FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2890872081> ?p ?o ?g. }

• W2890872081 endingPage "6248" @default.
• W2890872081 startingPage "6235" @default.
• W2890872081 abstract "Recurrent periods of over-excitation in the paraventricular nucleus (PVN) of the hypothalamus could contribute to chronic over-activation of this nucleus and thus enhanced sympathetic drive. Stimulation of the PVN glutamatergic population utilizing channelrhodopsin-2 leads to an immediate frequency-dependent increase in baseline blood pressure. Partial lesions of glutamatergic neurons of the PVN (39.3%) result in an attenuated rise in blood pressure following Deoxycorticosterone acetate (DOCA)-salt treatment and reduced index of sympathetic activity. These data suggest that stimulation of PVN glutamatergic neurons is sufficient to cause autonomic dysfunction and drive the increase in blood pressure during hypertension.Neuro-cardiovascular dysregulation leads to increased sympathetic activity and neurogenic hypertension. The paraventricular nucleus (PVN) of the hypothalamus is a key hub for blood pressure (BP) control, producing or relaying the increased sympathetic tone in hypertension. We hypothesize that increased central sympathetic drive is caused by chronic over-excitation of glutamatergic PVN neurons. We tested how stimulation or lesioning of excitatory PVN neurons in conscious mice affects BP, baroreflex and sympathetic activity. Glutamatergic PVN neurons were unilaterally transduced with channelrhodopsin-2 using an adeno-associated virus (CamKII-ChR2-eYFP-AAV2) in wildtype mice (n = 7) to assess the impact of acute stimulation of excitatory PVN neurons selectively on resting BP in conscious mice. Stimulation of the PVN glutamatergic population resulted in an immediate frequency-dependent (2, 10 and 20 Hz) increase in BP from baseline by ∼9 mmHg at 20 Hz stimulation (P < 0.001). Additionally, in vGlut2-cre mice glutamatergic neurons of the PVN were bilaterally lesioned utilizing a cre-dependent caspase (AAV2-flex-taCASP3-TEVp). Resting BP and urinary noradrenaline (norepinephrine) levels were then recorded in conscious mice before and after DOCA-salt hypertension. Partial lesions of glutamatergic neurons of the PVN (39.3%, P < 0.05) resulted in an attenuated rise in BP following DOCA-salt treatment (P < 0.05 at 7 day time point, n = 8). Noradrenaline levels as an index of sympathetic activity between the lesion and wildtype groups showed a significant reduction after DOCA-salt treatment in the lesioned animals (P < 0.05). These experiments suggest that stimulation of PVN glutamatergic neurons is sufficient to cause autonomic dysfunction and drive the increase in BP." @default.
• W2890872081 created "2018-09-27" @default.
• W2890872081 creator A5035088257 @default.
• W2890872081 creator A5039018435 @default.
• W2890872081 creator A5040698154 @default.
• W2890872081 creator A5041333361 @default.
• W2890872081 creator A5049981072 @default.
• W2890872081 creator A5050387959 @default.
• W2890872081 creator A5072754212 @default.
• W2890872081 date "2018-09-20" @default.
• W2890872081 modified "2023-10-12" @default.
• W2890872081 title "Glutamatergic neurons of the paraventricular nucleus are critical contributors to the development of neurogenic hypertension" @default.
• W2890872081 cites W1562584139 @default.
• W2890872081 cites W1966409424 @default.
• W2890872081 cites W1970839656 @default.
• W2890872081 cites W1973599240 @default.
• W2890872081 cites W1974379519 @default.
• W2890872081 cites W1988771705 @default.
• W2890872081 cites W1992425723 @default.
• W2890872081 cites W2008219323 @default.
• W2890872081 cites W2009608137 @default.
• W2890872081 cites W2015104765 @default.
• W2890872081 cites W2017802065 @default.
• W2890872081 cites W2026049925 @default.
