Decreased cardiorespiratory effects of neuropeptide Y in the nucleus tractus solitarius in diabetes

1992 ◽  
Vol 262 (5) ◽  
pp. R865-R871
Author(s):  
J. C. Dunbar ◽  
E. Ergene ◽  
G. F. Anderson ◽  
R. A. Barraco
Keyword(s):  
Blood Pressure ◽  
Neuropeptide Y ◽  
Nucleus Tractus Solitarius ◽  
Brain Regions ◽  
Diabetic Rats ◽  
Minute Volume ◽  
Solitary Tract ◽  
Respiratory Parameters ◽  
Alpha Chloralose ◽  
The Brain

It has been observed that diabetes results in increased neuropeptide Y (NPY) in various brain regions, especially the paraventricular nucleus, which projects to the nucleus of the solitary tract (NTS). Because previous studies indicated a pathophysiological relationship between diabetes and NPY, we investigated the effect of diabetes on the sensitivity of NTS-mediated responses to NPY administration. Rats were made diabetic using streptozocin (55 mg/kg iv) and maintained for 48 to 50 days. Normal and streptozocin-diabetic rats were anesthetized with urethan and alpha-chloralose, instrumented for cardiovascular and respiratory monitoring, and positioned in a stereotaxic apparatus. The brain stem was exposed surgically. NPY (0.15 nmol/kg) was microinjected into the NTS and the cardiovascular and respiratory parameters were monitored for 60 min. Diabetes increased systolic (SAP), diastolic (DAP), and mean (Pa) blood pressure but not pulse pressure (PP) and heart rate (HR). Respiratory parameters were not altered. NPY significantly decreased SAP, DAP, Pa, PP, HR, respiratory rate, and minute volume in normal animals. In diabetic animals, NPY also decreased SAP, DAP, and Pa but pronouncedly increased PP. Although NPY decreased the SAP and Pa in diabetic animals, the response was attenuated compared with normal animals. The respiratory parameters and HR of diabetic animals, unlike normal animals, did not respond to NPY administration. We conclude that chronic diabetes results in a decreased sensitivity to NTS-mediated responses and that the hyporesponsiveness of the NTS to NPY modulation may be important in the tendency toward elevated blood pressure and hypertension in diabetes.

Nucleus tractus solitarius and control of blood pressure in chronic sinoaortic denervated rats

1992 ◽  
Vol 263 (2) ◽  
pp. R258-R266 ◽  
Author(s):  
A. M. Schreihofer ◽  
A. F. Sved
Keyword(s):  
Blood Pressure ◽  
Plasma Levels ◽  
Nucleus Tractus Solitarius ◽  
Inhibitory Influence ◽  
Baroreceptor Reflexes ◽  
Alpha Chloralose ◽  
And Control ◽  
Bilateral Destruction ◽  
Conscious Control

To determine the role of the nucleus tractus solitarius (NTS) in the tonic maintenance of arterial pressure (AP) following chronic baroreceptor denervation, the present study examined the effect of inhibition of the NTS on AP in chronic sinoaortic denervated (SAD) and control rats. One to two weeks after complete SAD (no residual arterial baroreceptor reflexes) mean AP was not significantly different from that of control rats. Bilateral microinjections of muscimol and lidocaine into the NTS markedly increased AP in alpha-chloralose-anesthetized control rats. However, microinjections of these neuroinhibitory drugs had no effect on AP in SAD rats. Similarly, 1 h after bilateral destruction of the NTS conscious control rats were hypertensive, while AP in SAD rats was not changed. Plasma levels of vasopressin (VP), which were also elevated in control rats 1 h after NTS lesions, were not significantly altered in SAD rats. These results demonstrate that inhibition of the NTS has no effect on AP or plasma levels of VP in chronic SAD rats. This suggests neither the NTS nor afferents to the NTS supply a tonic inhibitory influence on AP after chronic baroreceptor denervation.

