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10.33549/PHYSIOLRES.934334

In 2011 Fujita and coworkers proposed that beta-adrenergic stimulation causes decreased serine/threonine-protein kinase WNK4 transcription leading to the activation of Na-Cl cotransporter (NCC) which participates in salt sensitivity and salt hypertension development in rodents.

Is renal beta-adrenergic-WNK4-NCC pathway important in salt hypertension of dahl rats?

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10.1111/jcmm.14863

In this study, we generated ribosomal‐depleted RNA sequencing data from normal mouse kidneys and from injured mouse kidneys induced by deoxycorticosterone acetate‐salt hypertension and identified at least 4900 circRNA candidates.

CircNr1h4 regulates the pathological process of renal injury in salt‐sensitive hypertensive mice by targeting miR‐155‐5p

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10.1016/j.phrs.2019.01.012

In deoxycorticosterone acetate (DOCA)‐salt hypertension mice, chronic injection of FR (0.

Anti‐hypertensive mechanisms of cyclic depsipeptide inhibitor ligands for Gq/11 class G proteins

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10.1152/ajpheart.00063.2019

Together, these results support that activation of PRR contributes to increased excitability and firing discharge of MNNs and increased plasma levels of VP in DOCA-salt hypertension.

EXACERBATED EFFECTS OF PRORENIN ON HYPOTHALAMIC MAGNOCELLULAR NEURONAL ACTIVITY AND VASOPRESSIN PLASMA LEVELS DURING SALT-SENSITIVE HYPERTENSION.

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10.1038/s41598-019-52808-z

Abcc6 loss-of-function is associated with greater cardiovascular calcification and fibrosis in mice subjected to DOCA-Salt hypertension.

Evidence of Cardiovascular Calcification and Fibrosis in Pseudoxanthoma Elasticum Mouse Models Subjected to DOCA-Salt Hypertension

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10.1152/ajpheart.00780.2018

NEW & NOTEWORTHY PRR knockdown in PVN neurons attenuates the development of DOCA-salt hypertension and autonomic dysfunction through a decrease in ERK1/2 activation in the PVN and RVLM during hypertension.

(Pro)renin receptor knockdown in the paraventricular nucleus of the hypothalamus attenuates hypertension development and AT1 receptor-mediated calcium events.

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10.1161/HYPERTENSIONAHA.119.13175

In a different set of 14-day Ang II-salt-treated rats, mini-osmotic pumps were used to infuse either a nonselective COX (cyclooxygenase) inhibitor ketorolac, L-PGDS inhibitor AT56, or DP1R inhibitor BWA868C to test the role of brain COX-PGD2-DP1R signaling in Ang II-salt hypertension.

Brain Prostaglandin D2 Increases Neurogenic Pressor Activity and Mean Arterial Pressure in Angiotensin II-Salt Hypertensive Rats.

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10.1038/s41440-019-0239-1

DOCA-salt hypertension was induced by DOCA (20 mg/kg s.

Reversal of cardiac, vascular, and renal dysfunction by non-quinazoline α1-adrenolytics in DOCA-salt hypertensive rats: a comparison with prazosin, a quinazoline-based α1-adrenoceptor antagonist

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10.1039/c8fo01818a

In the present study, the renal-protective effect of hawthorn fruit extract (HW) on high-salt hypertension and its effect on metabolic patterns are determined.

The protective role of hawthorn fruit extract against high salt-induced hypertension in Dahl salt-sensitive rats: impact on oxidative stress and metabolic patterns.

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10.1124/jpet.119.258954

KO of Dusp5 enhanced the myogenic tone of the renal afferent arteriole and interlobular artery in vitro with or without induction of deoxycorticosterone acetate-salt hypertension.

Knockout of Dual-Specificity Protein Phosphatase 5 Protects Against Hypertension-Induced Renal Injury

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10.1161/STROKEAHA.118.023928

Methods— Aneurysms were induced by a single stereotaxic injection of elastase into the cerebrospinal fluid at the skull base, combined with systemic deoxycorticosterone-salt hypertension, without or with high-salt diet, for mild or severe outcomes, respectively.

Noninvasive Vagus Nerve Stimulation Prevents Ruptures and Improves Outcomes in a Model of Intracranial Aneurysm in Mice

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10.14739/2310-1237.2019.1.166145

The aim of our study was to establish the morphodensitometric features of locus coeruleus (LC) neurons nuclei in the brain stem of rats with arterial hypertension of various origin (essential – SHR and endocrine-salt hypertension (ESH)).

Морфоденситометричні характеристики ядер нейронів блакитної плями стовбура мозку щурів при експериментальній артеріальній гіпертензії

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Salt Hypertension - In 2011 Fujita and coworkers proposed that beta-adrenergic stimulation causes decreased serine/threonine-protein kinase WNK4 transcription leading to the activation of Na-Cl cotransporter (NCC) which participates in salt sensitivity and salt hypertension development in rodents. [1] In this study, we generated ribosomal‐depleted RNA sequencing data from normal mouse kidneys and from injured mouse kidneys induced by deoxycorticosterone acetate‐salt hypertension and identified at least 4900 circRNA candidates. [2] In deoxycorticosterone acetate (DOCA)‐salt hypertension mice, chronic injection of FR (0. [3] Together, these results support that activation of PRR contributes to increased excitability and firing discharge of MNNs and increased plasma levels of VP in DOCA-salt hypertension. [4] Abcc6 loss-of-function is associated with greater cardiovascular calcification and fibrosis in mice subjected to DOCA-Salt hypertension. [5] NEW & NOTEWORTHY PRR knockdown in PVN neurons attenuates the development of DOCA-salt hypertension and autonomic dysfunction through a decrease in ERK1/2 activation in the PVN and RVLM during hypertension. [6] In a different set of 14-day Ang II-salt-treated rats, mini-osmotic pumps were used to infuse either a nonselective COX (cyclooxygenase) inhibitor ketorolac, L-PGDS inhibitor AT56, or DP1R inhibitor BWA868C to test the role of brain COX-PGD2-DP1R signaling in Ang II-salt hypertension. [7] DOCA-salt hypertension was induced by DOCA (20 mg/kg s. [8] In the present study, the renal-protective effect of hawthorn fruit extract (HW) on high-salt hypertension and its effect on metabolic patterns are determined. [9] KO of Dusp5 enhanced the myogenic tone of the renal afferent arteriole and interlobular artery in vitro with or without induction of deoxycorticosterone acetate-salt hypertension. [10] Methods— Aneurysms were induced by a single stereotaxic injection of elastase into the cerebrospinal fluid at the skull base, combined with systemic deoxycorticosterone-salt hypertension, without or with high-salt diet, for mild or severe outcomes, respectively. [11] The aim of our study was to establish the morphodensitometric features of locus coeruleus (LC) neurons nuclei in the brain stem of rats with arterial hypertension of various origin (essential – SHR and endocrine-salt hypertension (ESH)). [12]