Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
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Silver sea bream (Sparus sarba) is extremely euryhaline and can survive in a wide range of salinities (0-70 per thousand). The status of the renin-angiotensin system (RAS) in sea bream adapted to different salinities was studied. As indicated by plasma Ang II levels, a suppressed status of the RAS was found to occur under brackish water conditions; while under hypersaline conditions, an activated RAS prevailed, especially in fish adapted to double strength seawater (70 per thousand). Captopril successfully blocked the conversion of Ang I to Ang II, causing a dramatic drop in plasma Ang II levels, and such decrease was accompanied by lowered plasma cortisol levels. The pattern of changes in branchial Na-K-ATPase activity in different salinities was similar to those of plasma Ang II and cortisol, suggesting a causal regulatory role of Ang II on branchial Na-K-ATPase activity. Intraperitoneal injection of Ang II elicited a dose-dependent increase in branchial Na-K-ATPase activity in both 33- and 6 per thousand-adapted sea bream, but a relatively more intense stimulation of enzyme activity occurred in hyposmotic-adapted fish. Abrupt hyposmotic transfer rapidly lowered plasma Ang II level but elevated branchial Na-K-ATPase and transiently elevated plasma cortisol, indicating that these parameters are not solely controlled by Ang II but are also influenced by other hormonal factors that change during salinity transfer. Blood volumes of both 33- and 6 per thousand-adapted sea bream exhibited high stability during short-term salinity transfers and after long-term salinity adaptation. Captopril significantly reduced resting blood pressure in both 33- and 6 per thousand-adapted sea bream, indicating that the RAS was involved in maintenance of resting blood pressure in both hyperosmotic and hyposmotic environments. Blood pressure was highly stable during abrupt salinity transfer and captopril blockade did not alter such stability. The vasopressive effect of angiotensins was more potent in 6 per thousand-adapted sea bream. These results showed that the RAS is involved in the maintenance of fluid and pressure homeostasis in sea bream and hyposmotic-adapted sea bream has an abated RAS status.
Gen Comp Endocrinol 2006 Oct
PMID:Differential status of the renin-angiotensin system of silver sea bream (Sparus sarba) in different salinities. 1679 51

Phenylethanolamine N-methyltransferase (PNMT) is a final enzyme in catecholamine synthesizing cascade that converts noradrenaline to adrenaline. Although most profuse in adrenal medulla, PNMT is expressed also in the heart, particularly in cardiac atria and ventricles. In atria, the PNMT mRNA is much more abundant compared to ventricles. In present study we aimed to find out whether there is a difference in modulation of the PNMT gene expression in cardiac atria and ventricles. We used three methodological approaches: cold as a model of mild stress, hypoxia as a model of cardiac ischemic injury, and transgenic rats (TGR) with incorporated mouse renin gene (mREN-2)27, to determine involvement of renin-angiotensin pathway in the PNMT gene expression. We have found that PNMT gene expression was modulated differently in cardiac atria and ventricles. In atria, PNMT mRNA levels were increased by hypoxia, while cold stress decreased PNMT mRNA levels. In ventricles, no significant changes were observed by cold or hypoxia. On the other hand, angiotensin II elevated PNMT gene expression in ventricles, but not in atria. These results suggest that PNMT gene expression is modulated differently in cardiac atria and ventricles and might result in different physiological consequences.
Gen Physiol Biophys 2006 Dec
PMID:Gene expression of the phenylethanolamine N-methyltransferase is differently modulated in cardiac atria and ventricles. 1735 29

