Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the relationship between right atrial pressure (RAP) and atrial natriuretic peptide (ANP) release during prolonged exercise in a hot environment (30 degrees C, 20% relative humidity), we studied with a Swan-Ganz catheter five male volunteers exercising on a cycle ergometer at 60% of peak aerobic power for 50 min. The ANP level increased from 14 +/- 3 (SE) to 69 +/- 10 pg/ml (P < 0.001) during the first 10 min of exercise as RAP rose from 4.3 +/- 0.8 to 6.9 +/- 1.1 mmHg (P < 0.001). The 10-min ANP level was significantly correlated with RAP (r = 0.88, P < 0.05) but not with heart rate, pulmonary arterial blood temperature, plasma norepinephrine, or plasma epinephrine. The 10-min RAP value was inversely correlated with blood volume (r = -0.98, P < 0.01) and also with stroke volume (r = -0.96, P < 0.01). In the next 20 min of exercise, ANP continued to increase to 101 +/- 12 pg/ml (P < 0.02 vs. 10 min) and remained at this level until 50 min of exercise, whereas RAP decreased and reached a level not significantly different from baseline at 50 min (5.7 +/- 1.0 mmHg; P < 0.01 vs. 10 min). This dissociation of ANP and RAP may have been related to the significant increases from the 10-min values of heart rate, blood temperature, norepinephrine (all P < 0.01), and epinephrine (P < 0.02) during the same period. These results suggest that ANP release is primarily controlled by atrial distension at the onset of exercise but that other stimulators may be involved thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Right atrial pressure and ANP release during prolonged exercise in a hot environment. 806 45

Hemodynamic and neurohumoral responses to supine bicycle exercise were evaluated in 16 patients with congestive heart failure (New York Heart Association functional class II-III) and in 8 normal controls. We determined cardiac output by the dye-dilution method, and forearm hemodynamics by plethysmography. The patients had lower resting cardiac and stroke indexes (p < 0.05) than the normal controls. During exercise, the increase in the cardiac index due to an increase in heart rate, was less than that in the controls. Resting and exercise systemic vascular resistance indices were higher in the patients (p < 0.05). The patients had lower resting forearm blood flow and higher forearm vascular resistance (p < 0.05), and the increases during exercise were comparable in the 2 groups. However, forearm venous tone and venous pressure increased more in the patients (p < 0.05). Exercise duration was shorter in the patients (p < 0.01). Resting plasma angiotensin II and norepinephrine were similar in the 2 groups, but plasma 6-keto-prostaglandin F1 alpha and atrial natriuretic peptide were higher in the patients. During exercise, all of these neurohumoral parameters rose more in the patients than in the controls (p < 0.05). Thus, the patients exhibited impaired central and peripheral hemodynamics both at rest and during exercise. The excessive exercise responses of all of the neurohumoral factors suggest that both vasoconstrictor and vasodilator systems are activated in heart failure.
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PMID:Hemodynamic and neurohumoral responses to exercise in patients with congestive heart failure. 809 32

The systemic hemodynamic, renal and hormonal responses to SQ 28,603 (N-[2-(mercaptomethyl)-1-oxo-3-phenylpropyl]-beta-alanine) the selective inhibitor of neutral endopeptidase 3.4.24.11, the angiotensin-converting enzyme inhibitor captopril and their combination were determined in conscious dogs after 1 or 3 weeks of rapid ventricular pacing. Coadministration of captopril (100 or 10 mumol/kg i.v.) and SQ 28,603 (10 mumol/kg i.v.) significantly reduced mean arterial pressure, systemic vascular resistance and renal vascular resistance and increased cardiac output, stroke volume and renal blood flow in the conscious dogs paced for 1 week. This pattern of hemodynamic improvement was not predicted by the activity of the individual inhibitors. The combination of inhibitors did not significantly increase sodium excretion because of the variability introduced by the depressor activity; however, the pressure-natriuresis curve was steeper and shifted leftward, indicating that sodium excretion was maintained at lower renal perfusion pressures. The increases in urinary and plasma levels of cyclic GMP and atrial natriuretic peptide stimulated by SQ 28,603 were not affected by captopril. The data indicated that the hemodynamic and renal responses produced by SQ 28,603, presumably by elevating atrial natriuretic peptide levels, were enhanced by suppression of angiotensin II or that the combination of inhibitors protected other vasodilator/natriuretic peptides from degradation. Qualitatively similar responses to SQ 28,603, captopril and the combination of inhibitors were obtained in dogs paced for 3 weeks. In summary, the combined angiotensin-converting enzyme and neutral endopeptidase 3.4.24.11 inhibitors improved systemic hemodynamics and maintained renal function in conscious dogs with pacing-induced heart failure.
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PMID:Systemic hemodynamics, renal function and hormonal levels during inhibition of neutral endopeptidase 3.4.24.11 and angiotensin-converting enzyme in conscious dogs with pacing-induced heart failure. 839 22

