Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1) Measurements of renin secretion from single arterioles at time intervals down to 20 seconds showed that the renin secretion is episodic, the amount of renin released during each episode corresponding to the estimated content of one secretory granule. 2) A decrease in osmolality elicits episodic release of renin from single arterioles, stimulates renin release from isolated glomeruli transiently, and is associated with swelling of the secretory granules and formation of contacts between granules and the plasmalemma. 3) Increases in osmolality produce sustained inhibition of the renin secretion, and prevents swelling of the organelles of the juxtaglomerular epithelioid cells. 4) Treatment of isolated glomeruli with weak permeable bases has a biphasic effect on renin release: an initial transient stimulation, which can be blocked with sucrose, and a delayed inhibition which may be associated with an increase in intracellular pH. 5) Results with the monovalent cation ionophores nigericin and monensin, are similar to those obtained with weak permeable bases, and suggest that their effects are due to swelling and alkalinization of acidic cellular organelles. 6) A decrease in the extracellular calcium concentration results in sustained stimulation of renin secretion to a variable level dependent on the season. 7) After stimulation with a low extracellular calcium concentration, the sensitivity of secretion rate to osmotic stimuli is proportionally increased. A high extracellular osmolality blocks the stimulatory effect of a low calcium concentration. 8) Renin release is not correlated to the release of adenylate kinase.
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PMID:Studies on renin release in vitro. 268 Mar 10

Adenosine produced by the macula densa cells in response to changes in the tubular NaCl-concentration has been suggested to inhibit renin release in vivo. In order to test this suggestion we studied: incubated kidney cortical slices (KS) which contain both the macula densa and the entire afferent arteriole; superfused single microdissected glomeruli (LAG) without macula densa but with the afferent arteriole preserved; and superfused batches of selected glomeruli (SAG) containing only the juxtaglomerular cells closest to the glomerulus. For superfusion and incubation a bicarbonate Ringer solution was used. The specificity of the renin release process was validated by measuring adenylate kinase as a marker for cytoplasmatic leak. Adenosine (10 micrograms/ml) halved basal renin release from incubated KS as compared to controls (P less than 0.001, n = 8, 8). Renin release from LAG stimulated by calcium depletion was also inhibited (P less than 0.05, n = 8, 9) whereas basal release was not affected (n = 6, 12). No effect was detected neither on basal nor on calcium stimulated renin release from SAG. We conclude that adenosine inhibits renin release in vitro by a mechanism independent of a functioning nephron, and which involves only the JG-cells located in the afferent arteriole at some distance from the glomerulus.
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PMID:Effects of adenosine on renin release from isolated rat glomeruli and kidney slices. 389 16

The introduction of an assay for adenylate kinase into the study of renin release from isolated glomeruli is a useful tool in determining the specificity of the release process. Interestingly, even the absolute values of AK activity yield information that might be of value in understanding the effects on net renin output in media of grossly unphysiological composition. In qualitative terms, though, the AK measurements provide evidence against an unspecific loss of cytoplasmatic proteins as the cause of increased release of renin after removal of calcium or sodium bicarbonate. This renin release must have come from a compartment other than the cytoplasma of the juxtaglomerular cells. The in vivo position of the juxtaglomerular cells remaining in the present preparation, situated at the polkissen only few microns from the only hypoosmotic area in the body, suggests that the extreme osmosensitivity of renin release from isolated glomeruli represents a physiologic phenomenon. Because urea and sodium chloride are the predominant solutes in the tubular fluid at the macula densa, available data from isolated glomeruli are consistent with a macula densa feedback mechanism if it is accepted that a decrease in tubular sodium chloride concentration (and osmolality) increases the release of renin.
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PMID:Isolated glomeruli in vitro: an approach to the macula-densa-mediated renin release. 675 42