Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment of severe hypertension is beneficial, but reversibility of target-organ damage has not been characterized. Serial studies were performed in 15 patients with severe essential hypertension (age of 56 +/- 3 years, mean +/- SEM) treated for 1 year with 60 to 150 mg/day of continuous-release nifedipine; 3 patients required 50 mg of chlorthalidone/day to lower diastolic blood pressure (BP) to less than 95 mm Hg. Left ventricular (LV) structure and function was evaluated with two-dimensional-directed M-mode echocardiography, digitized from videotape and analyzed blindly. BP was markedly reduced from 194 +/- 8/115 +/- 4 to 146 +/- 4/88 +/- 14 mm Hg (p less than 0.0001) and maintained at this level for 1 year. Posterior wall and septal LV thickness, elevated at entry (12.9 +/- 0.1 and 13.4 +/- 0.1 mm), dropped steadily over 1 year into the normal range (10.0 +/- 0.03 and 11.2 +/- 0.1 mm, p less than 0.001). LV mass index, above 95% for normals at entry, decreased by 19% at 6 months (129 +/- 10 to 104 +/- 7 g/m2, p less than 0.01), and remained at this level at 1 year. LV fractional shortening rose steadily over 1 year from 34 to 42% (p less than 0.02). Atrial natriuretic peptide, which reflects LV filling pressures, was markedly elevated at entry, but was significantly reduced by 6 months (76 +/- 22 vs. 45 +/- 14 pg/ml, p less than 0.05). Sustained reduction of arterial BP with continuous-release nifedipine for 1 year normalizes LV mass, improves LV systolic function, and reduces circulating levels of atrial natriuretic peptide.
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PMID:Effect of nifedipine GITS on left ventricular mass and diastolic function in severe hypertension. 171 75

Recent studies have demonstrated that elevation of plasma atrial natriuretic factor (ANF) levels may produce significant bronchodilation in the constricted asthmatic airway. The current study was designed to examine the effect of both physiologic and pharmacologic plasma levels of ANF on bronchial reactivity to histamine in asthmatic subjects. A total of eight atopic men with well-controlled asthma were studied, mean (SD) FEV1 3.50 (0.73) L, equivalent to 87 (11)% of predicted; bronchial reactivity as measured by histamine PC20 was 0.77 mg/ml (geometric mean). On four separate study days infusions of 1, 3, or 10 pmol/kg/min of ANF or placebo were administered in a double-blind, randomized manner. Once steady-state plasma levels had been achieved, measurement of bronchial reactivity was repeated. Mean (SEM) basal ANF level was 18.5 (3.5) pg/ml and rose to 41 (4.3), 157 (15), and 500 (30) pg/ml with increasing doses of ANF. With placebo infusion geometric mean histamine PC20 was 0.77 mg/ml and rose to 1.15 mg/ml (p less than 0.05), 1.90 mg/ml (p less than 0.001), and 3.38 mg/ml (p less than 0.001), corresponding to a 1.5-, 2.5-, and 4.4-fold protection with respective ANF infusions. There was no significant change in plasma epinephrine. These results show that at both physiologic and pathophysiologic plasma levels ANF may significantly decrease bronchial reactivity to histamine in asthma.
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PMID:Influence of elevated plasma levels of atrial natriuretic factor on bronchial reactivity in asthma. 182 92