Because clinical indices of hydration state are insensitive, the estimation of correct postdialysis dry weight is still major problem. Recently, some new techniques have been introduced to assess postdialysis dry weight more accurately. The plasma concentrations of the biochemical markers atrial natriuretic peptide (ANP) and cGMP are related to intravascular hydration state. The echographically measured inferior caval vein diameter (VCD) is linked to right atrial pressure and blood volume (BV). Regional noninvasive conductivity measurements provide information about regional extracellular fluid volume (EFV). In this study of postdialysis ANP and cGMP concentrations, VCD and EFV yielded postdialysis diagnoses of hydration state in 18 patients on maintenance dialysis. In order to verify the established diagnosis, hemodynamic and BV changes during dialysis were studied. In postdialysis underhydrated patients, differentiated according to VCD and EFV standards, a pronounced decrease in BV, stroke volume, and left ventricular end-diastolic diameter compared with postdialysis normohydrated patients was observed. Hemodynamic and BV changes during dialysis were identical in the groups selected according to postdialysis ANP level. Only a difference in BV decrease was demonstrated between the groups selected according to postdialysis cGMP. Predialysis and postdialysis VCD correlated well with the corresponding EFV (r = 0.7 and r = 0.8, respectively). Because VCD and EFV were related and interpretation yielded diagnoses of postdialysis hydration state that were substantiated by the finding of classical hemodynamic features of underhydration, both are an asset in the diagnosis of postdialysis dry weight. cGMP values are less informative, and ANP does not provide any information at all.
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PMID:Assessment of postdialysis dry weight: a comparison of techniques. 840 74

Plasma atrial natriuretic peptide (ANP) was measured with radioimmunoassay in 39 patients with acute stroke. The mean level was 144.3 +/- 8.7 pg/ml; this was significantly higher in comparison with those in normal controls (55.8 +/- 4.7 pg/ml, n = 20) and hypertension patients (87.7 +/- 8.0 pg/ml, n = 15). Serial measurement of ANP level in 6 patients showed that it was elevated on the first day of the stroke, reached to its peak on the second or third day and returned to normal after two weeks. Five patients had hyponatremia following the attack of stroke and the plasma ANP level was further elevated. It is suggested that elevated plasma ANP level might be a pathogenetic factor of the accompanying hyponatremia in stroke.
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PMID:[Increased concentration of plasma atrial natriuretic peptide in patients with acute stroke and its significance]. 840 32

The cardiovascular consequences of endothelin (ET) blockade with the ETA-receptor antagonist FR 139317 were evaluated by determining the long-term effects of the drug on hemodynamic, hormonal, renal and structural parameters in stroke-prone spontaneously hypertensive rats (SHR-SP). Young SHR-SP on a high-sodium diet develop malignant hypertension accompanied by renovascular and cerebrovascular lesions. In control SHR-SP the systolic blood pressure increased from 196 +/- 3 to 260 +/- 4 mm Hg, whereas in animals treated with FR 139317 (20 mg/kg intraperitoneally, twice daily) it increased only from 196 +/- 4 to 212 +/- 3 mm Hg during a treatment period of 6 weeks. There was also an increase in heart weight. At the end of the experiment the plasma levels of atrial natriuretic peptide and brain natriuretic peptide were significantly lower in the group treated with FR 139317 than in the controls. The endothelin plasma levels were significantly higher and the plasma renin activity was lower in the group treated with the endothelin receptor antagonist. These data indicate that endothelin is involved in the maintenance of high blood pressure and cardiac hypertrophy in malignant hypertension, as exemplified by SHR-SP.
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PMID:Prolonged endothelin blockade prevents hypertension and cardiac hypertrophy in stroke-prone spontaneously hypertensive rats. 855 37

