Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
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Query: UNIPROT:P41181 (
collecting duct
)
5,183
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Recent studies revealed that angiotensin II (Ang II) interacts with two pharmacologically different subtypes of cell surface receptors. Type I Ang II (AT1) receptor is characterized by signal transduction mediated through G protein and phospholipase C. In this study, the micro-localization of mRNAs coding for AT1 receptor and angiotensinogen was carried out in the rat kidney, using an assay of reverse transcription and polymerase chain reaction (RT-PCR) in individual microdissected renal tubule segments along the nephron, glomeruli, vasa recta bundle, and arcuate arteries. Large signals for AT1 receptor were detected in the glomerulus, proximal convoluted tubule (PCT), proximal straight tubule (PST), cortical
collecting duct
, and vascular system. Small signals were also seen in medullary thick ascending limb, outer medullary
collecting duct
, and inner medullary
collecting duct
(IMCD).
Angiotensinogen
mRNA is expressed largely in PCT, PST, and a small amount in glomerulus and vasa recta. Our data demonstrate that Ang II could be produced locally in proximal tubule and vasa recta bundle, and that the AT1 receptor was widely distributed not only in the glomerulus and vessels but also in tubules from PCT to IMCD.
...
PMID:PCR localization of angiotensin II receptor and angiotensinogen mRNAs in rat kidney. 831 39
The presence of renin production by the principal cells of the
collecting duct
has opened new perspectives for the regulation of intrarenal angiotensin II (Ang II).
Angiotensinogen
(
AGT
) and angiotensin-converting enzyme (ACE) are present in the tubular fluid coming from the proximal tubule and
collecting duct
. All the components needed for Ang II formation are present along the nephron, and much is known about the mechanisms regulating renin in juxtaglomerular cells (JG); however, those in the
collecting duct
remain unclear. Ang II suppresses renin via protein kinase C (PKC) and calcium (Ca
2+
) in JG cells, but in the principal cells, Ang II increases renin synthesis and release through a pathophysiological mechanism that increases further intratubular Ang II de novo formation to enhance distal Na
+
reabsorption. Transgenic mice overexpressing renin in the
collecting duct
demonstrate the role of
collecting duct
renin in the development of hypertension. The story became even more interesting after the discovery of a specific receptor for renin and prorenin: the prorenin receptor ((P)RR), which enhances renin activity and fully activates prorenin. The interactions between (P)RR and prorenin/renin may further increase intratubular Ang II levels. In addition to Ang II, other mechanisms have been described in the regulation of renin in the
collecting duct
, including vasopressin (AVP), bradykinin (BK), and prostaglandins. Current active investigations are aimed at elucidating the mechanisms regulating renin in the distal nephron segments and understand its role in the pathogenesis of hypertension.
...
PMID:Role of Collecting Duct Renin in the Pathogenesis of Hypertension. 2869
