Collecting duct renin regulates potassium homeostasis in mice.

Aim: The kaliuretic action of the renin-angiotensin-aldosterone system (RAAS) is well established as highlighted by hyperkalemia side effect of RAAS inhibitors but such action is usually ascribed to systemic RAAS. The present study addresses the involvement of intrarenal RAAS in K homeostasis with emphasis on locally generated renin within the collecting duct (CD).

Methods: Wild-type (Floxed) and CD-specific deletion of renin (CD renin KO) mice were treated for 7 days with a high K (HK) diet to investigate the role of CD renin in kaliuresis regulation and further define the underlying mechanism with emphasis on analysis of intrarenal aldosterone biosynthesis.

Mutagenesis of the Cleavage Site of Pro Renin Receptor Abrogates Angiotensin II-Induced Hypertension in Mice.

[Figure: see text].

Soluble (pro)renin receptor induces endothelial dysfunction and hypertension in mice with diet-induced obesity via activation of angiotensin II type 1 receptor.

Until now, renin-angiotensin system (RAS) hyperactivity was largely thought to result from angiotensin II (Ang II)-dependent stimulation of the Ang II type 1 receptor (AT1R). Here we assessed the role of soluble (pro)renin receptor (sPRR), a product of site-1 protease-mediated cleavage of (pro)renin receptor (PRR), as a possible ligand of the AT1R in mediating: (i) endothelial cell dysfunction in vitro and (ii) arterial dysfunction in mice with diet-induced obesity. Primary human umbilical vein endothelial cells (HUVECs) treated with a recombinant histidine-tagged sPRR (sPRR-His) exhibited IκBα degradation concurrent with NF-κB p65 activation.

Soluble (pro)renin receptor treats metabolic syndrome in mice with diet-induced obesity via interaction with PPARγ.

The therapies available for management of obesity and associated conditions are limited, because they are often directed toward an individual component of metabolic syndrome and are associated with adverse effects. Here, we report the multifaceted therapeutic potential of histidine-tagged recombinant soluble (pro)renin receptor (sPRR), termed sPRR-His, in a mouse model of diet-induced obesity (DIO). In the DIO model, 2-week administration of sPRR-His lowered body weight and remarkably improved multiple metabolic parameters in the absence of fluid retention.

(Pro)renin receptor mediates albumin-induced cellular responses: role of site-1 protease-derived soluble (pro)renin receptor in renal epithelial cells.

Proteinuria is a characteristic of chronic kidney disease and also a causative factor that promotes the disease progression, in part, via activation of the intrarenal renin-angiotensin system (RAS). (Pro)renin receptor (PRR), a newly discovered component of the RAS, binds renin and (pro)renin to promote angiotensin I generation. The present study was performed to test the role of soluble PRR (sPRR) in albumin overload-induced responses in cultured human renal proximal tubular cell line human kidney 2 (HK-2) cells.

Delayed administration IL-1β neutralizing antibody improves cognitive function after transient global ischemia in rats.

In order to study the protective effects on motor and cognitive function by inhibiting IL-1β as delayed as 24h after global ischemia, we designed behavioral testing protocol and histology detection after 10 min transient global ischemia followed by IL-1β or its antibody intracerebroventricular injection. We found benefit of IL-1β antibody treatment 24h after ischemia in cognitive function recovery. But no obvious amelioration in motor function was found.

Retinal pigment epithelium development, plasticity, and tissue homeostasis.

The retinal pigment epithelium (RPE) is a simple epithelium interposed between the neural retina and the choroid. Although only 1 cell-layer in thickness, the RPE is a virtual workhorse, acting in several capacities that are essential for visual function and preserving the structural and physiological integrities of neighboring tissues. Defects in RPE function, whether through chronic dysfunction or age-related decline, are associated with retinal degenerative diseases including age-related macular degeneration.

[Central interleukin-1beta involved in modulation of motor behavior in novelty stress rats].

Objective: To investigate the effect of central interleukin-1beta (IL-1beta) on motor behavioral responses in novelty stress rats.

Methods: The novelty stress was elicited by novel environmental stimuli with novelty stress box. The intracerebrolventricular (ICV) cannula and microinjection were performed with rat brain stereotaxic system.

p38 MAPK mediates cardiovascular and behavioral responses induced by central IL-1 beta and footshock in conscious rats.

Aim: To investigate the roles of p38 mitogen-activated protein kinase (p38 MAPK) in the cardiovascular and behavioral responses induced by intracerebral ventricular injection (i.c.v.

Cardiovascular effects of urotensin II in different brain areas.

It has been shown that intracerebroventricular injection of urotensin II (UII)-induced hypotensive and bradycardiac responses. Here, we tested the cardiovascular roles of UII in different brain areas by microinjection of UII into the A1 and A2 areas (noradrenergic cells found in the lower part of the medulla that have been designated either A1 or A2 areas), the paraventricular and the arcuate nucleus. In urethane-anaesthetized rats, we observed that: (1) microinjection of UII into the A1 area induced dose-related depressor and bradycardiac responses; (2) mean arterial blood pressure (mABP) and heart rate (HR) did not change significantly after microinjection of UII into the A2 area; and (3) significant increases in mABP and HR were induced after microinjection of 10 pmol UII into either the paraventricular or arcuate nucleus.

Interleukin-1 beta is involved in the pressor response of amygdaloid neurons excited by sodium glutamate.

The effects of interleukin-1beta in the paraventricular nucleus or caudal arcuate nucleus on hypertensive and tachycardiac responses induced by excitation of the central amygdaloid nucleus were studied. We observed that microinjection of sodium glutamate into central amygdaloid nucleus resulted in hypertension and tachycardia. Microinjection of interleukin-1beta into paraventricular nucleus or caudal arcuate nucleus induced significant pressor and tachycardiac responses while pretreatment with microinjection of rabbit anti-rat interleukin-1beta antibody into bilateral paraventricular nuclei or arcuate nuclei attenuated the hypertensive response induced by microinjection of 40 nmol sodium glutamate into central amygdaloid nucleus.