The hemodynamic and renal effects of strong diuretic atrial natriuretic peptide (ANP) were investigated in 12 patients with acute myocardial infarction. Strong diuretic ANP was administered as a bolus injection of 100 micrograms and followed by a continuous infusion of 2 micrograms/kg within 10 minutes into the right atrium via a catheter. We found that strong diuretic ANP induced an increase in cardiac index and stroke volume index. Right atrial pressure, pulmonary arterial pressure, pulmonary capillary wedge pressure, systemic vascular resistance and pulmonary vascular resistance were decreased after ANP infusion. The maximal responses were observed immediately after the infusion was completed. No significant change of arterial blood pressure and heart rate was observed. Furthermore, strong diuretic ANP also increased the urine volume, urinary sodium, urinary chloride and urinary potassium. These results suggest that strong diuretic ANP infusion may induce significant changes of hemodynamics and may be used to prevent the development of severe circulatory volume overload in patients with AMI.
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PMID:[Hemodynamic and renal effects of strong diuretic atrial natriuretic peptide in patients with acute myocardial infarction]. 873 59

Exercise tolerance of heart transplant patients is often limited. Central and peripheral factors have been proposed to explain such exercise limitation but, to date, the leading factors remain to be determined. We examined how a short-term endurance exercise training programme may improve exercise capacity after heart transplantation, and whether atrial natriuretic peptide (ANP) release may contribute to the beneficial effects of exercise training by minimizing ischaemia and/or cardiac and circulatory congestion through its vasodilatation and haemoconcentration properties. Seven heart transplant recipients performed a square-wave endurance exercise test before and after 6 weeks of supervised training, while monitoring haemodynamic parameters, ANP and catecholamine concentrations. After training, the maximal tolerated power and the total mechanical work load increased from 130.4 (SEM 6.5) to 150.0 (SEM 6.0) W (P < 0.05) and from 2.05 (SEM 0.1) to 3.58 (SEM 0.14) kJ.kg-1 (P < 0.001). Resting heart rate decreased from 100.0 (SEM 3.4) to 92.4 (SEM 3.5) beats.min-1 (P < 0.05) but resting and exercise induced increases in cardiac output, stroke volume, right atrial, pulmonary capillary wedge, systemic and pulmonary artery pressures were not significantly changed by training. Exercise-induced decrease of systemic vascular resistance was similar before and after training. After training arterio-venous differences in oxygen content were similar but maximal lactate concentrations decreased from 6.20 (SEM 0.55) to 4.88 (SEM 0.6) mmol.l-1 (P < 0.05) during exercise. Similarly, maximal exercise noradrenaline concentration tended to decrease from 2060 (SEM 327) to 1168 (SEM 227) pg.ml-1. A significant correlation was observed between lactate and catecholamines concentrations. The ANP concentration at rest and the exercise-induced ANP concentration did not change throughout the experiment [104.8 (SEM 13.1) pg.ml-1 vs 116.0 (SEM 13.5) pg.ml-1 and 200.0 (SEM 23.0) pg.ml-1 vs 206.5 (SEM 25.9) pg.ml-1, respectively]. The results of this study suggested that the significant improvement in exercise capacity observed after this short-term endurance training period may have arisen mainly through peripheral mechanisms, associated with the possible decrease in plasma catecholamine concentrations and reversal of muscle deconditioning and/or prednisone-induced myopathy.
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PMID:Effect of short-term endurance training on exercise capacity, haemodynamics and atrial natriuretic peptide secretion in heart transplant recipients. 878 55

