Disease relevance of REN

• We propose that the sensitivity of 18-hydroxylase to oxygen accounts for the dissociation of renin and aldosterone during hypoxia in vivo [1].
• The crystal structure of recombinant bovine chymosin (EC 3.4.23.4; renin), which was cloned and expressed in Escherichia coli, has been determined using X-ray data extending to 2.3 A resolution [2].
• Serum renin, lactate, and pyruvate values remained normal; creatinine clearances were not significantly different than control values, and there were no significant changes in body weight [3].
• Cultured neuroblastoma cells and neuroblastoma-glioma cells have been shown to contain renin activity, angiotensin-converting enzyme activity, and angiotensins [4].
• TAH implantation caused systemic and pulmonary hypertension (P less than 0.01), salt retention, edema, and significant elevations of plasma renin, aldosterone, and arginine vasopressin [5].

Psychiatry related information on REN

• It is concluded that some intrarenal functional or structural change induced by water deprivation sensitizes the renin-secreting mechanism to colloid osmotic stimuli [6].

High impact information on REN

• Endothelial cells modulate renin secretion from isolated mouse juxtaglomerular cells [7].
• Taken together, our findings provide first evidence for a local control function of the endothelium on cAMP stimulated renin secretion from renal juxtaglomerular cells, which could in part be mediated by endothelin [7].
• Matrix-assisted laser desorption ionization is used to obtain Fourier-transform ion cyclotron resonance mass spectra of model peptides (e.g., gramicidin S, angiotensin I, renin substrate, melittin, and bovine insulin) [8].
• These data document the lack of any significant stimulatory influence of decreased pulse pressure on renin secretion in a chronic awake calf model [9].
• Although renal blood flow decreased slightly from control (667 +/- 84 ml/min) during the nonpulsatile perfusion period (555 +/- 73 ml/min), renin secretion did not increase significantly from control (482 +/- 81 ng angiotensin I/ml per hr per min) during the bypass period (531 +/- 99) [9].

Chemical compound and disease context of REN

• The dopamine antagonist, metoclopramide, injected i.v. (1 mg X kg-1 body weight) did not modify plasma renin activity, aldosterone or cortisol concentrations in either group [10].

Biological context of REN

• Insulin-like growth factor I alters renal function and stimulates renin secretion in late gestation fetal sheep [11].
• The more potent inhibitors (IC50 = 20-50 nM) were found to be selective inhibitors for renin over porcine pepsin and bovine cathepsin D (little or no inhibition was observed at 10(-5) M) [12].
• 6. Synthesis of prostaglandins by the kidney is important to mechanisms which control renin release and renal vascular resistance [13].
• Local reduction of perfusion pressure in small arteries and arterioles by the injection of microspheres induced a short-lasting decrease in renal plasma flow and a transient stimulation of renin release [14].
• The vasoconstriction induced by the crude renin substrate probably does not involve the AII receptors [14].

Anatomical context of REN

• After pump implantation and recovery, control measurements of renal vein and arterial plasma renin activity, arterial pressure, and renal artery flow were obtained [9].
• Regulation of the adrenal renin angiotensin system in cultured bovine zona glomerulosa cells: effect of catecholamines [15].
• Thus we have shown that renin/prorenin production by theca cells in vitro can be directly regulated by LH in a cAMP-dependent manner [16].
• The effect of water deprivation on the osmotic release of renin was evaluated in conscious rats previously prepared with right nephrectomy and cannulations of left renal artery and lower abdominal aorta [6].
• These cultured cells could be stimulated with LH to produce renin and prorenin [16].

Associations of REN with chemical compounds

• In the presence of endothelial cells both spontaneous and forskolin (10 microM) or isoproterenol (10 microM) stimulated renin release were markedly attenuated [7].
• Catecholamines had a weak stimulating effect on aldosterone secretion and were potent stimulators of adrenal renin activity in cells and medium [15].
• The results of this study therefore suggest that theophylline-stimulated renin release may be mediated through a prostaglandin pathway [17].
• The addition of progesterone (the major steroid product of the MA-10 cells) did not induce a significant increase in renin activity [18].
• The treatment of Leydig cell cultures with bovine LH (bLH), hCG, or with (Bu)2cAMP elicited a dose- and time-dependent induction of renin activity and a concomitant increase in steroid biosynthesis [18].

Regulatory relationships of REN

• Transforming growth factor-beta 1 inhibits aldosterone and stimulates adrenal renin in cultured bovine zona glomerulosa cells [19].
• Addition of TNF alpha to cultured bovine thecal cells resulted in a dose-dependent inhibition of LH- or 8-bromo-cAMP-stimulated production of prorenin and renin by the cells in a noncytotoxic manner [20].

Other interactions of REN

• Contrary to its effect on aldosterone, TGF beta 1 stimulates the synthesis and release of adrenal renin and prorenin [19].
• Plasma renin concentration increased by 275 +/- 52% during infusion of IGF-I (P < 0.005) [11].
• STUDY OBJECTIVE--The aim of the study was to investigate plasma concentrations of atrial natriuretic peptide, aldosterone, and renin during experimentally induced acute central venous congestion [21].
• It inhibited bovine and rat trypsin, showed weak inhibition of bovine chymotrypsin and was inactive against rat chymotrypsin and bovine renin, kallikrein, thrombin and trypsinogen [22].

Analytical, diagnostic and therapeutic context of REN

• Utilizing cocultures of mouse renal juxtaglomerular cells with bovine microvascular endothelial cells, we have examined whether endothelial cells exert direct influence on renin secretion from renal juxtaglomerular cells [7].
• A diurnal cycle of renin secretin was observed during the pulseless perfusions [9].
• Furthermore, immunofluorescence microscopy with antirenin antisera confirmed the presence of renin within these cells [23].
• Biosynthetic radiolabeling, followed by immunoprecipitation, demonstrated de novo synthesis of a renin precursor in the endothelial cells, which was processed to a more mature protein [23].
• Brain renin has been purified 1,670,000-fold to homogeneity from bovine anterior pituitary in seven steps, including affinity chromatography on pepstatin-aminohexyl-agarose [24].

References