Increased vasopressin transmission from the paraventricular nucleus to the rostral medulla augments cardiorespiratory outflow in chronic intermittent hypoxia-conditioned rats.
about
Neural Control of Blood Pressure in Chronic Intermittent HypoxiaMaternal defense is modulated by beta adrenergic receptors in lateral septum in miceAngiotensin converting enzyme 1 in the median preoptic nucleus contributes to chronic intermittent hypoxia hypertension.Chronic intermittent hypoxia and hypercapnia inhibit the hypothalamic paraventricular nucleus neurotransmission to parasympathetic cardiac neurons in the brain stem.Modulation of cardiorespiratory function mediated by the paraventricular nucleus.Visualization of oxytocin release that mediates paired pulse facilitation in hypothalamic pathways to brainstem autonomic neurons.Central role of carotid body chemoreceptors in disordered breathing and cardiorenal dysfunction in chronic heart failure.Chronic intermittent hypoxia increases blood pressure and expression of FosB/DeltaFosB in central autonomic regions.Activation of the hypothalamic paraventricular nucleus by forebrain hypertonicity selectively increases tonic vasomotor sympathetic nerve activity.Novel mechanism within the paraventricular nucleus reduces both blood pressure and hypothalamic pituitary-adrenal axis responses to acute stress.An Essential role for DeltaFosB in the median preoptic nucleus in the sustained hypertensive effects of chronic intermittent hypoxiaNeurogenic mechanisms underlying the rapid onset of sympathetic responses to intermittent hypoxia.Effect of postnatal intermittent hypoxia on growth and cardiovascular regulation of rat pups.Membrane trafficking of NADPH oxidase p47(phox) in paraventricular hypothalamic neurons parallels local free radical production in angiotensin II slow-pressor hypertensionVasopressin and oxytocin in control of the cardiovascular systemSympathetic network drive during water deprivation does not increase respiratory or cardiac rhythmic sympathetic nerve activityOxytocin neuron activation prevents hypertension that occurs with chronic intermittent hypoxia/hypercapnia in rats.Rats selectively bred for differences in aerobic capacity have similar hypertensive responses to chronic intermittent hypoxia.Knockdown of tyrosine hydroxylase in the nucleus of the solitary tract reduces elevated blood pressure during chronic intermittent hypoxia.Essential hypertension: an approach to its etiology and neurogenic pathophysiology.Chronic intermittent hypoxia increases sympathetic control of blood pressure: role of neuronal activity in the hypothalamic paraventricular nucleus.Coupling between respiratory and sympathetic activities as a novel mechanism underpinning neurogenic hypertension.Neuronal control of breathing: sex and stress hormones.Parasympathetic Vagal Control of Cardiac Function.Vasopressin V1a receptors mediate the hypertensive effects of [Pyr1 ]apelin-13 in the rat rostral ventrolateral medulla.In vivo bioluminescence imaging reveals redox-regulated activator protein-1 activation in paraventricular nucleus of mice with renovascular hypertension.Superoxide anions involved in sympathoexcitation and pressor effects of salusin-β in paraventricular nucleus in hypertensive rats.The Hypothalamic PVN Contributes to Acute Intermittent Hypoxia-Induced Sympathetic but not Phrenic Long-Term Facilitation.Role of angiotensin-converting enzyme 1 within the median preoptic nucleus following chronic intermittent hypoxia.Salusin-β in paraventricular nucleus increases blood pressure and sympathetic outflow via vasopressin in hypertensive rats.Chronic intermittent hypoxia-hypercapnia blunts heart rate responses and alters neurotransmission to cardiac vagal