Doppler echocardiographic indices of diastolic function and systemic haemodynamics were studied in response to infusions of atrial natriuretic peptide (0.5, 1, 2, 5 pmol.kg-1.min-1) and placebo (0.9% (w/v) saline) in ten normal male subjects. Compared with placebo, atrial natriuretic peptide infusion produced a significant and dose-related reduction in the isovolumic relaxation time [(mean and 95% CI) -5.9 (-9.2 to -2.6) ms (P < 0.01) at 5 pg.kg-1 min-1] and a significant increase in the ratio between early and late transmitral peak velocities [0.46 (0.02 to 0.89) (P < 0.05) at 5 pg.kg-1 min-1]. No significant changes in heart rate, blood pressure or aortic stroke distance were observed with infusion of atrial natriuretic peptide compared with placebo. These data suggest that pathophysiological plasma concentrations of atrial natriuretic peptide improve diastolic function by increasing the rate of myocardial relaxation.
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PMID:Acute effects of atrial natriuretic peptide on left ventricular diastolic function. a pulsed wave Doppler study in man. 888 69

Studies in healthy human subjects subjected to lower body positive pressure (LBPP) have failed to elucidate many of the physiologic effects of this maneuver. In 7 healthy, well-hydrated men we studied the following responses to LBPP (35 mm Hg, 1 hour, supine position): systemic and renal hemodynamics; urine volume (UV), urine osmolality (Uosm), and urine sodium level (UNaV); free water (CH20) and osmolar (Cosm) clearances; plasma renin activity (PRA); levels of aldosterone (PA), cortisol (CORT), norepinephrine (NE), atrial natriuretic peptide (ANP), and vasopressin (AVP); osmolality (Posm); and serum sodium level. Subjects were restudied on a control day with zero trouser pressure. The recorded changes (p < 0.05) when comparing the LBPP day with the control day were as follows: fractional Na+ reabsorption increased (98.7% +/- 0.2% to 99.3% +/- 0.1%) and UNaV decreased (0.19 +/- 0.03 mEq/min to 0.10 +/- 0.01 mEq/min), with concomitant increases in PRA (1.7 +/- 0.2 ng/ml/90 min to 4.5 +/- 1.8 ng/ml/90 min), PA (7.7 +/- 0.7 ng/dl to 9.3 +/- 1.5 ng/dl), and CORT (13.0 +/- 2.6 mg/dl to 19.2 +/- 3 mg/dl); the increase in blood pressure with LBPP (96 +/- 3 mm Hg to 112 +/- 4 mm Hg) was greater than that during control conditions. Renal plasma flow tended to display an interactive pattern across days, with a slight decline during LBPP (5%) and a slight elevation under control conditions (9%). On the LBPP day only, filtered Na+ declined (15 +/- I mEq/min to 12 +/- 1 mEq/min) as a function of reduced glomerular filtration rate (112 +/- 5 ml/min to 91 +/- 7 ml/min), blood volume decreased (by 2.7% +/- 0.7%), CO decreased (5.5 +/- 0.3 L/min to 4.7 +/- 0.3 L/min), and stroke volume declined (101 +/- 6 ml to 84 +/- 3 ml). On both days, NE increased (control, 221 +/- 23 pg/ml to 340 +/- 33 pg/ml; LBPP, 236 +/- 17 pg/ml to 369 +/- 31 pg/ml) and ANP increased (control, 47 +/- 7 pg/ml to 97 +/- 21 pg/ml; LBPP, 49 +/- 10 pg/ml to 104 +/- 30 pg/ml). We concluded that LBPP reduces renal sodium excretion. The mechanism for this reduction is not known, although it did occur in association with an increase in plasma renin activity, which in turn results from mechanical reduction of renal perfusion, stress-related CORT stimulation, a reflex-based elevation in peripheral vascular resistance leading to a reflex increase in plasma renin activity, or a combination of these.
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PMID:Hemodynamic, renal, and hormonal responses to lower body positive pressure in human subjects. 896 Jun 42


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