Cardiovascular diseases associated with molecular variants of individual components of renin-angiotensin system are reported to constitute inherited predisposition in humans. Molecular variant frequencies are race- and population-dependent. We examined frequencies of the M235T variant of angiotensinogen gene and I/D polymorphism of gene for angiotensin-converting enzyme in Slovak population: in hypertensive patients, coronary heart disease (CHD), dilated cardiomyopathy (DCM) and myocardial infarction (MI) patients compared to healthy subjects. Frequency of M235T was significantly increased in hypertensive, CHD and DCM patients compared to controls (0.48 and 0.50 vs. 0.40, p < 0.001). Significant increase in D allele frequency compared to controls was observed in the group of patients after MI (0.58 vs. 0.50, p < 0.001), CHD (0.59 vs. 0.50, p < 0.001) and DCM (0.60 vs. 0.50, p < 0.001). These results correlate with other Caucasian populations. In Slovak population, M235T is associated with increased blood pressure and D allele of ACE gene is associated with MI, chronic CHD and DCM, rather than with hypertension. Our results suggest that in Slovak population, D alelle and M235T variant represent a risk factor for several cardiovascular diseases and these polymorphisms might have a cumulative effect on development of cardiovascular diseases.
Gen Physiol Biophys 2007 Mar
PMID:Cardiovascular diseases and molecular variants of the renin-angiotensin system components in Slovak population. 1757 51

In mammals, a large body of evidence supports the existence of a brain renin-angiotensin system (RAS) acting independently or synergistically with the endocrine RAS to maintain diverse physiological functions, notably cardiovascular homeostasis. The RAS is of ancient origin and although most components of the RAS are present within the brain of teleost fishes, little is known regarding the central physiological actions of the RAS in these vertebrates. The present review encompasses the most relevant functional data for a role of the brain RAS in cardiovascular regulations in our experimental animal model, the unanesthetized trout Oncorhynchus mykiss. This paper mainly focuses on the central effect of angiotensin II (ANG II) on heart rate, blood pressure, heart rate variability and cardiac baroreflex, after intracerebroventricular injection or local microinjection of the peptide within the dorsal vagal motor nucleus. The probable implications of the parasympathetic nervous system in ANG II-evoked changes in the cardiac responses are also discussed.
Gen Comp Endocrinol 2008 May 15
PMID:Central cardiovascular actions of angiotensin II in trout. 1840 98

The goal of this work was to verify the hypothesis about the possible role of some genes of the renin-angiotensin system in the innate immunity to tuberculosis. The insertion/deletion polymorphism (I/D) of the gene of the angiotensin-converting enzyme (ACE) is known to have an effect on the concentration of the angiotensin II in human body and also an indirect effect on various branches of metabolism. On the one hand, people with homozygote deletion of the ACE gene (DD genotype) are vulnerable to adiposity, arterial hypertension, hypercholesterolemia, and a number of other pathological conditions. On the other hand, it was shown that hypocholesterolemia is the general phenomenon for the patients with pulmonary tuberculosis (Perez-Guzman C. et al., Chest (2005)). In this work, we studied the I/D polymorphism of the gene ACE (genotypes DD, ID, and II), single nucleotide polymorphism (SNP) of the gene AT1R (1166 A/C), and SNP in 3123 positions of the gene AT2R (3123 A/C) in 200 patients with tuberculosis, 202 patients with essential hypertension, and 208 apparently healthy subjects. A group of patients with essential hypertension was used as a contrast group. According to the hypothesis stated above, the excess in the number of patients with the DD genotype (ACE) should be statistically significant in the group of patients with hypertension as compared to the group of patients with tuberculosis (chi2 = 9.64; chi2 = 0.0019; OR = 2.0; CI 1.2-3.3). There was a trend toward an increase in the rate of the DD genotype in the group of patients with tuberculosis relative to healthy subjects. Similar trend was observed in healthy subjects relative to the group of patients with hypertension. However, this difference was found to be statistically insignificant. The genotypes and allelotypes were compared in the group of patients with tuberculosis versus both the two control groups (healthy subjects and patients with hypertension). The significant difference from control was observed only in male rather than female patients with tuberculosis. It was shown that the greatest contribution to the distinction between groups was due to the genes ACE and AT2R. The combination of the genotypes of genes ACE and AT2R (ID+3123C) was met significantly more frequently in male patients with tuberculosis as compared to control group of healthy subjects (chi2 = 9.70; chi2 = 0.002; OR = 2.3; CI 1.2-4.3). The results obtained in this work are discussed in terms of the hypothesis stated above.
Mol Gen Mikrobiol Virusol 2008
PMID:[Polymorphism of genes of the renin-angiotensin system ACE, AT1R, and AT2R in patients with pulmonary tuberculosis]. 1848 44

