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)

Renal function, plasma renin activity, plasma aldosterone concentration and urine excretion of free norepinephrine were evaluated in 13 cirrhotics without previous or ongoing ascites and in 13 healthy subjects, after 6 days of controlled electrolyte intake (40 mmol of Na and 70 mmol of K per day) and during 24 h of recumbency. Plasma concentrations of the atrial natriuretic peptide (ANP) were also measured in 8 patients and 8 controls. Despite a low-normal filtered load of sodium (14.6 +/- 1.2 vs. 17.1 +/- 1.2 mmol/min), cirrhotic patients showed supernormal natriuresis (141.5 +/- 14.1 vs. 78.8 +/- 8.6 mmol/day; p < 0.001). Whereas the fractional excretion of sodium in these patients was twice that of controls (0.70 +/- 0.05 vs. 0.36 +/- 0.04%; p < 0.001), potassium excretion (42.5 +/- 2.7 vs. 43.1 +/- 2.7 mmol/day) and urine volume (1270 +/- 98 vs. 1452 +/- 148 ml/day) did not differ. In cirrhotics, plasma renin activity was reduced (0.50 +/- 0.12 vs. 1.39 +/- 0.33 ng/ml/h; p < 0.02), and plasma aldosterone concentration tended to be lower (66 +/- 10 vs. 86 +/- 9 pg/ml; p = 0.09), while urine norepinephrine excretion did not significantly differ from controls (961 +/- 120 vs. 782 +/- 43 ng/h). ANP was higher in patients than in controls (92 +/- 17 vs. 48 +/- 9 pg/ml; p < 0.05). Natriuresis was directly correlated with ANP (r = 0.69, p < 0.005) and ANP/plasma aldosterone ratio (r = 0.63; p < 0.01) in patients and healthy subjects taken together.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bed-rest-induced hypernatriuresis in cirrhotic patients without ascites: does it contribute to maintain 'compensation'? 148 52

The negative effect of artificial ventilation with positive pressure on renal function, expresses itself as a decrease of water and sodium excretion, being directly related with the raise of intrathoracic pressure. Factors participating in this process are: lowering in cardiac output, arousal of sympathic nervous system, increase in vasopressin action, activation of renin-angiotensin-aldosterone system and decrease of atrial natriuretic peptide release. This disorder of hydromineral metabolism produces: Impairment of hemodynamic equilibrium, favors the increase of hypoxia and renal failure. The effects of mechanical ventilation on renal function can be attenuated with the adoption of the following measures: a) techniques (use of low levels of PEEP and early disconnection of respirator); b) therapeutic (dopamine 2-3 mcg/kg/min, rational use of diuretics and fluids); y c) monitoring of renal function and hydro-mineral equilibrium.
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PMID:[The kidney in mechanical ventilation]. 148 39

Administration of a large dose of atrial natriuretic peptide is associated with an increase in glomerular filtration rate, diuresis and natriuresis in normal-sodium rats. However, glomerular hyperfiltration induced by atrial natriuretic peptide is markedly decreased in low-sodium rats. Glomerular insensitivity to atrial natriuretic peptide may be due to increased activity of the renin-angiotensin system in low-sodium rats and to an accompanying hypersensitivity to adenosine. The results indicate that attenuated glomerular responses to atrial natriuretic peptide are restored by the administration of adenosine deaminase in low-sodium rats. Moreover atrial natriuretic peptide markedly increases the urinary excretion of adenosine deaminase, which may be due to increased permeability of glomeruli to the enzyme.
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PMID:Adenosine deaminase restores the ability of atrial natriuretic peptide to induce glomerular hyperfiltration in low-sodium rats. 149 57

Sodium balance plays a primary role in blood pressure regulation. Atrial natriuretic peptide, a recently discovered natriuretic substance, seems to participate in renal sodium handling, but its behavior in essential hypertension has not been fully defined. In our study, to avoid the "contamination" of factors other than hypertension, we evaluated the plasma levels of atrial natriuretic peptide in young men at military draft age. Our main results showed that plasma atrial natriuretic peptide levels are higher in young hypertensives with low plasma renin activity and low urinary excretion of active kallikrein. The influence of a positive genetic background for essential hypertension on plasma atrial natriuretic peptide levels was also investigated. Our data showed slightly elevated levels of the atrial hormone in young normotensives with a family history of hypertension.
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PMID:[Cardiac and renal sodium-modulating hormones in juvenile arterial hypertension. The physiopathological aspects and therapeutic results of a trial at the Policlinico Militare Celio in Rome]. 149 65