The influence of preeclampsia on the circulating concentrations of the 28-amino-acid carboxy terminus (C-terminus) (i.e., atrial natriuretic factor) and the amino terminus (N-terminus) of the 126-amino-acid atrial natriuretic factor prohormone (pro ANF) was studied in the third trimester with the use of three specific radioimmunoassays that recognize: (1) atrial natriuretic factor (i.e., amino acids 99 to 126), (2) the whole 98-amino-acid N-terminus, and (3) amino acids 31 to 67 from the midportion of the N-terminus of the prohormone. The C-terminus was significantly increased (p less than 0.001) in the third trimester in women with preeclampsia, the mean +/- SEM of 15 subjects was 150 +/- 7 pg/ml versus 89 +/- 7 pg/ml in the third trimester in 12 women during normal pregnancies and 65 +/- 2 pg/ml in 19 healthy nonpregnant women. The whole 98-amino-acid N-terminus, likewise, was significantly increased (p less than 0.001) in women with preeclampsia to 4706 +/- 629 pg/ml versus 2160 +/- 79 pg/ml in women in the third trimester of normal pregnancies and versus the circulating concentration of 1847 +/- 127 pg/ml in healthy nonpregnant women. ProANF 31 to 67 mean circulating concentration in preeclampsia was 4638 +/- 725 pg/ml, which was also significantly (p less than 0.001) increased compared with its mean circulating concentration in the third trimester of normal pregnancy of 1758 +/- 83 pg/ml or that in healthy nonpregnant women (1400 +/- 105 pg/ml). The circulating concentrations of both the N-terminus and C-terminus of the atrial natriuretic factor prohormone decreased within 24 hours after delivery in contrast to a normal pregnancy in which they both increase post partum. These results indicate a marked difference in the metabolism of both the N-terminus and the C-terminus of the atrial natriuretic factor prohormone in women with preeclampsia versus that in women with normal pregnancies or that in healthy nonpregnant women.
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PMID:The N-terminal and C-terminal portions of the atrial natriuretic factor prohormone increase during preeclampsia. 182 48

Atrial natriuretic peptide (ANP) was measured in arterial and venous umbilical cord plasma at the time of delivery by cesarean section in pre-eclamptic (n = 7) and normal women (n = 6). In addition venous samples were obtained from pre-eclamptic (n = 7) and normal pregnant women (n = 7) near term. ANP plasma levels were higher in pregnant women with pre-eclampsia than in normal pregnant women (27.9 +/- 4.4 [mean +/- SEM] and 14.1 +/- 2.5 pmol l-1, respectively, P less than 0.05). Immediately after delivery plasma ANP in pre-eclamptic mothers was 66.7 +/- 12.8 pmol l-1 compared to 13.9 +/- 2.2 pmol l-1 in normal mothers (P less than 0.01). However, in the pre-eclamptic group the levels of ANP in arterial and venous umbilical cord plasma (19.5 +/- 4.2 and 16.7 +/- 4.3 pmol l-1, respectively) were significantly (P less than 0.01) lower than ANP levels in arterial and venous cord plasma (39.6 +/- 1.0 and 31.1 +/- 4.2 pmol l-1, respectively) from normal mothers. It is concluded that the increased ANP plasma level in pre-eclamptic women originates from a maternal source. In addition, since the ANP level is lower in cord plasma than in maternal plasma in pre-eclampsia, feto-placental volume homeostasis may also be changed in pre-eclampsia.
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PMID:Atrial natriuretic peptide concentrations in umbilical cord plasma from pre-eclamptic women. 182 94

