Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Based on analysis of 399 symptomatic patients with mitral valve prolapse (MVP) and the reported experience of others, we developed a clinical classification in order to improve nosology, provide better identification and promote insight into the mechanism of symptoms in patients with MVP. The heading of anatomic MVP designates those in whom symptoms or complications were primarily or directly related to valvular dysfunction and the heading of MVP syndrome designates those patients in whom symptoms cannot be explained on the basis of valvular dysfunction alone. Patients with MVP syndrome present with a symptom complex which results from various forms of neuroendocrine or autonomic dysfunction; the most common symptoms include chest pain, palpitations, cardiac arrhythmias, orthostatic phenomena, syncope, presyncope, fatigue, exercise intolerance, dyspnea and neuropsychiatric symptoms (Table 1). Mechanisms underlying the condition have been shown to include increased adrenergic activity, disturbances of catecholamine regulation, hyperresponsiveness to adrenergic stimulation, anomalous beta-adrenergic receptors, dysfunction of the parasympathetic portion of the autonomic nervous system, disturbances in renin-aldosterone regulation, decreased intravascular volume, diminished left ventricular diastolic volume in the upright position as well as abnormal secretion of atrial natriuretic factor (Table 2). In MVP syndrome, alterations of the heart, kidney, the adrenals and the autonomic nervous system coexist and interact, creating a complex "neuro-endocrine cardiovascular process" which may account for many of the symptoms otherwise unexplained on the basis of the valvular abnormality alone.
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PMID:Mitral valve prolapse syndrome: neuro-endocrinological aspects. 284 39

The purpose of this investigation was to test the hypothesis that endurance exercise trained (ET) subjects would demonstrate a greater reduction in orthostatic tolerance as compared to untrained (UT) subjects following prior exposure to -6 degrees head-down tilt (HDT) because vasoactive hormone and enzyme responses to head-up tilt (HUT) would be decreased following HDT so as to predispose ET subjects to orthostatic intolerance. Six ET subjects (VO2peak = 4.52 +/- 0.20 L/min) were matched for age and height with six UT subjects (VO2peak = 3.26 +/- 0.22 L/min; p < 0.01). After 30 min of supine rest, subjects were exposed to 30 min of head-up tilt (HUT) at 70 degrees, then on a separate occasion, 4 h of HDT (-6 degrees) followed by 30 min of HUT. The HUT involved passive standing for 30 min or until subjects became presyncopal. Blood sampled from the antecubital vein at min 1, 15, and 30, or at presyncope was analyzed for atrial natriuretic peptide (ANP), aldosterone (PA), arginine vasopressin (AVP), plasma renin activity (PRA), and norepinephrine (NE), while BP and HR were continuously monitored. All subjects tolerating 30 min of HUT, after either condition, had significantly increased (p < 0.05) levels of PRA at the 30th min. Following 4 h of HDT, five of six UT subjects and only one of six ET subjects endured 30 min of HUT. The most marked difference during HUT after prior exposure to HDT was a significant increase in AVP (p < 0.05) at the onset of HUT observed only for the UT subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hormonal responses during orthostasis following 4 hours of head-down tilt. 835 13

We tested the hypothesis that one bout of maximal exercise performed at the conclusion of prolonged simulated microgravity would improve blood pressure stability during an orthostatic challenge. Heart rate (HR), mean arterial blood pressure (MAP), norepinephrine (NE), epinephrine (E), arginine vasopressin (AVP), plasma renin activity (PRA), atrial natriuretic peptide (ANP), cardiac output (Q), forearm vascular resistance (FVR), and changes in leg volume were measured during lower body negative pressure (LBNP) to presyncope in seven subjects immediately prior to reambulation from 16 days of 6 degrees head-down tilt (HDT) under two experimental conditions: 1) after maximal supine cycle ergometry performed 24 h before returning to the upright posture (exercise) and 2) without exercise (control). After HDT, the reduction of LBNP tolerance time from pre-HDT levels was greater (P = 0.041) in the control condition (-2.0 +/- 0.2 min) compared with the exercise condition (-0.4 +/- 0.2 min). At presyncope after HDT, FVR and NE were higher (P < 0.05) after exercise compared with control, whereas MAP, HR, E, AVP, PRA, ANP, and leg volume were similar in both conditions. Plasma volume (PV) and carotid-cardiac baroreflex sensitivity were reduced after control HDT, but were restored by the exercise treatment. Maintenance of orthostatic tolerance by application of acute intense exercise after 16 days of simulated microgravity was associated with greater circulating levels of NE, vasoconstriction, Q, baroreflex sensitivity, and PV.
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PMID:Application of acute maximal exercise to protect orthostatic tolerance after simulated microgravity. 889 72