Role of adrenal catecholamines in cerebrovasodilation evoked from brain stem

1987 ◽  
Vol 252 (6) ◽  
pp. H1183-H1191
Author(s):  
C. Iadecola ◽  
P. M. Lacombe ◽  
M. D. Underwood ◽  
T. Ishitsuka ◽  
D. J. Reis
Keyword(s):  
Brain Function ◽  
Blood Gases ◽  
Brain Regions ◽  
Elevated Plasma ◽  
Regional Cerebral Blood ◽  
Medullary Reticular Formation ◽  
Alpha Chloralose ◽  
The Brain ◽  
Stimulation Of

We studied whether adrenal medullary catecholamines (CAs) contribute to the metabolically linked increase in regional cerebral blood flow (rCBF) elicited by electrical stimulation of the dorsal medullary reticular formation (DMRF). Rats were anesthetized (alpha-chloralose, 30 mg/kg), paralyzed, and artificially ventilated. The DMRF was electrically stimulated with intermittent trains of pulses through microelectrodes stereotaxically implanted. Blood gases were controlled and, during stimulation, arterial pressure was maintained within the autoregulated range for rCBF. rCBF and blood-brain barrier (BBB) permeability were determined in homogenates of brain regions by using [14C]iodoantipyrine and alpha-aminoisobutyric acid (AIB), respectively, as tracers. Plasma CAs (epinephrine and norepinephrine) were measured radioenzymatically. DMRF stimulation increased rCBF throughout the brain (n = 5; P less than 0.01, analysis of variance) and elevated plasma CAs substantially (n = 4). Acute bilateral adrenalectomy abolished the increase in plasma epinephrine (n = 4), reduced the increases in flow (n = 6) in cerebral cortex (P less than 0.05), and abolished them elsewhere in brain (P greater than 0.05). Comparable effects on rCBF were obtained by selective adrenal demedullation (n = 7) or pretreatment with propranolol (1.5 mg/kg iv) (n = 5). DMRF stimulation did not increase the permeability of the BBB to AIB (n = 5). We conclude that the increases in rCBF elicited from the DMRF has two components, one dependent on, and the other independent of CAs. Since the BBB is impermeable to CAs and DMRF stimulation fails to open the BBB, the results suggest that DMRF stimulation allows, through a mechanism not yet determined, circulating CAs to act on brain and affect brain function.

Sex, the brain and hypertension: brain oestrogen receptors and high blood pressure risk factors

2015 ◽  
Vol 130 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Meredith Hay
Keyword(s):  
Risk Factors ◽  
Blood Pressure ◽  
Older Women ◽  
Premenopausal Women ◽  
Brain Regions ◽  
Oestrogen Receptors ◽  
The Common ◽  
Key Sites ◽  
The Brain ◽  
Underlying Risk

Hypertension is a major contributor to worldwide morbidity and mortality rates related to cardiovascular disease. There are important sex differences in the onset and rate of hypertension in humans. Compared with age-matched men, premenopausal women are less likely to develop hypertension. However, after age 60, the incidence of hypertension increases in women and even surpasses that seen in older men. It is thought that changes in levels of circulating ovarian hormones as women age may be involved in the increase in hypertension in older women. One of the key mechanisms involved in the development of hypertension in both men and women is an increase in sympathetic nerve activity (SNA). Brain regions important for the regulation of SNA, such as the subfornical organ, the paraventricular nucleus and the rostral ventral lateral medulla, also express specific subtypes of oestrogen receptors. Each of these brain regions has also been implicated in mechanisms underlying risk factors for hypertension such as obesity, stress and inflammation. The present review brings together evidence that links actions of oestrogen at these receptors to modulate some of the common brain mechanisms involved in the ability of hypertensive risk factors to increase SNA and blood pressure. Understanding the mechanisms by which oestrogen acts at key sites in the brain for the regulation of SNA is important for the development of novel, sex-specific therapies for treating hypertension.

Abstract 25: Angiotensin AT 1A Receptors on Leptin Receptor-Expressing Cells are Required for the Blood Pressure and Metabolic Rate Effects of Leptin

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Justin L Grobe ◽  
Kristin E Claflin
Keyword(s):  
Blood Pressure ◽  
Metabolic Rate ◽  
Body Mass ◽  
Leptin Receptor ◽  
Receptor Gene ◽  
Brain Regions ◽  
Leptin Resistance ◽  
Brown Adipose ◽  
Obesity Hypertension ◽  
The Brain

