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)

This investigation focuses on the hormonal response to electrolyte changes and water loss in patients suffering from heat exhaustion, hospitalized in Muna during Hajj seasons. The concentrations of cortisol, aldosterone, renin (PRA), vasopressin (ADH) parathyroid hormone (PTH), adrenocorticotrophic hormone (ACTH) and growth hormone (GH) were determined in venous blood samples drawn from the patients upon admission, during, and after treatment. Highly elevated PRA mean values (396.77 +/- 88.58-462.18 +/- 106.95 ng.ml-1.h-1) were recorded, with no statistically significant difference between the readings. A similar trend was seen for cortisol (42.92 +/- 4.30-60.20 +/- 11.90 ug/dl). Vasopressin (ADH) showed a highly elevated value upon admission (42.48 +/- 18.82 pg/ml), which decreased to 23.66 +/- 8.27 pg/ml during treatment, and declined further to 7.67, ranging between 4.04 and 11.30 pg/ml, thereafter. Statistically speaking, however, there was no significant difference between these readings. PTH concentration, on the other hand, increased from an initial value of 143.31 +/- 47.64 to 245.90 +/- 107.34 pmol/l after treatment, but again there was no significant difference between the values. ACTH concentrations showed no detectable values throughout this study. The GH concentration was within normal throughout, ranging from 4.42 +/- 0.87 to 5.19 +/- 1.78 ng/ml. Aldosterone concentration was significantly reduced in the patients upon admission, with an initial value of 187.93 +/- 21.41 pg/ml (p < 0.05 as compared to normal mean value). During and after treatment, aldosterone values were still significantly lower than normal mean (152.63 +/- 13.47, p < 0.05; 145.2 +/- 17.55, p < 0.01, respectively), thereby shedding some light on the possible etiology of persistent metabolic acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Physiological studies on heat exhaustion victims among Mecca pilgrims. 764 64

Continuous pump-driven veno-venous hemofiltration (CVVH) has become an established method for treatment of acute renal failure (ARF). Since severe disturbances of (micro-) circulation are intimately involved in the bad outcome of these patients, the profile of endocrinological regulators of circulation was prospectively and serially measured in patients undergoing pump-driven CVVH (n = 15). 15 patients with similar APACHE II score, but without ARF and without CVVH were also studied. Endothelin-1 (ET-1), atrial natriuretic peptide (ANP), vasopressin, renin, and catecholamine (epinephrine, norepinephrine) plasma levels were measured before start of CVVH (= "baseline") (in the non-CVVH patients: admission to intensive care unit) and during the next 5 days. Various hemodynamic parameters were additionally monitored. MAP, HR, PAP, CI, and right ventricular hemodynamics (RVEF, RVEDV, RVESV) remained almost unchanged in the CVVH patients and were without differences to the non-CVVH group within the entire investigation period. PCWP and RAP were higher in the CVVH patients already at baseline (RAP, 17.8 +/- 4.0 mmHg; PCWP, 22.1 +/- 4.5 mmHg) (p < .02) and remained elevated in the further course of the investigation. Renin plasma level was higher already at baseline in the CVVH patients (907 +/- 184 pg/ml) (p < .05) and further increased during CVVH (to 1453 +/- 186 pg/mL). Vasopressin increased only in the CVVH group (from 3.80 +/- .66 to 11.85 +/- 1.05 pg/mL) (p < .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in regulators of circulation in patients undergoing continuous pump-driven veno-venous hemofiltration. 2597 10