Plasma vasoactive hormone concentrations [epinephrine (p(Epi)), norepinephrine (p(NE)), ANG II (p(ANG II)), vasopressin (p(VP)), endothelin-1 (p(ET-1))] and plasma renin activity (p(RA)) were measured periodically and compared during lower body negative pressure (LBNP) to test the hypothesis that responsiveness of the renin-angiotensin system, the latter being one of the most powerful vasoconstrictors in the body, is of major importance for LBNP tolerance. Healthy men on a controlled diet (2,822 cal/day, 2 mmol. kg(-1). day(-1) Na(+)) were exposed to 30 min of LBNP from -15 to -50 mmHg. LBNP was uneventful for seven men [25 +/- 2 yr, high-tolerance (HiTol) group], but eight men (26 +/- 3 yr) reached presyncope after 11 +/- 1 min [P < 0.001, low-tolerance (LoTol) group]. Mean arterial pressure (MAP) did not change measurably, but central venous pressure and left atrial diameter decreased similarly in both groups (5-6 mmHg, by approximately 30%, P < 0.05). Control (0 mmHg LBNP) hormone concentrations were similar between groups, however, p(RA) differed between them (LoTol 0.6 +/- 0.1, HiTol 1.2 +/- 0.1 ng ANG I. ml(-1). h(-1), P < 0.05). LBNP increased (P < 0. 05) p(RA) and p(ANG II), respectively, more in the HiTol group (9.9 +/- 2.2 ng ANG I. ml(-1). h(-1) and 58 +/- 12 pg/ml) than in LoTol subjects (4.3 +/- 0.9 ng ANG I. ml(-1). h(-1) and 28 +/- 6 pg/ml). In contrast, the increase in p(VP) was higher (P < 0.05) in the LoTol than in the HiTol group. The increases (P < 0.05) for p(NE) were nonsignificant between groups, and p(ET-1) remained unchanged. Thus there may be a causal relationship between attenuated activation of p(RA) and p(ANG II) and presyncope, with p(VP) being a possible cofactor. Measurement of resting p(RA) may be of predictive value for those with lower hypotensive tolerance.
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PMID:Low LBNP tolerance in men is associated with attenuated activation of the renin-angiotensin system. 1095 39

Orthostatic intolerance (OI) is a major problem after spaceflight. Its etiology remains uncertain, but reports have pointed toward an individual susceptibility to OI. We hypothesized that individual predisposition plays an important role in post-bed rest OI. Twenty-four healthy male subjects were equilibrated on a constant diet, after which they underwent tilt-stand test (pre-TST). They then completed 14-16 days of head-down-tilt bed rest, and 14 of the subjects underwent repeat tilt-stand test (post-TST). During various phases, the following were performed: 24-h urine collections and hormonal measurements, plethysmography, and cardiovascular system identification (a noninvasive method to assess autonomic function and separately quantify parasympathetic and sympathetic responsiveness). Development of presyncope or syncope defined OI. During pre-TST, 11 subjects were intolerant and 13 were tolerant. At baseline, intolerant subjects had lower serum aldosterone (P < 0.01), higher excretion of potassium (P = 0.01), lower leg venous compliance (P = 0.03), higher supine parasympathetic responsiveness (P = 0.02), and lower standing sympathetic responsiveness (P = 0.048). Of the 14 subjects who completed post-TST, 9 were intolerant and 5 were tolerant. Intolerant subjects had lower baseline serum cortisol (P = 0.03) and a higher sodium level (P = 0.02) compared with tolerant subjects. Thus several physiological characteristics were associated with increased susceptibility to OI. We propose a new model for OI, whereby individuals with greater leg venous compliance recruit compensatory mechanisms (activation of the renin-angiotensin-aldosterone system and sympathetic nervous system, and withdrawal of the parasympathetic nervous system) in the face of daily postural challenges, which places them at an advantage to face orthostatic stress. With head-down-tilt bed rest, the stimulus to recruit compensatory mechanisms disappears, and differences between the two subgroups attenuate.
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PMID:Role of individual predisposition in orthostatic intolerance before and after simulated microgravity. 1507 9

