Peripheral Receptor Targets for Analgesia

2009 ◽  
Keyword(s):  
Receptor Targets ◽  
Peripheral Receptor

Apolipoprotein E Is Upregulated in Olfactory Bulb Glia Following Peripheral Receptor Lesion in Mice

2001 ◽  
Vol 172 (1) ◽  
pp. 128-136 ◽  
Author(s):  
Britto P. Nathan ◽  
Rafia Nisar ◽  
Shari Randall ◽  
Jody Short ◽  
Michael Sherrow ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Apolipoprotein E ◽  
Peripheral Receptor

Abstract 103: Soluble (Pro)Renin Receptor Targets Renal V2 Vasopressin Receptor to Enhance Urine Concentrating Capability

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Fei Wang ◽  
Nirupama Ramkumar ◽  
Kexin Peng ◽  
Xiaohan Lu ◽  
Long Zhao ◽  
...  
Keyword(s):  
Biological Fluid ◽  
Collecting Duct ◽  
Urine Volume ◽  
Neutralizing Antibody ◽  
Fold Increase ◽  
Medium Level ◽  
V2 Vasopressin Receptor ◽  
Receptor Targets ◽  
Renal Expression

The extracellular domain of (pro)renin receptor (PRR) is cleaved to produce a 28 kDa soluble receptor (sPRR) which is detected in biological fluid and elevated under certain pathological conditions. Our recent work suggests that sPRR derived from collecting duct intercalated cells acts in a paracrine fashion to regulate water transport in the principal cells. The present study attempted to further define the role of sPRR in vasopressin (AVP) signaling with emphasis on V2R regulation. In primary rat IMCD cells, treatment with a recombinant sPRR termed as sPRR-His at 10 nM for 12 h induced a 2.8 -fold increase in V2R protein and a 2-fold increase in V2R mRNA. Following AVP treatment, V2R protein expression was increased by 3-fold, which was blunted by a PRR antagonist (PRO20) and a PRR neutralizing antibody. Mice with CD-specific (CD PRR KO) developed a medium level of diabetes insipidus (urine volume: KO: 2.2±0.4 versus Floxed: 1.2±0.3 ml/day; P <0.05), accompanied with a 60% reduction of renal V2R protein and a 25% reduction of urinary sPRR excretion. Adminstration of sPRR-His at for 3 d almost completely rescued the polyuria phenotype of CD PRR KO mice (urine volume: KO+sPRR-His: 1.6±0.3 vs. KO: 2.4±0.5 ml/day, p <0.05) associated with restoration of renal V2R protein and AQP2 protein abundances. Interestingly, nephron-specific PRR KO (Neph PRR KO) exhibited more robust polyuria (urine volume: KO: 7.3±1.1 vs. Floxed: 1.2±0.5 ml/day, p <0.01) associated with suppressed renal expression of AQP2, NKCC2, and V2R. Administration of sPRR-His to Neph PRR KO mice partially attenuated polyuria (urine volume: KO+sPRR-His: 4.1±1.2 vs. KO: 7.3±1.1 ml/day, p <0.01) accompanied by restored renal expression of V2R and AQP2, as well as AVP sensitivity. In contrast, the downregulation of NKCC2 expression in the null mice was unaffected by sPRR-His infusion nor was the upregulation of autophagosome marker microtubule-associated protein 1A/1B-light chain 3 (LC3b). Together, our data suggests that sPRR selectively targets the CD to determine V2R expression and hence AVP sensitivity and urine concentrating capability, independently of autophagosome accumulation.

scholarly journals Site-1 protease–derived soluble (pro)renin receptor targets vasopressin receptor 2 to enhance urine concentrating capability

JCI Insight ◽  
2019 ◽  
Vol 4 (7) ◽  
Author(s):  
Fei Wang ◽  
Chuanming Xu ◽  
Renfei Luo ◽  
Kexin Peng ◽  
Nirupama Ramkumar ◽  
...  
Keyword(s):  
Vasopressin Receptor ◽  
Receptor Targets

Effect of volume expansion and veratrine on salt gland secretion in the goose

1977 ◽  
Vol 232 (5) ◽  
pp. R185-R189
Author(s):  
I. H. Zucker ◽  
C. Gilmore ◽  
J. Dietz ◽  
J. P. Gilmore
Keyword(s):  
Volume Expansion ◽  
Plasma Osmolality ◽  
Salt Gland ◽  
Sodium Concentration ◽  
Ringer Solution ◽  
Gland Secretion ◽  
Similar Increase ◽  
Volume Load ◽  
Salt Gland Secretion ◽  
Peripheral Receptor

The influence of acute intravascular volume expansion on salt gland secretion of conscious, adult geese was investigated. The intravenous administration of 5% dextran in Krebs-bicarbonate-Ringer solution in an amount equivalent to 30% of the estimated blood volume caused a transient but highly significant increase in salt gland secretion independent of changes in plasma osmolality or sodium concentration. Intravenous veratrine (60 microng) caused a similar increase in salt gland secretion only when administered after the volume load. Intravenous 5% NaCl always caused a prolonged and significant increase in salt gland secretion which was not potentiated by veratrine. Volume expansion and hypertonic saline caused a significant tachycardia while veratrine caused a significant bradycardia. It is concluded that a volume component may contribute to the initiation of salt gland secretion in the goose and that the peripheral receptor involved is most likely vascular in origin.

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