Circulating leptin and the local brain renin-angiotensin system (RAS) both contribute to the control of food intake (FI), resting metabolic rate (RMR) and blood pressure (BP), and both have been postulated to contribute to obesity-hypertension. Here we examined the provocative hypothesis that the brain RAS is required for (or mediates) the RMR- and BP-stimulating effects of leptin. To create animals lacking the AT 1A receptor specifically in cells expressing the leptin receptor (“KO”), mice with a flox’ed version of the endogenous angiotensin AT 1A receptor gene (AT 1A flox ) were crossed with mice expressing cre-recombinase via the leptin receptor promoter (ObR-Cre). Body mass, body composition, blood chemistry, glucose tolerance, and FI behaviors were essentially unchanged through 34 weeks of age in mice maintained on standard chow (Teklad 7013). In contrast, anesthetized BP (MAP; control n=9, 91.6 ± 4.1, vs KO n=8, 78.0 ± 3.7 mmHg) and heart rate (351 ± 13, vs 308 ± 11 BPM) were reduced in KO mice (both P<0.05). Further, interscapular brown adipose (BAT SNA, 112 ± 22, vs 22 ± 35 % above baseline at 3 hr) and renal (154 ± 19, vs 53 ± 23 % above baseline at 3 hr) sympathetic nerve activity responses to acute leptin injection (60 μg, i.v.) were completely abolished (both P<0.05). When maintained on a 45% high fat diet (OpenSource D12451 ) to increase endogenous leptin production, KO mice exhibited accelerated body mass (control n=15, -0.1 ± 0.1, vs KO n=4, +1.7 ± 0.5 g/wk) and fat mass (+2.9 ± 0.5, vs +4.9 ± 1.1 g/5 wk) gains (both P<0.05), likely due to normal FI behaviors but a 18% reduction in RMR (control n=16, 0.196 ± 0.011, vs KO n=7, 0.161 ± 0.004 kcal/hr at 30°C, P<0.05). We conclude that expression of angiotensin AT 1A receptors on leptin-sensitive cells is required for the metabolic rate and cardiovascular effects of leptin. Ongoing studies are focused on identifying the brain regions and subsets of leptin receptor-expressing cells in which this RAS-leptin cross-talk occurs, and the directionality and molecular mediators of this interaction. We hypothesize that uncontrolled or pathological activity of the brain RAS may thus help explain the clinically variable effects of leptin, and contribute to the mechanism(s) of selective leptin resistance and obesity-hypertension.

Angiotensin II attenuates baroreflexes at nucleus tractus solitarius of rats

1986 ◽  
Vol 250 (2) ◽  
pp. R193-R198 ◽  
Author(s):  
R. Casto ◽  
M. I. Phillips
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Baroreflex Sensitivity ◽  
Nucleus Tractus Solitarius ◽  
Ang Ii ◽  
Spontaneously Hypertensive ◽  
Baroreceptor Reflexes ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
The Brain

Microinjection of angiotensin II (ANG II) into the nucleus tractus solitarius (NTS) has been shown to produce a dose-dependent increase in blood pressure and heart rate. We have tested the effect of subpressor infusions of ANG II (10 ng . kg-1 . min-1) in the NTS on reflex bradycardia after intravenous administration of the vasoconstrictor phenylephrine (1-12 micrograms) in normotensive urethan-anesthetized rats. ANG II within the brain is thought to contribute to the decreased baroreflex sensitivity in spontaneously hypertensive rats (SHR). The sensitivity of the baroreflex was significantly decreased by the infusion of ANG II (1.01 +/- 0.08) compared with control (2.41 +/- 0.51) in the normotensive animals. Baroreflex sensitivity was significantly decreased in SHR (0.40 +/- 0.21) compared with normotensive animals. We conclude that ANG II within the NTS can inhibit the function of baroreceptor reflexes in normotensive animals, suggesting that the endogenous peptide may perform an inhibitory role in the baroreflex arc, and this is further evidence that central ANG II is involved in blood pressure of SHR.

scholarly journals PROFIL PENDERITA STROKE DENGAN HIPERTENSI DI BAGIAN RAWAT INAP NEUROLOGI RSUP PROF. DR. R. D. KANDOU MANADO PERIODE JULI 2013 – JUNI 2014

e-CliniC ◽  
2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Caroline G. Senaen ◽  
Mieke A. H. N Kembuan ◽  
Rizal Tumewah
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Stroke ◽  
Brain Regions ◽  
Neurological Deficits ◽  
Diastolic Hypertension ◽  
Blood Pressures ◽  
Male Patients ◽  
Grade 3 ◽  
The Brain ◽  
Symptoms And Signs

