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Tytuł pozycji:

Mechanisms Responsible for Genetic Hypertension in Schlager BPH/2 Mice.

Tytuł:
Mechanisms Responsible for Genetic Hypertension in Schlager BPH/2 Mice.
Autorzy:
Jackson KL; Neuropharmacology Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Head GA; Neuropharmacology Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Gueguen C; Neuropharmacology Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Stevenson ER; Neuropharmacology Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.
Lim K; Neuropharmacology Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.; Department of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Melbourne, VIC, Australia.
Marques FZ; Neuropharmacology Laboratory, Baker Heart and Diabetes Institute, Melbourne, VIC, Australia.; Hypertension Research Laboratory, School of Biological Sciences, Monash University, Clayton, VIC, Australia.
Źródło:
Frontiers in physiology [Front Physiol] 2019 Oct 18; Vol. 10, pp. 1311. Date of Electronic Publication: 2019 Oct 18 (Print Publication: 2019).
Typ publikacji:
Journal Article; Review
Język:
English
Imprint Name(s):
Original Publication: Lausanne : Frontiers Research Foundation
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Contributed Indexing:
Keywords: GABA receptor A; Schlager mice; allopregnanolone; amygdala; hypothalamus; neurogenic hypertension; orexin; sympathetic nervous system
Entry Date(s):
Date Created: 20191105 Latest Revision: 20200930
Update Code:
20240104
PubMed Central ID:
PMC6813185
DOI:
10.3389/fphys.2019.01311
PMID:
31681017
Czasopismo naukowe
It has been 45 years since Gunther Schlager used a cross breeding program in mice to develop inbred strains with high, normal, and low blood pressure (BPH/2, BPN/3, and BPL/1 respectively). Thus, it is timely to gather together the studies that have characterized and explored the mechanisms associated with the hypertension to take stock of exactly what is known and what remains to be determined. Growing evidence supports the notion that the mechanism of hypertension in BPH/2 mice is predominantly neurogenic with some of the early studies showing aberrant brain noradrenaline levels in BPH/2 compared with BPN/3. Analysis of the adrenal gland using microarray suggested an association with the activity of the sympathetic nervous system. Indeed, in support of this, there is a larger depressor response to ganglion blockade, which reduced blood pressure in BPH/2 mice to the same level as BPN/3 mice. Greater renal tyrosine hydroxylase staining and greater renal noradrenaline levels in BPH/2 mice suggest sympathetic hyperinnervation of the kidney. Renal denervation markedly reduced the blood pressure in BPH/2 but not BPN/3 mice, confirming the importance of renal sympathetic nervous activity contributing to the hypertension. Further, there is an important contribution to the hypertension from miR-181a and renal renin in this strain. BPH/2 mice also display greater neuronal activity of amygdalo-hypothalamic cardiovascular regulatory regions. Lesions of the medial nucleus of the amygdala reduced the hypertension in BPH/2 mice and abolished the strain difference in the effect of ganglion blockade, suggesting a sympathetic mechanism. Further studies suggest that aberrant GABAergic inhibition may play a role since BPH/2 mice have low GABA A receptor δ, α4 and β2 subunit mRNA expression in the hypothalamus, which are predominantly involved in promoting tonic neuronal inhibition. Allopregnanolone, an allosteric modulator of GABA A receptors, which increase the expression of these subunits in the amygdala and hypothalamus, is shown to reduce the hypertension and sympathetic nervous system contribution in BPH/2 mice. Thus far, evidence suggests that BPH/2 mice have aberrant GABAergic inhibition, which drives neuronal overactivity within amygdalo-hypothalamic brain regions. This overactivity is responsible for the greater sympathetic contribution to the hypertension in BPH/2 mice, thus making this an ideal model of neurogenic hypertension.
(Copyright © 2019 Jackson, Head, Gueguen, Stevenson, Lim and Marques.)

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