Several components are responsible for circulatory control at the central, regional, and microcirculatory level. Angiotensin-converting enzyme (ACE) inhibitors are known to act beneficially on circulation by various mechanisms. The influence of continuous i.v. administration of the ACE inhibitor enalaprilat on regulators of circulation was studied in 45 critically ill patients. According to a prospective randomized sequence, either 0.25 mg/h (group 1, n = 15) or 0.5 mg/h (group 2, n = 15) of enalaprilat or saline solution as placebo (control group, n = 15) were continuously given. Infusion was started on the day of admission to the intensive care unit (ICU) and continued for the next 5 days. From arterial blood samples, plasma levels of endothelin-1 (ET), atrial natriuretic peptide (ANP), renin, vasopressin, angiotensin-II, and catecholamines (epinephrine, norepinephrine) were measured. All measurements were carried out before infusion (= baseline values) and during the next 5 days. In both enalaprilat groups, mean arterial blood pressure (MAP) decreased similarly; heart rate (HR) and central venous pressure (CVP) did not change, and were without differences in comparison to the untreated control. Except for ET, plasma levels of all vasoactive substances exceeded normal range at baseline. Angiotensin-II plasma concentrations significantly decreased during enalaprilat infusion (0.25 mg/h: from 53.1 +/- 11.3 to 22.1 +/- 9.3 pg/ml; 0.50 mg/h: 62.1 +/- 14.4 to 17.9 +/- 7.9 pg/ml), but they remained significantly elevated in the untreated control patients. Vasopressin plasma level increased only in the control group (p < 0.01) and decreased in the patients in whom 0.50 mg/h of enalaprilat was infused.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Continuous i.v. administration of the angiotensin-converting enzyme inhibitor enalaprilat in the critically ill: effects on regulators of circulatory homeostasis. 776 7

Transgenic mice overexpressing a transthyretin promoter-ANF structural fusion gene have a life-long reduction in arterial blood pressure compared to nontransgenic littermates. The present study was designed to test the hypothesis that the high plasma level of ANF in the transgenic mice inhibits the renin-angiotensin and/or vasopressin systems, thereby causing the hypotension. Mice were anaesthetized with Inactin and arterial pressure and heart rate were monitored before and during Saralasin infusion and vasopressin V1 receptor blockade. Effectiveness of the blockade was determined by injection of angiotensin and vasopressin before and during Saralasin and V1 receptor antagonist administration. Saralasin was associated with hypotension in both transgenic and nontransgenic mice. The decrease in blood pressure was proportionally greater in the transgenic animals. Vasopressin receptor blockade had little effect on blood pressure in either group. Heart rates were not different between the groups during any maneuver. We conclude that the chronic hypotensive effect of ANF overproduction does not involve the inhibition of either renin-angiotensin or vasopressin systems. The data, however, suggest that the renin-angiotensin system may be stimulated in the ANF-transgenic mice.
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PMID:Blood pressure regulation in ANF-transgenic mice: role of angiotensin and vasopressin. 799 80

To elucidate the effects of exercise in water on the maternal circulation, twenty normal pregnancies were examined under the following three conditions; 1) on the land at rest, 2) during water immersion and 3) after the exercise in water. Their gestational ages were from 25 to 37 weeks (31 +/- 4 weeks, mean +/- S.D., n = 20). We examined the blood pressure, the urine volume throughout the examination, CBC and the levels of vasopressin, plasma renin activity and human atrial natriuretic peptide (hANP). The blood volume calculated from the Hb and Ht were significantly (p < 0.001) increased during the water immersion (105.8 +/- 2.5%), even after the exercise (101.6 +/- 2.9%). Vasopressin was decreased during the water immersion and increased after the exercise, but plasma renin activity was decreased in these two conditions. The hANP concentration was significantly (p < 0.001) increased after the exercise in water and correlated with the urine volume (ml/hour) during the examination. These results show that the decline in blood pressure and the increase in the urine volume during the maternal swimming were caused by the decreased plasma renin activity and the increased hANP concentration resulted from the blood volume expansion during the exercise in water.
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PMID:[Effect of exercise in water on maternal blood circulation]. 812 82

We studied the effects of prostaglandin E1 (PGE1) on decrease in urine output during surgery in patients for radical total hysterectomy under general anesthesia. The patients were randomly allocated into two groups. Five patients (control group) were given no PGE1 and served as control. Seven patients (PGE1 group) were given continuous infusion of PGE1 at a rate of 50 ng.kg-1 x min-1 after first measurement (baseline). Urine output in control group decreased by 68%, but in PGE1 group it did not change from the baseline. Urine sodium and fractional sodium excretion in control group decreased, but in PGE1 group they increased. Creatinine clearance increased from the baseline in both groups. Antidiuretic hormone in control group increased by 30%, but in PGE1 group decreased by 53%. Plasma renin activity, angiotensin I, angiotensin II in both groups increased, and those in the control group were higher than those in PGE1 group. However, aldosterone in the control group was lower than that in PGE1. These results indicate that diuretic effect of PGE1 could be mediated by suppression of antidiuretic hypersecretion induced by surgical stress, inhibition of the action of antidiuretic hormone, and suppression of sodium and water reabsorption in proximal and distal tubules. Also, PGE1 did not directly stimulate renin-angiotensin system.
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PMID:[Prostaglandin E1 suppresses hypersecretion of antidiuretic hormone induced by surgical stress]. 816 28

