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

We studied sympathetic and renin-angiotensin systems activity in a series of 175 patients suffering from acute myocardial infarction. These two systems were both overactivated especially in the cases complicated by hemodynamically documented left heart failure. The response of these systems to acute heart failure was in the same range for patients younger or older than 65 years and the witness (norepinephrine and plasma renin levels) of sympathetic and renin-angiotensin activities were good independent prognostic factors of in-hospital mortality.
Bull Mem Acad R Med Belg 1991
PMID:[Activity of the sympathetic nervous system and of the renin-angiotensin system in the acute stage of myocardial infarction]. 181 13

In nephrology, intensive research has focused in recent years on the interplay between NO produced by the different isoforms of NO synthase (NOS) and complex renal functions. In this regard, the juxtaglomerular apparatus is of particular interest. First, it is the main site for control of renal blood flow by autoregulation and of glomerular filtration rate by tubuloglomerular feedback, as well as of renin secretion. Second, two constitutive NOS, nNOS and eNOS, are expressed, respectively, in the macula densa cells and in the endothelium of the afferent and efferent arteriole. It was thus not unexpected that NO could interact with the physiological variables. Indeed, NO attenuates rapidly the autoregulatory efficacy of renal blood flow as well as the sensitivity of the tubuloglomerular feedback by inhibiting Ca++ influx mainly in the afferent arteriole. On the other hand, renin secretion may be stimulated as well as inhibited by NO. These opposing effects, although as yet unexplained, could be related to the source of NO. If so, the hypothetical dual effect of NO could be secondary to a difference in modulation of each NOS isoform by their specific stimuli and results in secretion or not of renin. This hypothesis seems to be applicable to changes in extracellular volume.
Bull Mem Acad R Med Belg 2000
PMID:[Paracrine kidney activity and homeostasis: the emergence of nitric oxide. A conceptual perspective]. 1147 97

In 1992, a new type of progressive renal fibrosis was reported in patients after the intake of weight-reducing pills containing a Chinese herb (Aristolochia fangchi) rich of nephrotoxic and carcinogenic aristolochic acids (AA). Up to now, Chinese herb nephropathy (CHN), also called aristolochic acid nephropathy (AAN), has been observed in more than 100 patients in Belgium, but also in numerous patients all around the world. The main histological characteristics of CHN are tubular atrophy and interstitial fibrosis leading to severe renal functional impairment and end-stage renal failure. Urothelial carcinomas were also found in about 50% CHN patients suffering from end-stage renal failure. Experimentally, the main features of CHN were successfully reproduced after 35 days of daily AA injections to rats. Starting from this model, we demonstrated that other potential nephrotoxic substances (dexfenfluramine, diuretics) also contained in the weight-reducing pills, did not enhance the renal toxicity of AA. Interestingly, the inhibition of renin angiotensin system did not prevent the development of renal lesions, suggesting that, in contrast with other animal models, physiopathological mechanisms leading to renal fibrosis might be largely independent of angiotensin II. From clinical observations to experimental studies, we currently increased our knowledge in the understanding of pathophysiological mechanisms of nephropathies of toxic origin. Botanicals which are known or suspected to contain AA are still sold on Web sites or over-the-counter markets. It is not surprising then to find new AAN cases reported in the medical literature. Therefore, further studies are needed to elucidate pathways of AA-related nephrotoxicity and carcinogenicity in order to develop therapeutic strategies.
Bull Mem Acad R Med Belg 2006
PMID:[Nephropathy caused by Chinese plants and aristolochic acids: from clinical observation to experimental model]. 1728 6

It has been shown that the brain has its own intrinsic renin-angiotensin system (RAS) and angiotensin-(1-7) (Ang-(1-7)) is particularly interesting, because it appears to counterbalance most of the Ang II effects. Ang-(1-7) exerts its biological function through activation of the G-protein-coupled receptor Mas. Interestingly, hippocampus is one of the regions with higher expression of Mas. However, the role of Ang-(1-7)/Mas axis in hippocampus-dependent memories is still poorly understood. Here we demonstrated that Mas ablation, as well as the blockade of Mas in the CA1-hippocampus, impaired object recognition memory (ORM). We also demonstrated that the blockade of Ang II receptors AT1, but not AT2, recovers ORM impairment of Mas-deficient mice. Considering that high concentrations of Ang-(1-7) may activate AT1 receptors, nonspecifically, we evaluate the levels of Ang-(1-7) and its main precursors Ang I and Ang II in the hippocampus of Mas-deficient mice. The Ang I and Ang II levels are unaltered in the whole hipocampus of MasKo. However, Ang-(1-7) concentration is increased in the whole hippocampus of MasKo mice, as well as in the CA1 area. Taken together, our findings suggest that the functionality of the Ang-(1-7)/Mas axis is essential for normal ORM processing.
Neurobiol Learn Mem 2012 Jan
PMID:Angiotensin-(1-7)/Mas axis integrity is required for the expression of object recognition memory. 2206 10