The renin-angiotensin system is an enzyme-linked hormonal cascade that plays an important role in body fluid and cardiovascular regulation. The system is initiated by the action of renin on the precursor protein, angiotensinogen (AGT), whose sequence information is scarce because of its high variability among species. In the present study, we cloned AGT in chondrichthyans (elasmobranchs: Triakis scyllium, Dasyatis akajei,Leucoraja erinacea and a holocephalan: Callorhinchus milii). Homology was low among AGTs thus far identified; 25-28% between elasmobranchs and tetrapods and 33-61% even within chondrichthyans. All chondrichthyan angiotensin (ANG) II's have a unique Pro3 instead of Val3 as seen in all other species. In addition, holocephalan ANG II has an unusual His4 instead of Tyr4. In addition, and the N-terminal amino acid, which is usually Asp1 in tetrapods and Asn1 in fishes, was highly variable (Asp, Asn or Tyr) in chondrichthyans. Molecular phylogenetic analysis showed that chondrichthyan AGT precursors are clustered into a group separated from those of tetrapods and teleosts. The AGT gene was most abundantly expressed in the liver, followed by the kidney, interrenal tissue and rectal gland of Triakis where biological actions of ANG II have been demonstrated. Collectively, we identified diversified AGT genes for the first time in chondrichthyes and showed that their ANG II's have unique amino acid residues at positions 1, 3 and 4. High variability of ANG II sequences in chondrichthyans is discussed in relation to their unique regulatory mechanisms such as urea-based osmoregulation.
Gen Comp Endocrinol 2009 Mar
PMID:Identification of angiotensinogen genes with unique and variable angiotensin sequences in chondrichthyans. 1907 Nov 26

Ageing and hypertension are the major risk factors for the development of cardiovascular and renal diseases, and the renin-angiotensin system has been shown responsible for these pathologies. Thus, the aim of this study was to compare the effects of losartan, angiotensin II type-1 receptor blocker, on systolic (SBP), diastolic (DBP), and mean (MBP) blood pressure, pulse pressure (PP) and heart rate as well as regional haemodynamics, cardiac hypertrophy and biochemical parameters in adult (L(9): 9-month-old) and aged (L(18): 18-month-old) spontaneously hypertensive rats (SHRs). Aged match untreated SHRs served as controls (U(9): 9-month-old and U(18): 18-month-old). Aortal blood flow and resistance were significantly improved by losartan treatment in L(9) vs. U(9) (p < 0.05). In aged SHRs, losartan significantly reduced SBP, MBP, PP, right ventricle weight index, and improved age-related impairment of left ventricular weight index (U(18): 4.21 +/- 0.09 mg/g vs. U(9): 3.54 +/- 0.34 mg/g, p < 0.05 and vs. L(18): 3.65 +/- 0.07 mg/g, p < 0.001), carotid, renal, and aortal vascular resistance, and glomerular filtration rate (U(18): 2.75 +/- 0.27 ml/min/kg vs. U(9): 4.84 +/- 0.85 ml/min/kg, p < 0.05 and vs. L(18): 3.65 +/- 0.07 ml/min/kg, p < 0.05). These results demonstrate significantly impaired systemic and regional haemodynamics and left ventricular hypertrophy in old SHRs. Losartan decreased age and hypertension associated cardiovascular risk by decreasing vascular resistance and pressure overload, ventricular hypertrophy, and preserving kidney function.
Gen Physiol Biophys 2009
PMID:Effects of angiotensin II type-1 receptor blocker losartan on age-related cardiovascular risk in spontaneously hypertensive rats. 1989 88