• W2890872081 cites W2029668809 @default.
• W2890872081 cites W2033133965 @default.
• W2890872081 cites W2039408689 @default.
• W2890872081 cites W2039482567 @default.
• W2890872081 cites W2052742427 @default.
• W2890872081 cites W2057913521 @default.
• W2890872081 cites W2058068599 @default.
• W2890872081 cites W2061072142 @default.
• W2890872081 cites W2079578502 @default.
• W2890872081 cites W2082523159 @default.
• W2890872081 cites W2088672561 @default.
• W2890872081 cites W2089652976 @default.
• W2890872081 cites W2091666749 @default.
• W2890872081 cites W2100762371 @default.
• W2890872081 cites W2103921111 @default.
• W2890872081 cites W2109011905 @default.
• W2890872081 cites W2111678533 @default.
• W2890872081 cites W2118121453 @default.
• W2890872081 cites W2121887640 @default.
• W2890872081 cites W2122782518 @default.
• W2890872081 cites W2128246009 @default.
• W2890872081 cites W2132670847 @default.
• W2890872081 cites W2138926810 @default.
• W2890872081 cites W2139368311 @default.
• W2890872081 cites W2145522884 @default.
• W2890872081 cites W2146868259 @default.
• W2890872081 cites W2153842331 @default.
• W2890872081 cites W2162260301 @default.
• W2890872081 cites W2162699802 @default.
• W2890872081 cites W2164385322 @default.
• W2890872081 cites W2228536968 @default.
• W2890872081 cites W2520827615 @default.
• W2890872081 cites W2598403127 @default.
• W2890872081 cites W2600107558 @default.
• W2890872081 cites W2737890831 @default.
• W2890872081 cites W2755782582 @default.
• W2890872081 cites W2793514054 @default.
• W2890872081 cites W4235269668 @default.
• W2890872081 cites W4244742774 @default.
• W2890872081 doi "https://doi.org/10.1113/jp276229" @default.
• W2890872081 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6292814" @default.
• W2890872081 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30151830" @default.
• W2890872081 hasPublicationYear "2018" @default.
• W2890872081 type Work @default.
• W2890872081 sameAs 2890872081 @default.
• W2890872081 citedByCount "38" @default.
• W2890872081 countsByYear W28908720812018 @default.
• W2890872081 countsByYear W28908720812019 @default.
• W2890872081 countsByYear W28908720812020 @default.
• W2890872081 countsByYear W28908720812021 @default.
• W2890872081 countsByYear W28908720812022 @default.
• W2890872081 countsByYear W28908720812023 @default.
• W2890872081 crossrefType "journal-article" @default.
• W2890872081 hasAuthorship W2890872081A5035088257 @default.
• W2890872081 hasAuthorship W2890872081A5039018435 @default.
• W2890872081 hasAuthorship W2890872081A5040698154 @default.
• W2890872081 hasAuthorship W2890872081A5041333361 @default.
• W2890872081 hasAuthorship W2890872081A5049981072 @default.
• W2890872081 hasAuthorship W2890872081A5050387959 @default.
• W2890872081 hasAuthorship W2890872081A5072754212 @default.
• W2890872081 hasBestOaLocation W28908720811 @default.
• W2890872081 hasConcept C112592302 @default.
• W2890872081 hasConcept C126322002 @default.
• W2890872081 hasConcept C134018914 @default.
• W2890872081 hasConcept C169760540 @default.
• W2890872081 hasConcept C170493617 @default.
• W2890872081 hasConcept C191237925 @default.
• W2890872081 hasConcept C24998067 @default.
• W2890872081 hasConcept C2777003273 @default.
• W2890872081 hasConcept C2777953023 @default.
• W2890872081 hasConcept C2780648746 @default.
• W2890872081 hasConcept C2908647359 @default.
• W2890872081 hasConcept C61174792 @default.
• W2890872081 hasConcept C71924100 @default.

• next