity

2004 ◽  
Vol 1262 ◽  
pp. 458-461 ◽  
Author(s):  
Richard Ceska ◽  
Vojtech Melenovsky ◽  
Jan Malik ◽  
Eva Kralikova ◽  
Tomas Stulc ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Sympathetic Activity ◽  
Hypolipidemic Drugs

Low Frequency Music Slows Heart Rate and Decreases Sympathetic Activity

2018 ◽  
Vol 10 (4) ◽  
pp. 180 ◽  
Author(s):  
James D. Halbert ◽  
Debra R. Van Tuyll ◽  
Carl Purdy ◽  
Guang Hao ◽  
Steven Cauthron ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Activity ◽  
Stress Condition ◽  
Mental Arithmetic ◽  
Low Frequency ◽  
Cvd Risk ◽  
Beneficial Effects ◽  
Main Effect ◽  
Underlying Mechanisms

Objectives: Increasing blood pressure (BP) increases the risk of developing cardiovascular disease (CVD). Lower frequency music may lower BP and heart rate (HR), therefore, decreases the CVD risk. Methods: Participants were 16 high BP individuals aged 20 to 50 years. The protocol consisted of 2 visits (experimental & control). Music was tuned between 440 Hz and 432 Hz, and the frequencies changed every 10 minutes. HR variability, diastolic function, oxytocin, and amylase were recorded at each phase. An (ANOVA) was used to examine the effects of music. Results: Mental arithmetic significantly increased BP and HR (all ps<0.01). There were significant differences between the stress condition and all other conditions, all p’s < .02. There was a significant main effect for Music Order, F (1, 6) = 6.23, p = .047, ƞp2= .51, β = .55. Participants had lower HR listening to 432 Hz music (M = -7.20, se = 2.47) than 440 Hz music (M = -5.33, se = 2.71), t(7) = 2.53, p = .04, d ‘ = .41. Conclusion: Listening to low frequency music has cardiovascular benefits including slowing heart rate and promoting relaxation. Further study is needed to determine the underlying mechanisms of music induced beneficial effects.

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