The renin-secreting juxtaglomerular cells (JGC) in the media of the afferent arteriole at the vessel pole are the major source of circulating renin. The control of renin secretion is complex with increases in cAMP being the major stimulus and increases in intracellular free Ca2+ concentration ([Ca2+]i) being inhibitory. We measured [Ca2+]i in the afferent arteriole from mostly JGC. Manoeuvres that increase cAMP (e.g. isoproterenol) or dibutyryl-cAMP elicited an increase in [Ca2+]i which was approximately 40% of that induced by angiotensin II (3 nmol/l). The Ca2+ response occurred in 50-90% of the cases, and increasing the stimulus increased responder frequency but not response size. The response was (almost) abolished by removal of extracellular Ca2+, prevented by inhibitors of store-operated Ca2+ channels (Gd3+ and 2-aminoethoxydiphenyl-borate), but was unaffected by isradipine or protein kinase A inhibitors. It was not produced by an activator of EPACs (exchange protein activated by cAMP) and was not accompanied by changes in membrane potential. The data suggest that in rat JGC, cAMP, perhaps directly, activates store-operated Ca2+ channels to increase [Ca2+]i. One could speculate that this increase in [Ca2+]i serves to finely adjust the stimulating effect cAMP-increasing signals on the renin-angiotensin system.
Gen Physiol Biophys 2009 Dec
PMID:Cyclic AMP increases cytoplasmic free calcium in renin-secreting cells from rat kidney. 2009 63

Atrial fibrillation (AF) is the most common sustained arrhythmia in man. Over the past years, importance of the renin-angiotensin-aldosterone system in AF pathophysiology has been recognized. Lately, the role of aldosterone in AF pathophysiology and mineralocorticoid receptor (MR) antagonism in "upstream" AF treatment is discussed with special regards concerning the effects on AF-induced structural remodeling. However, there is more and more evidence that MR antagonism also influences atrial electrophysiology and, respectively, AF-induced electrical remodeling, whereas the molecular mechanisms are almost unknown. The aim of this mini-review is to give an overview about the role of aldosterone in AF pathophysiology in principle and to summarize current available data concerning affection of cardiac ion channels by aldosterone and MR antagonism. Finally, as modulation of oxidative stress is discussed as one main therapy principle of "upstream" treatment of AF, potential mechanisms how modulation of oxidative stress by aldosterone and accordingly MR antagonism might alter atrial ion currents are delineated. Summarized, publications concerning potential mechanisms of aldosterone- and MR antagonism-modulated cardiac ion channels in various experimental settings are almost exclusively limited to the ventricular level and, partly, they are also contradictorily. Translation of these data to the atria is problematic because atrial and ventricular electrophysiology exhibit remarkable differences. It can be concluded that further research on the "atrial level" is needed in order to clarify the potential impact of the affection of atrial ion channels by aldosterone and accordingly MR antagonism in "upstream" therapy of AF.
Gen Physiol Biophys 2011 Mar
PMID:Effects of aldosterone and mineralocorticoid receptor antagonism on cardiac ion channels in the view of upstream therapy of atrial fibrillation. 2146 Apr 7

Hypercholesterolemia and low testosterone concentrations in men are associated with a high risk factor for atherosclerosis. It is known that cholesterol serves as the major precursor for the synthesis of the sex hormones. The bioactive peptides of the renin-angiotensin-system localized in the gonads play a key role in the relation between cholesterol and testosterone by modulating steroidogenesis and inhibiting testosterone production. In the present work, we evaluated the effects of diet-induced hypercholesterolemia on circulating testosterone levels and its relationship with the testicular RAS-regulating specific aminopeptidase activities in male mouse. A significant decrease in serum circulating levels of testosterone was observed after induced hypercholesterolemia. The changes found in aminopeptidase activities suggest a role of Ang III and Ang IV in the regulation of steroidogenesis.
Gen Comp Endocrinol 2011 Aug 01
PMID:Diet-induced hypercholesterolemia impaired testicular steroidogenesis in mice through the renin-angiotensin system. 2153 44


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