Adipose afferent reflex response to insulin is mediated by melanocortin 4 type receptors in the paraventricular nucleus in insulin resistance rats

2015 ◽  
Vol 214 (4) ◽  
pp. 450-466 ◽  
Author(s):  
L. Ding ◽  
N. Tong ◽  
X.-M. Feng ◽  
D. Chen ◽  
H.-S. Wang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Paraventricular Nucleus ◽  
Reflex Response

Role of paraventricular nucleus in the cardiogenic sympathetic reflex in rats

2005 ◽  
Vol 288 (2) ◽  
pp. R420-R426 ◽  
Author(s):  
Matthew R. Zahner ◽  
Hui-Lin Pan
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Paraventricular Nucleus ◽  
Reflex Response ◽  
Renal Sympathetic Nerve Activity ◽  
Basal Blood Pressure ◽  
Blood Pressure Responses ◽  
Spinal Afferents

Myocardial ischemia stimulates cardiac spinal afferents to initiate a sympathoexcitatory reflex. However, the pathways responsible for generation of increased sympathetic outflow in this reflex are not fully known. In this study, we determined the role of the paraventricular nucleus (PVN) in the cardiogenic sympathetic reflex. Renal sympathetic nerve activity (RSNA) and blood pressure were recorded in anesthetized rats during epicardial application of 10 μg/ml bradykinin. Bilateral microinjection of muscimol (0.5 nmol), a GABAA receptor agonist, was performed to inhibit the PVN. In 10 vehicle-injected rats, epicardial bradykinin significantly increased RSNA 178.4 ± 48.5% from baseline, and mean arterial pressure from 76.9 ± 2.0 to 102.3 ± 3.3 mmHg. Microinjection of muscimol into the PVN significantly reduced the basal blood pressure and RSNA ( n = 12). After muscimol injection, the bradykinin-induced increases in RSNA (111.6 ± 35.9% from baseline) and mean arterial pressure (61.2 ± 1.3 to 74.5 ± 2.7 mmHg) were significantly reduced compared with control responses. The response remained attenuated even when the basal blood pressure was restored to the control. In a separate group of rats ( n = 9), bilateral microinjection of the ionotropic glutamate antagonist kynurenic acid (4.82 or 48.2 nmol in 50 nl) had no significant effect on the RSNA and blood pressure responses to bradykinin compared with controls. These results suggest that the tonic PVN activity is important for the full manifestation of the cardiogenic sympathoexcitatory response. However, ionotropic glutamate receptors in the PVN are not directly involved in this reflex response.

scholarly journals A projection from the hypothalamic paraventricular nucleus to the nucleus tractus solitarii is critical for cardiorespiratory responses to hypoxia

2019 ◽  
Author(s):  
◽  
Brian Ruyle
Keyword(s):  
Paraventricular Nucleus ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nucleus Tractus Solitarii ◽  
Reflex Response ◽  
Protective Mechanism ◽  
Adaptive Responses ◽  
Nerve Activity ◽  
Cardiorespiratory Responses ◽  
Obstructive Sleep

The arterial chemoreflex is an essential protective mechanism for adaptive responses to hypoxia. Stimulation of peripheral chemoreceptors initiates a reflex response that generates compensatory physiological responses, including increased ventilation, arterial pressure and sympathetic nerve activity. However, chemoreflex dysfunction, including over-excitation of chemoreflex pathways, leads to respiratory instability and increased sympathetic nerve activity (SNA) in disease states including heart failure, hypertension and obstructive sleep apnea (170, 199, 232). Determining the mechanisms involved in the central chemoreflex neurocircuitry and its plasticity in health and disease may lead to the development of targeted therapies in cardiorespiratory disease. This dissertation seeks to provide new insight into the neural circuits that drive chemoreflex function. Compensatory responses to chemoreflex stimulation are generated through coordinated interactions between nuclei in the brainstem, forebrain and spinal cord. However, the underlying neurocircuitry, including relevant connections between these nuclei, and the signaling mechanisms that take place within each region are not completely understood. The nucleus tractus solitarii (nTS) and the paraventricular nucleus (PVN) are two central nuclei known to drive chemoreflex function and are implicated in altered cardiorespiratory responses resulting from chemoreflex dysfunction. These two regions form reciprocal connections but the extent to which these connections influence cardiorespiratory regulation and specifically chemoreflex function is unclear. The overarching goal of this dissertation is to examine whether a population of PVN neurons that project to the nTS is involved in shaping cardiorespiratory responses to chemorefle activation by hypoxia. The experiments performed in the three studies (Chapters 2-4) test the overall hypothesis that a descending PVN-nTS projection is an essential component of chemoreflex neurocircuitry; chemoreflex-evoked activation of this pathway is critical for compensatory cardiorespiratory responses to hypoxia.

Superoxide anions in the paraventricular nucleus mediate cardiac sympathetic afferent reflex in insulin resistance rats

2014 ◽  
Vol 212 (4) ◽  
pp. 267-282 ◽  
Author(s):  
H.-J. Sun ◽  
H. Zhou ◽  
X.-M. Feng ◽  
Q. Gao ◽  
L. Ding ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Paraventricular Nucleus ◽  
Superoxide Anions ◽  
Cardiac Sympathetic Afferent Reflex

Differential role of the paraventricular nucleus of the hypothalamus in modulating the sympathoexcitatory component of peripheral and central chemoreflexes

2005 ◽  
Vol 289 (3) ◽  
pp. R789-R797 ◽  
Author(s):  
Maram K. Reddy ◽  
Kaushik P. Patel ◽  
Harold D. Schultz
Keyword(s):  
Paraventricular Nucleus ◽  
Potassium Cyanide ◽  
Reflex Response ◽  
Nerve Activity ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Arterial Blood ◽  
Central Chemoreceptors ◽  
Stimulation Of

In the present study we investigated the involvement of the hypothalamic paraventricular nucleus (PVN) in the modulation of sympathoexcitatory reflex activated by peripheral and central chemoreceptors. We measured mean arterial blood pressure (MAP), heart rate (HR), renal sympathetic nerve activity (RSNA), and phrenic nerve activity (PNA) before and after blocking neurotransmission within the PVN by bilateral microinjection of 2% lidocaine (100 nl) during specific stimulation of peripheral chemoreceptors by potassium cyanide (KCN, 75 μg/kg iv, bolus dose) or stimulation of central chemoreceptors with hypercapnia (10% CO2). Typically stimulation of peripheral chemoreceptors evoked a reflex response characterized by an increase in MAP, RSNA, and PNA and a decrease in HR. Bilateral microinjection of 2% lidocaine into the PVN had no effect on basal sympathetic and cardiorespiratory variables; however, the RSNA and PNA responses evoked by peripheral chemoreceptor stimulation were attenuated ( P < 0.05). Bilateral microinjection of bicuculline (50 pmol/50 nl, n = 5) into the PVN augmented the RSNA and PNA response to peripheral chemoreceptor stimulation ( P < 0.05). Conversely, the GABA agonist muscimol (0.2 nmol/50 nl, n = 5) injected into the PVN attenuated these reflex responses ( P < 0.05). Blocking neurotransmission within the PVN had no effect on the hypercapnia-induced central chemoreflex responses in carotid body denervated animals. These results suggest a selective role of the PVN in processing the sympathoexcitatory and ventilatory component of the peripheral, but not central, chemoreflex.

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