Orthostatic intolerance (OI) is a major problem following spaceflight, and, during flight, astronauts also experience sleep restriction. We hypothesized that sleep restriction will compound the risk and severity of OI following simulated microgravity and exaggerate the renal, cardioendocrine, and cardiovascular adaptive responses to it. Nineteen healthy men were equilibrated on a constant diet, after which they underwent a tilt-stand test. They then completed 14-16 days of simulated microgravity [head-down tilt bed rest (HDTB)], followed by repeat tilt-stand test. During HDTB, 11 subjects were assigned to an 8-h sleep protocol (non-sleep restricted), and 8 were assigned to a sleep-restricted protocol with 6 h of sleep per night. During various phases, the following were performed: 24-h urine collections, hormonal measurements, and cardiovascular system identification. Development of presyncope or syncope defined OI. There was a significant decrease in time free of OI (P = 0.02) and an increase in OI occurrence (P = 0.06) after HDTB among all subjects. However, the increase in OI occurrence did not differ significantly between the two groups (P = 0.60). The two groups also experienced similar physiological changes with HDTB (initial increase in sodium excretion; increased excretion of potassium at the end of HDTB; increase in plasma renin activity secretion without a change in serum or urine aldosterone). No significant change in autonomic function or catecholamines was noted. Simulated microgravity leads to increased OI, and sleep restriction does not additively worsen OI in simulated microgravity. Furthermore, conditions of sleep restriction and nonsleep restriction are similar with respect to renal, cardioendocrine, and cardiovascular responses to simulated microgravity.
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PMID:Sleep restriction does not affect orthostatic tolerance in the simulated microgravity environment. 1523 56

Exposure to LBNP results in body fluid shift to lower extremities similarly as under influence of orthostatic stress. In susceptible persons it leads to syncope. For better understanding why certain individuals are more susceptible to orthostatic challenges it seemed necessary to collect more data on hemodynamic and neuroendocrine adjustments occurring before onset of presyncopal symptoms Accordingly, in this study heart rate (HR), blood pressure (BP), stroke volume (SV), cardiac output (CO), hematocrit, plasma catecholamines, adrenomedullin, ACTH and plasma renin activity (PRA) were measured in 24 healthy men during graded LBNP (-15, -30 and -50 mmHg). Thirteen subjects completed the test (HT group) whereas 11 had presyncope signs or symptoms at -30 mmHg or at the beginning of -50 mmHg (LT group). Comparison of these groups showed that LT subjects had lower baseline total peripheral resistance and higher plasma adrenomedullin. During LBNP plasma catecholamine and PRA increases were even greater in LT than in HT group while plasma adrenomedullin elevations were similar in both groups. Plasma ACTH increased only in LT group following presyncope symptoms. Low tolerant group showed more rapid decline of SV and CO than HT subjects from the beginning of LBNP. It is suggested that measurements of SV at the level of LBNP which did not evoke any adverse symptoms may be of predictive value for lower orthostatic tolerance.
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PMID:Hemodynamic and neuroendocrine predictors of lower body negative pressure (LBNP) intolerance in healthy young men. 1598 1