Alveolar hypoxia and resulting tissue hypoxia initiates the pathophysiological sequence of high altitude pulmonary edema (HAPE). Very rapid ascent to high altitude without prior acclimatization results in HAPE, even in subjects with excellent tolerance to high altitude. Upon acute altitude exposure, HAPE-susceptible individuals react with increased secretion of norepinephrine, epinephrine, renin, angiotensin, aldosterone and atrial natriuretic peptide. In response to exercise at high altitude, subjects developing acute mountain sickness and HAPE secrete more aldosterone and antidiuretic hormone than subjects who remain well. This results in sodium and water retention, reduction of urine output, increase in body weight and development of peripheral edemas. The hypoxic pulmonary vascular response is enhanced in HAPE-susceptible subjects, thus favouring the development of severe pulmonary hypertension on exposure to high altitude. It has been postulated that uneven pulmonary vasoconstriction enhances filtration pressure in non-vasoconstricted lung areas, leading to interstitial and alveolar edema. The high protein content of the edema fluid in HAPE characterizes this edema as a permeability edema. The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to 4559 m and thus prevents HAPE in most cases. This finding illustrates the crucial role of hypoxic pulmonary hypertension in the development of HAPE. The causal treatment of HAPE is descent, evacuation and administration of oxygen. Treatment of HAPE patients with nifedipine results in a reduction of pulmonary artery pressure, clinical improvement, increased oxygenation, decrease of the alveolar arterial oxygen gradient and progressive clearing of pulmonary edema on chest x-ray. Thus nifedipine offers a pharmacological tool for the treatment of HAPE.
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PMID:[Pathophysiology, prevention and therapy of altitude pulmonary edema]. 149 42

We have previously proposed the ovarian ERAANPS (endothelin-rein- angiotensin-atrial natriuretic peptide system). The present study was undertaken to examine in vivo the effects of herbal medicines [Tokishakuyakusan (TS), Keishibukuryogan (KB), Shakuyakukanzoto (SK) and Unkeito (UT)] on endothelin-1 (ET), renin and angiotensin II (A II) in the ovaries, of immature rats treated with 10 IU PMS for 48 h. ET and all components of renin-angiotensin system (RAS) were found at high levels in the ovary. Concomitant treatment with PMS plus TS, KB, SK or UT, especially TS and UT, tended to decrease the ET levels in ovary, while components of RAS tended to increase. However, ET, renin and A II levels in plasma were not at all affected after treatment with TS, KB, SK or UT. These results suggest that TS, KB, SK or UT may regulate the ovarian ERAANPS.
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PMID:Effects of tokishakuyakusan, keishibukuryogan, shakuyakukanzoto and unkeito on ovarian endothelin, renin and angiotensin II in pregnant mare's serum gonadotropin-treated immature rats. 151 58

C-type natriuretic peptide (CNP), the third member of the natriuretic peptide family, is thus far known to be distributed mainly in the central nervous system and is considered to act as a neuropeptide, in contrast to atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), which act as cardiac hormones. Recently, we and others have demonstrated that the ANP-B receptor, which is selectively activated by CNP, is localized not only in the central nervous system but in peripheral tissues, including blood vessels. This finding has made us speculate regarding the peripheral production of CNP. In the present study, cultured endothelial cells were examined for CNP production by RIA and Northern blot analysis. CNP-like immunoreactivity was detected in the conditioned media of endothelial cells. Northern blot analysis detected CNPmRNA with a size of 1.2 kb. In addition, transforming growth factor (TGF)-beta, one of the key growth factors for vascular remodeling, markedly stimulated the expression of CNPmRNA and induced a tremendous increase in CNP secretion. We could also detect CNP transcript in the bovine thoracic aorta using the reverse transcription-polymerase chain reaction method. The present study demonstrates the endothelial production of CNP and suggests that a member of the natriuretic peptide family may act as a local regulator in vascular walls. Since evidence for the pathophysiological importance of the vascular renin-angiotensin system has been accumulating and the natriuretic peptide system is known to be antagonistic to the renin-angiotensin system, the possible existence of "vascular natriuretic peptide system" may prove to be of physiological and clinical relevance.
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PMID:Endothelial production of C-type natriuretic peptide and its marked augmentation by transforming growth factor-beta. Possible existence of "vascular natriuretic peptide system". 152 22