We studied renal sodium handling during water diuresis in children in the early phase of relapse of minimal lesion nephrotic syndrome (MLNS). Findings were related to presence or absence of symptoms suggestive of hypovolaemia, and to neurohumoral factors, and were compared to results of similar studies in the same children in remission. Nine children (aged 7.8 +/- 3.1 years) presented with hypovolaemic symptoms, and 10 (7.4 +/- 4.3 years) without such symptoms. Both groups displayed severe proteinuria, hypoproteinaemia and oedema. Symptomatic patients showed tendency for a low glomerular filtration rate, and significantly impaired urine dilution, decreased fractional sodium and lithium excretions, and elevated diluting segment reabsorption [CH2O/(CH2O + CNa)] and sodium/potassium exchange [UK/(UK + UNa)]. In the non-symptomatic patients these parameters were normal. Plasma renin and aldosterone were significantly elevated in the symptomatic children, and strongly correlated with all parameters of tubule sodium reabsorption. Weaker associations were found for plasma noradrenaline and atrial natriuretic peptide. Vasopressin was also relatively high in the symptomatic group, but showed no association with impaired urine dilution. The diffusely stimulated tubular sodium reabsorption in the symptomatic children, in association with stimulated neurohumoral factors, indicates that secondary sodium retention contributes to oedema formation in at least a subset of children developing a nephrotic relapse. This may be limited to the early stage, and be more pronounced in some patients than in others. The tubular defect responsible for maintenance of oedema in stabilized MLNS remains unclear.
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PMID:Renal sodium handling in children with nephrotic relapse: relation to hypovolaemic symptoms. 894 79

Despite a number of difficulties in performing experiments during weightlessness, a great deal of information has been obtained concerning the effects of spaceflight on the regulation of body fluid and electrolytes. Many paradoxes and questions remain, however. Although body mass, extracellular fluid volume, and plasma volume are reduced during spaceflight and remain so at landing, the changes in total body water are comparatively small. Serum or plasma sodium and osmolality have generally been unchanged or reduced during the spaceflight, and fluid intake is substantially reduced, especially during the first of flight. The diuresis that was predicted to be caused by weightlessness, has only rarely been observed as an increased urine volume. What has been well established by now, is the occurrence of a relative diuresis, where fluid intake decreases more than urine volume does. Urinary excretion of electrolytes has been variable during spaceflight, but retention of fluid and electrolytes at landing has been consistently observed. The glomerular filtration rate was significantly elevated during the SLS missions, and water and electrolyte loading tests have indicated that renal function is altered during readaptation to Earth's gravity. Endocrine control of fluid volumes and electrolyte concentrations may be altered during weightlessness, but levels of hormones in body fluids do not conform to predictions based on early hypotheses. Antidiuretic hormone is not suppressed, though its level is highly variable and its secretion may be affected by space motion sickness and environmental factors. Plasma renin activity and aldosterone are generally elevated at landing, consistent with sodium retention, but inflight levels have been variable. Salt intake may be an important factor influencing the levels of these hormones. The circadian rhythm of cortisol has undoubtedly contributed to its variability, and little is known yet about the influence of spaceflight on circadian rhythms. Atrial natriuretic peptide does not seem to play an important role in the control of natriuresis during spaceflight. Inflight activity of the sympathetic nervous system, assessed by measuring catecholamines and their metabolites and precursors in body fluids, generally seems to be no greater than on Earth, but this system is usually activated at landing. Collaborative experiments on the Mir and the International Space Station should provide more of the data needed from long-term flights, and perhaps help to resolve some of the discrepancies between U.S. and Russian data. The use of alternative methods that are easier to execute during spaceflight, such as collection of saliva instead of blood and urine, should permit more thorough study of circadian rhythms and rapid hormone changes in weightlessness. More investigations of dietary intake of fluid and electrolytes must be performed to understand regulatory processes. Additional hormones that may participate in these processes, such as other natriuretic hormones, should be determined during and after spaceflight. Alterations in body fluid volume and blood electrolyte concentrations during spaceflight have important consequences for readaptation to the 1-G environment. The current assessment of fluid and electrolyte status during weightlessness and at landing and our still incomplete understanding of the processes of adaptation to weightlessness and readaptation to Earth's gravity have resulted in the development of countermeasures that are only partly successful in reducing the postflight orthostatic intolerance experienced by astronauts and cosmonauts. More complete knowledge of these processes can be expected to produce countermeasures that are even more successful, as well as expand our comprehension of the range of adaptability of human physiologic processes.
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PMID:Regulation of body fluid volume and electrolyte concentrations in spaceflight. 904 37