Abstract: Stroke is a disease of acute neurological deficits caused by brain blood vessel disorder that occurs suddenly and causes symptoms and signs that correspond to the affected brain regions. High blood pressure, also known as hypertension, is one of the major risk factors of hemorrhagic stroke and ischemic stroke. Hypertension can lead to rupture or narrowing of blood vessels of the brain. This study aimed to identify the profile of stroke patients with hypertension in inpatients of Neurology Department Prof. Dr R. D. Kandou Hospital Manado from July 2013 to June 2014. This was a descriptive retrospective study. In this study, there were 162 patients with stroke who met the inclusion criteria. There were 74 male patients and 88 female patients. Most patients were 55-65 years, had high school education, and were housewives. Most systolic blood pressures were at grade 3 and diastolic hypertension at grade 2. Based on types of stroke, most patients had ischemic stroke.Keywords: gender, age, education, occupation, blood pressure, type of strokeAbstrak: Stroke adalah suatu penyakit defisit neurologis akut yang disebabkan oleh gangguan pembuluh darah otak yang terjadi secara mendadak dan menimbulkan gejala dan tanda yang sesuai dengan daerah otak yang terganggu. Tekanan darah tinggi atau yang dikenal dengan hipertensi merupakan salah satu faktor resiko utama, baik untuk stroke hemoragik maupun stroke iskemik. Hipertensi dapat mengakibatkan pecahnya maupun penyempitan pembuluh darah otak. Penelitian ini bertujuan untuk mengetahui profil penderita stroke dengan hipertensi di Bagian Rawat Inap Neurologi RSUP Prof. Dr. R. D. Kandou Manado periode Juli 2013 – Juni 2014. Penelitian ini menggunakan metode retrospektik deskriptif dengan 162 pasien stroke yang memenuhi kriteria inklusi. Pasien stroke berjenis kelamin laki – laki sebanyak 74 dan perempuan 88 orang. Sebagian besar pasien stroke berusia 55 – 65 tahun, pendidikan SMA dan pekerjaan terbanyak ialah ibu rumah tangga. Berdasarkan tekanan sistolik, sebagian besar dengan hipertensi derajat 3 sedangkan berdasarkan tekanan diastolik yaitu hipertensi derajat 2. Berdasarkan jenis stroke terbanyak ialah stroke iskemik.Kata kunci: jenis kelamin, umur, pendidikan, pekerjaan, tekanan darah, jenis stroke

scholarly journals SAT-605 Characterization of Dual Projection Patterns of Refeeding-Activated Neurons in the Parasubthalamic Nucleus

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Gabor Wittmann ◽  
Nicholas Cosentino ◽  
Ronald M Lechan
Keyword(s):  
Food Intake ◽  
Nucleus Tractus Solitarius ◽  
Brain Regions ◽  
Central Nucleus ◽  
Free Access ◽  
Target Area ◽  
Sprague Dawley ◽  
Bed Nucleus ◽  
Alexa Fluor ◽  
The Brain