The vascular disturbance associated with ciclosporin (CS) nephrotoxicity is poorly defined in both the normal and transplanted human kidney. Six bone marrow transplant recipients were studied before, during and after administration of CS. By analysis of time activity curves and clearance of Tc-99m DTPA, renal blood flow (RBF), filtration fraction (FF) and GFR were shown to fall on CS (GFR: p less than 0.001; RBF, FF: p less than 0.01). These haemodynamic variables did not fully recover with dose reduction or after discontinuation of therapy. Plasma renin activity (PRA) aldosterone and atrial natriuretic peptide did not change although there appeared a tendency for PRA to fall on CS. There was a reversible normokalemic metabolic acidosis. CS levels stayed within the therapeutic range. The partial reversibility of GFR, RBF and FF is consistent with CS-induced functional disturbance and reflects sensitivity to microvascular and tubular injury of the normal human kidney.
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PMID:Disturbance in renal haemodynamics and physiology in bone marrow transplant recipients treated with ciclosporin A. 153 79

To assess the interaction of endothelin (ET) with atrial natriuretic peptide (ANP) on cardiovascular and renal function, arginine vasopressin (AVP) release, and the renin-angiotensin-aldosterone system, either a low or high dose of ET (4 or 12 pmol.kg-1.min-1) was administered with ANP (26 pmol.kg-1.min-1) for 45 min after the initial infusion of ANP alone in anesthetized dogs. In the other groups, either ANP or saline alone was administered for 90 min. ANP alone decreased blood pressure (BP), cardiac output (CO), plasma aldosterone, and plasma renin activity (PRA), increased urinary Na and K excretion (UNaV and UKV, respectively) and urine flow (UF), but did not affect plasma AVP. The low dose of ET had no effect on these ANP-induced changes. However, the high dose of ET curtailed the responses to ANP, increased BP and PRA, and decreased UNaV, UKV, and UF associated with decreased renal plasma flow and glomerular filtration rate. High ET also further potentiated the decrease in CO and the increase in total peripheral resistance induced by ANP and increased plasma AVP. These results indicate that a dose of ET one-half that of ANP (on the molar ratio) may have completely counteracted vascular, hormonal, and renal responses to ANP.
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PMID:Interaction of ANP with endothelin on cardiovascular, renal, and endocrine function. 153 32

Plasma levels of alpha-human atrial natriuretic peptide (alpha-hANP), renin activity and angiotensin II were studied in 17 patients undergoing partial hepatectomy. Central venous pressure (CVP), heart rate (HR), mean arterial pressure (MAP) and the serum sodium concentration (Na), which affect plasma ANP levels, were measured during the operation. At 90 minutes after the surgical incision, plasma alpha-hANP levels increased significantly from 38.6 +/- 4.02 pg.ml-1 to 62.7 +/- 8.24 pg.ml-1, but the changes in plasma alpha-hANP levels during the surgery were within normal levels. Plasma alpha-hANP levels were not related to changes in CVP, HR and Na. At 90 minutes after the incision when plasma alpha-hANP levels were elevated, plasma renin activity, angiotensin II and MAP also increased significantly. Therefore, we believe that activation of the sympathetic nervous system by surgical stimulation is one of the causes of the elevation of alpha-hANP levels during the operation. The increase in plasma alpha-hANP levels, however, was lower than those of the plasma renin activity and angiotensin II. Our results suggest that surgical stimulation acts to retain sodium and water in patients during partial hepatectomy.
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PMID:[Plasma levels of alpha-human atrial natriuretic peptide, renin activity and angiotensin II in partial hepatectomy]. 153 37


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