neurons.Optogenetic identification of hypothalamic orexin neuron projections to paraventricular spinally projecting neurons.Blood pressure is maintained during dehydration by hypothalamic paraventricular nucleus-driven tonic sympathetic nerve activity.Chronic intermittent hypoxia alters glutamatergic control of sympathetic and respiratory activities in the commissural NTS of rats.Carotid body denervation improves autonomic and cardiac function and attenuates disordered breathing in congestive heart failure.Dysregulation of the Renin-Angiotensin System and the Vasopressinergic System Interactions in Cardiovascular Disorders.Sympathoexcitation following intermittent hypoxia in rat is mediated by circulating angiotensin II acting at the carotid body and subfornical organBlockade of Rostral Ventrolateral Medulla Apelin Receptors Does Not Attenuate Arterial Pressure in SHR and -NAME-Induced Hypertensive Rats
P2860
Q28078657-56D932B7-4508-47E7-9F49-757279B2C638Q30466932-7D732E3E-5663-4E31-9A4C-89FE43D92132Q33740901-C969B7C4-42C7-4D49-86F4-FE4E15B3D4B9Q34051414-E16ED125-DF07-4811-87E0-E3C18FA5F84EQ34258985-C2EBD846-2DD1-4C1E-9D1C-3370AC2943A5Q34472905-F9E46E70-D514-4A6A-BA5D-728E987BD538Q34562968-655E8D7B-C92A-433F-8426-92A302D553FBQ35086929-BBC50B1D-011F-4AC6-9807-73F83A880C8CQ35138540-2BC68FB4-0F1C-4DD6-A2DE-1402C9E8B6E7Q35958646-A99C765C-0480-42B8-A5AA-57A6C3E191F3Q36152606-E1ED5BF1-6BC2-4C29-B19B-325BDB054354Q36382223-99E72205-3C95-4A74-831B-D4B512A6FB5FQ36390112-E31E5BC8-789C-4185-9454-C96D73AB940AQ36739777-5C1172DD-E78F-4242-999D-67DE86CF2123Q36798875-712CCC7E-13A4-4E8A-AE29-B057453CFBA7Q36924148-63BF1FAF-EA26-47B4-8E37-6949306A2B2FQ37071891-4A15F8FA-4184-4B50-949A-E4DCE34B3A8AQ37093696-97A47B2D-F5EA-4F48-A78B-059F941F393FQ37342330-365E70E9-4C1D-463A-8B72-2DDFBBEF5F37Q37412877-A5ACA586-6557-4CD7-A7EE-89A5C2D5944AQ37440591-4149721C-AC84-43E9-AFDC-199CF2EB2161Q37858914-24DA9A0C-57B8-49B0-881A-80874241476CQ38111735-2DA02AB7-5F48-4303-A274-A96AC3FDACD8Q38724274-06B41002-C7D4-41A6-AD5B-87966394D181Q38931663-40FA9AE0-53EC-44B7-8A1D-860BEF9F297DQ41881082-54F6DEBF-A6E1-4B6B-A324-073155C3241BQ44110037-38FDA189-DDDF-45AC-9DA2-CAEDE2318BB2Q47650944-A6BB3A1D-19A0-4E94-B029-663554955729Q47781593-98940E9F-5540-41D8-A100-230E3E993195Q48091184-C315E9FF-B8C1-45ED-8576-E97C88CB6D6AQ48106386-8FEE4AD4-8617-4107-B456-87350D407EADQ48325029-A28DCFB1-53E5-449B-A4E0-2B1111D12B8EQ48690718-A29DC92A-B352-43A4-9CC1-160ACD4453D9Q48743580-9F678CD4-6E2F-4E38-8D80-7129B0657B66Q54576764-D476092E-A479-4559-92B4-6B1157744B72Q55153307-9EF80A91-6F90-42E7-9E90-49A87851585AQ56379459-A371B1A4-889C-4778-A084-850C95CC1FA5Q59127752-5BC12FEC-5915-4C4E-9B23-F6E7412DE704
P2860
Increased vasopressin transmission from the paraventricular nucleus to the rostral medulla augments cardiorespiratory outflow in chronic intermittent hypoxia-conditioned rats.
description
2010 nî lūn-bûn
@nan
2010年の論文
@ja
2010年学术文章
@wuu
2010年学术文章
@zh
2010年学术文章
@zh-cn
2010年学术文章
@zh-hans
2010年学术文章
@zh-my
2010年学术文章
@zh-sg
2010年學術文章
@yue
2010年學術文章
@zh-hant
name
Increased vasopressin transmis ...... tent hypoxia-conditioned rats.
@en
Increased vasopressin transmis ...... tent hypoxia-conditioned rats.
@nl
type
label
Increased vasopressin transmis ...... tent hypoxia-conditioned rats.
@en
Increased vasopressin transmis ...... tent hypoxia-conditioned rats.
@nl
prefLabel
Increased vasopressin transmis ...... tent hypoxia-conditioned rats.
@en
Increased vasopressin transmis ...... tent hypoxia-conditioned rats.
@nl
P2093
P2860
P1476
Increased vasopressin transmis ...... tent hypoxia-conditioned rats.
@en
P2093
Joseph C Lamanna
Kannan V Balan
Musa A Haxhiu
Richard J Martin
Steven S Tjoe
Thomas E Dick
P2860
P304
P356
10.1113/JPHYSIOL.2009.184580
P407
P577
2010-01-05T00:00:00Z