The KAATSU training is a unique method of muscle training with restricting venous blood flow, which might be applied to prevent muscle atrophy during space flight, but the effects of KAATSU in microgravity remain unknown. We investigated the hemodynamic responses to KAATSU during actually simulated weightlessness (6 degrees head-down tilt for 24 h, n = 8), and compared those to KAATSU in the seated position before bed rest. KAATSU was applied to the proximal ends of both the thighs. In the seated position before bed rest, sequential incrementing of KAATSU cuff pressure and altering the level of blood flow restriction resulted in a decrease in stroke volume (SV) with an increase in heart rate (HR). KAATSU (150-200 mmHg) decreased SV comparable to standing. Following 24-h bed rest, body mass, blood volume (BV), plasma volume (PV), and diameter of the inferior vena cava (IVC) were significantly reduced. Norepinephrine (NOR), vasopressin (ADH), and plasma renin activity (PRA) tend to be reduced. A decrease in SV and CO induced by KAATSU during the simulated weightlessness was larger than that in the seated position before bed rest, and one of eight subjects developed presyncope due to hypotension during 100 mmHg KAATSU. High-frequency power (HF(RR)) decreased during KAATSU and standing, while low-frequency/high-frequency power (LF(RR)/HF(RR)) increased significantly. NOR, ADH and PRA also increased during KAATSU. These results indicate that KAATSU blood flow restriction reproduces the effects of standing on HR, SV, NOR, ADH, PRA, etc., thus stimulating a gravity-like stress during simulated weightlessness. However, syncope due to lower extremity blood pooling and subsequent reduction of venous return may be induced during KAATSU in microgravity as reported in cases of lower-body negative pressure.
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PMID:Hemodynamic responses to simulated weightlessness of 24-h head-down bed rest and KAATSU blood flow restriction. 1865 Nov 62

We hypothesized that orthostatic tolerance is higher in young, healthy black compared with white women. To determine orthostatic tolerance, 22 women (11 black and 11 white) underwent graded lower body negative pressure to presyncope. We measured blood pressure, heart rate, and R-R interval (ECG) continuously at baseline and through all of the levels of lower body negative pressure. Blood samples were taken at baseline along with presyncope for the measurement of plasma catecholamine concentrations, serum aldosterone concentration, and plasma renin activity. Cumulative stress index, the sum of the product of time and lower body negative pressure, was the indicator of orthostatic tolerance. Orthostatic tolerance in the black women was greater than in the white women [cumulative stress index: -1003 (375) versus -476 (197); P<0.05]. Although plasma concentrations of norepinephrine increased in both groups at presyncope, the increase was greater in black [Deltaplasma concentrations of norepinephrine: 167 (123)] versus white women [86 (64); P<0.05], as was the increase in PRA [DeltaPRA 2.6 (1.0) versus 0.6 (0.9) ng of angiotensin II x mL(-1) x h(-1); P<0.05, for black and white women, respectively). Although heart rate increased and R-R interval decreased to a greater extent during lower body negative pressure in black women compared with white women (ANOVA: P<0.05), baroreflex function (ie, slope R-R interval versus systolic blood pressure) was unaffected by race. These data indicate that orthostatic tolerance is greater in black compared with white women, which appears to be a function of greater sympathetic nervous system responses to orthostatic challenges.
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PMID:Greater orthostatic tolerance in young black compared with white women. 2045 5

Approximately 500,000 American premenopausal women have the postural orthostatic tachycardia syndrome (POTS). We tested the hypothesis that in POTS women during orthostasis, activation of the renin-angiotensin-aldosterone system is greater, leading to better compensated hemodynamics in the midluteal phase (MLP) than in the early follicular phase of the menstrual cycle. Ten POTS women and 11 healthy women (controls) consumed a constant diet 3 days before testing. Hemodynamics and renal-adrenal hormones were measured while supine and during 2-hour standing. We found that blood pressure was similar, heart rate and total peripheral resistance were greater, and cardiac output and stroke volume were lower in POTS subjects than in controls during 2-hour standing. In controls, hemodynamic parameters were indistinguishable between menstrual phases. In POTS subjects, cardiac output and stroke volume were lower and total peripheral resistance was greater in the early follicular phase than MLP after 30 minutes of standing; however, blood pressure and heart rate were similar between phases. Plasma renin activity (9+/-6 [SD] versus 13+/-9 ng/mL per hour; P=0.04) and aldosterone (43+/-22 versus 55+/-25 ng/dL; P=0.02) were lower in the early follicular phase than MLP in POTS subjects after 2 hours of standing. Catecholamine responses were similar between phases. The percentage rate of subjects having presyncope was greater in the early follicular phase than MLP for both groups (chi(2) P<0.01). These results suggest that the menstrual cycle modulates the renin-angiotensin-aldosterone system and affects hemodynamics during orthostasis in POTS. The high estrogen and progesterone in the MLP are associated with greater increases in renal-adrenal hormones and presumably more volume retention, which improve late-standing tolerance in these patients.
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PMID:Menstrual cycle affects renal-adrenal and hemodynamic responses during prolonged standing in the postural orthostatic tachycardia syndrome. 2047 33


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