Abstract We have observed that following a fast, animals terminate their food intake within 2h after refeeding accompanied by a pattern of neuronal activation as identified by c-fos immunostaining that involves a number of brain regions associated with the regulation of food intake including the nucleus tractus solitarius (NTS), parabrachial nucleus (PBN), central nucleus of the amygdala (CEA), hypothalamic arcuate and paraventricular nuclei, and bed nucleus of the stria terminalis. We also observed striking c-fos activation in the posterior-lateral hypothalamus called the parasubthalamic nucleus or PSTN, raising the possibility that it may also be an important anorectic center in the brain. To establish how the PSTN is integrated into the CNS, we performed dual-label retrograde tract tracing studies to characterize whether refeeding-activated PSTN neurons project to one, or more than one target area in the CNS. Adult, Sprague-Dawley rats received dual stereotaxic injections of Alexa Fluor 488- and Alexa Fluor 555-conjugated cholera toxin β subunit (CTB; 0.1%, 0.5–1 µl volume) into the 1) PBN and NTS, 2) PBN and CEA and 3) NTS and CEA. After 7–12 days, the animals were fasted for 24 h and then given free access to food for 2 h before euthanasia by transcardial perfusion with 4% paraformaldehyde. Brains with successful dual injections were further processed for c-fos immunohistochemistry. The results showed that 26.5±3.8% of PSTN neurons projecting to the PBN also project to the CEA, and 34.6±7.6% of PSTN neurons that project to the CEA also project to the PBN. In addition, 20.2±2.7% of PSTN neurons that project to the PBN also project to the NTS, and 38.1±9.7% of PSTN neurons that project to the NTS also project to the PBN. Furthermore, 35.0±12.5% of PSTN neurons that project to the CEA project to the NTS and 37.1±4.0% of PSTN neurons that project to the NTS project to the CEA. Finally, up to 15% of the neurons with dual projections to the PBN and CEA contained c-fos after refeeding; up to 18% of the neurons with dual projections to the PBN and NTS contained c-fos; and up to 30% of neurons with dual projections to the NTS and CEA contained c-fos. We conclude that a large number of PSTN neurons have more than one projection site within the brain, thus the PSTN appears to have the capability of simultaneously communicating information about appetite to several, major feeding-related sites within the brain, presumably to terminate feeding.

Cardiovascular actions of microinjections of angiotensin II in the brain stem of rats

1984 ◽  
Vol 246 (5) ◽  
pp. R811-R816 ◽  
Author(s):  
R. Casto ◽  
M. I. Phillips
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Brain Stem ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Ang Ii ◽  
The Brain

The blood pressure and heart rate responses to microinjection of angiotensin II (ANG II) into the brain stem of urethan-anesthetized rats were studied. Microinjection of ANG II into the area postrema (AP) resulted in significant elevation of blood pressure and significant reduction of heart rate. Microinjection into the region of the nucleus tractus solitarius (NTS) yielded a significant dose-dependent elevation in blood pressure and consistent increases in heart rate. The response to microinjection of ANG II into the region of the NTS was not due to leakage into the peripheral circulation, since intravenous administration of the ANG II antagonist, saralasin, did not attenuate the response. In fact, the cardiovascular response was increased after peripheral ANG II blockade, and the heart rate, which was consistently but not significantly elevated by NTS injection alone, was significantly elevated after saralasin pretreatment. Thermal ablation of the AP did not change the heart rate or the pressor response to microinjection of ANG II into the region of the NTS, indicating that the response was not mediated through the AP.

scholarly journals Brain Region-Dependent Effects of Neuropeptide Y on Conditioned Social Fear and Anxiety-Like Behavior in Male Mice

2021 ◽  
Vol 22 (7) ◽  
pp. 3695
Author(s):  
Johannes Kornhuber ◽  
Iulia Zoicas
Keyword(s):  
Neuropeptide Y ◽  
Brain Region ◽  
Basolateral Amygdala ◽  
Dorsal Hippocampus ◽  
Brain Regions ◽  
Dependent Manner ◽  
Contextual Fear ◽  
Social Fear ◽  
Fear And Anxiety ◽  
The Brain

Neuropeptide Y (NPY) has anxiolytic-like effects and facilitates the extinction of cued and contextual fear in rodents. We have previously shown that the intracerebroventricular administration of NPY reduces the expression of social fear in a mouse model of social fear conditioning (SFC). In the present study, we aimed to identify the brain regions that mediate these effects of NPY. We show that NPY (0.1 nmol/0.2 µL/side) reduces the expression of SFC-induced social fear in a brain-region-dependent manner. In more detail, NPY reduced the expression of social fear when administered into the dorsolateral septum (DLS) and central amygdala (CeA), but not when administered into the dorsal hippocampus (DH), medial amygdala (MeA) and basolateral amygdala (BLA). We also investigated whether the reduced expression of social fear might partly be due to a reduced anxiety-like behavior, and showed that NPY exerted anxiolytic-like effects when administered into the DH, DLS, CeA and BLA, but not when administered into the MeA. This study identifies the DLS and the CeA as brain regions mediating the effects of NPY on the expression of social fear and suggests that partly distinct neural circuitries mediate the effects of NPY on the expression of social fear and on anxiety-like behavior.

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