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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:dateCreated |
1984-9-24
|
| pubmed:abstractText |
Immunocytochemical techniques were used for the localization of the different components of the renin-angiotensin system (RAS) within the kidneys of various species. Special attention was paid to the renin-secreting granulated cells located mainly in the media of the afferent glomerular arteriole. It was demonstrated that variations of kidney renin caused by stimulation or inhibition of the RAS are reflected in changes of the length of the renin-positive part of the afferent arteriole upstream from its entry into the glomerulus. During stimulation, plain smooth-muscle cells are transformed into renin-generating granulated cells. Likewise, the marked species differences in kidney renin are paralleled by corresponding differences in the renin-positive part of the afferent vessel. In this context, the site of action and the relative importance of the stimuli inducing renin secretion, i.e., the beta 1-adrenoreceptor, the mechanoreceptor, and the so-called macula densa mechanism are discussed. Whereas the microtopography of the RAS in the kidney has been at least partly understood, little is known about the stimulus-secretion coupling at the level of the individual granulated cell. Thus, adequate electrophysiological data about granulated cells might help to understand some still obscure phenomena, e.g., the inhibitory effect of Ca2+ on renin secretion. Our investigations in the hydronephrotic kidney preparation of the mouse show that granulated cells do not differ significantly from "plain" smooth-muscle cells in their electrical characteristics. They have a membrane potential of -55 mV and are spontaneously active. Both cell types are depolarized by noradrenaline and angiotensin II (AII), although they remain unaffected by isoproterenol. Since isoproterenol is known to stimulate renin secretion, our results indicate that stimulus-secretion coupling via the beta 1-adrenoreceptor is likely to proceed without changes of membrane potential in granulated cells.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:issn |
0160-2446
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
6 Suppl 2
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
S383-93
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:6206347-Angiotensin I,
pubmed-meshheading:6206347-Angiotensin II,
pubmed-meshheading:6206347-Angiotensinogen,
pubmed-meshheading:6206347-Animals,
pubmed-meshheading:6206347-Arterioles,
pubmed-meshheading:6206347-Cricetinae,
pubmed-meshheading:6206347-Cricetulus,
pubmed-meshheading:6206347-Electrophysiology,
pubmed-meshheading:6206347-Guinea Pigs,
pubmed-meshheading:6206347-Histocytochemistry,
pubmed-meshheading:6206347-Immunochemistry,
pubmed-meshheading:6206347-Kidney Glomerulus,
pubmed-meshheading:6206347-Mice,
pubmed-meshheading:6206347-Rats,
pubmed-meshheading:6206347-Rats, Inbred Strains,
pubmed-meshheading:6206347-Renal Circulation,
pubmed-meshheading:6206347-Renin,
pubmed-meshheading:6206347-Swine
|
| pubmed:year |
1984
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| pubmed:articleTitle |
The afferent glomerular arteriole: immunocytochemical and electrophysiological investigations.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|