In congestive heart failure (CHF), low cardiac output decreases the fullness of the arterial circulation. This underfilling of the arterial vascular compartment unloads the baroreceptors, resulting in a sequence of events to maintain arterial circulatory integrity. Among them, the renin-angiotensin-aldosterone axis, the sympathetic nervous system, the non-osmotic release of vasopressin and the endothelins are activated to increase vascular resistance and enhance sodium and water renal retention. Simultaneously, vasodilatory and natriuretic substances such as the natriuretic peptides are activated to counterregulate these vasoconstrictors. In the initial phase of CHF, these events contribute to the cardiorenal adaptation. However, when CHF progresses, they become maladaptive and further depress vantricular performance and increase sodium and water retention. This vicious cycle of CHF provides the rationale for the use of neurohormonal antagonists in CHF. The beneficial effects of angiotensin converting enzyme inhibitors in CHF are well described. Vasopressin V1 receptor antagonists have been associated with peripheral vasodilation and improved cardiac function in some patients with CHF. In CHF animals, the vasopressin V2 receptor antagonist has been demonstrated to reverse the defect in water excretion. Bosentan, an endothelin antagonist, is associated with an increase of cardiac index in patients with CHF. A role for exogenous natriuretic peptides is also under investigation. Modulation of the neurohumoral systems associated with CHF opens a new perspective in the treatment of cardiac edema, principally by improving cardiac performance.
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PMID:Sodium and water retention in heart failure: pathogenesis and treatment. 918 6

Upright posture leads to rapid pooling of blood in the lower extremities and shifts plasma fluid into surrounding tissues. This results in a decrease in plasma volume (PV) and in hemoconcentration. There has been no integrative evaluation of concomitant neurohumoral and PV shifts with upright posture in normal subjects. We studied 10 healthy subjects after 3 days of stable Na+ and K+ intake. PV was assessed by the Evans blue dye method and by changes in hematocrit. Norepinephrine (NE), NE spillover, epinephrine (Epi), vasopressin, plasma renin activity, aldosterone, osmolarity, and kidney response expressed by urine osmolality and by Na+ and K+ excretion of the subjects in the supine and standing postures were all measured. We found that PV fell by 13% (375 +/- 35 ml plasma) over approximately 14 min, after which time it remained relatively stable. There was a concomitant decrease in systolic blood pressure and an increase in heart rate that peaked at the time of maximal decrease in PV. Plasma Epi and NE increased rapidly to this point. Epi approached baseline by 20 min of standing. NE spillover increased 80% and clearance decreased 30% with 30 min of standing. The increase in plasma renin activity correlated with an increase in aldosterone. Vasopressin increased progressively, but there was no change in plasma osmolarity. The kidney response showed a significant decrease in Na+ and an increase in K+ excretion with upright posture. We conclude that a cascade of neurohumoral events occurs with upright posture, some of which particularly coincide with the decrease in PV. Plasma Epi levels may contribute to the increment in heart rate with maintained upright posture.
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PMID:Effect of standing on neurohumoral responses and plasma volume in healthy subjects. 948 Sep 52


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