Atrial natriuretic peptide (ANP), a 28-amino acid peptide, is produced and secreted by cardiac atriocytes to modulate cardiovascular functions. Recently, biologically active receptors for ANP have been demonstrated in the spleen; we report here the production of ANP-(5-28) and its 15-kDa (K) mol wt (Mr) presumptive precursors by macrophages of rat splenic tissues. Splenic, hypothalamic, and heart tissues were collected from adult male Sprague-Dawley rats and acid extracted for ANP assay. The splenic content of immunoreactive (ir) ANP (mean +/- SEM, 428 +/- 68 pg/tissue; n = 7) was approximately a fifth of that found in the hypothalamus and about 4 orders of magnitude lower than that in the heart of the same animals. The Sephadex G-50 column profile of splenic extracts revealed two immunoreactive peaks; the major peak eluted in positions consistent with 15K Mr, while a minor peak coeluted with synthetic rat ANP-(1-28) of 3K Mr. HPLC analysis of the 3K Mr species showed a single peak of immunoreactivity, which eluted with a retention time similar to that of ANP-(5-28). In rat splenic sections, immunoperoxidase localization of ir-ANP revealed positive cells sparsely distributed in marginal sinuses and the red pulp of the tissue; employing a double staining technique, S22, a surface marker for macrophages, was colocalized on the same splenocytes. Furthermore, colorimetric in situ hybridization with antisense oligonucleotide probes labeled with digoxigenin, identified specific signals for pro-ANP mRNA in splenocytes of tissue sections. In monolayer cultures of vehicle-treated splenocytes, approximately 87% of the adherent cells stained positive for S22; this marker was colocalized with ir-ANP in approximately 15% of the cells. Twenty-four-hour treatment with lipopolysaccharide (50 micrograms/ml), a bacterial endotoxin, tripled the proportion of adherent cells (32 +/- 4%; P less than 0.01) staining positive for ir-ANP over that in control cultures (mean +/- SEM, 11 +/- 3%; 10(4) cells/sample; n = 5). Furthermore, an equivalent dose of lipopolysaccharide, but not Concanavalin-A (50 micrograms/ml), quadrupled ir-ANP content compared to that in vehicle-treated cultures (less than 5 pg/well). Thus, our findings suggest that ANP-(5-28) is produced by a small population of splenic macrophages and raise the possibility that the peptide may play a signalling role at the tissue level.
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PMID:Evidence for atrial natriuretic peptide-(5-28) production by macrophages of the rat spleen: an immunochemical and nonradioactive in situ hybridization approach. 183 Feb 72

Plasma concentrations of the immunoreactive N-terminus, C-terminus and 4,000-dalton midportion of the N-terminus of the atrial natriuretic factor (ANF) prohormone were measured before and after hemodialysis in 13 patients with end-stage renal disease. There was a significant (p less than 0.001) fall in the mean plasma concentration of the C-terminus (i.e. ANF, amino acids 99-126 of the prohormone) from 123 +/- 25 to 80 +/- 22 fmol/ml (mean +/- SEM) with dialysis. The whole N-terminus, on the other hand, increased from 9,336 +/- 2,011 to 11,021 +/- 2,134 fmol/ml after dialysis (p less than 0.002). Pro ANF 31-67 (i.e. amino acids 31-67 of the prohormone) increased postdialysis from 27,775 +/- 4,300 to 31,040 +/- 4,840 fmol/ml (p less than 0.003). Only 1.5% of pro ANF 1-98 and pro ANF 31-67 were cleared by the dialyzer membrane while 15% of ANF crossed the membrane. Thus, with hemodialysis the C-terminus decreases while the N-terminus and pro ANF 31-67 from the midportion of the N-terminus of the ANF prohormone increase in plasma which is partially explained by their respective abilities to cross the dialyzer membrane.
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PMID:Change in plasma immunoreactive N-terminus, C-terminus, and 4,000-dalton midportion of atrial natriuretic factor prohormone with hemodialysis. 183 Mar 73

Isotonic volume expansion results in atrial natriuretic factor release by cardiac myocytes. Because pregnancy produces well-established alterations in fluid homeostasis and cardiovascular function, changes in atrial natriuretic factor responses may also occur. This study compares plasma atrial natriuretic factor responses to short-term volume expansion in pregnant and nonpregnant sheep. Seven pregnant and six nonpregnant ewes were chronically instrumented and subjected to a series of four experiments consisting of a control group (no infusion) and groups that received 10 ml/kg, 25 ml/kg, and 40 ml/kg isotonic saline infusion over a 30-minute period. The order of the experiments was random and separated by greater than or equal to 48 hours. Plasma atrial natriuretic factor, osmolality, right atrial pressure, blood pressure, and urine flow were measured over a 150-minute observation period. After volume expansion, plasma atrial natriuretic factor levels rose significantly from 39 +/- 4 pg/ml (mean +/- SEM) to 49 +/- 7 pg/ml, 36 +/- 4 pg/ml to 62 +/- 19 pg/ml, and 39 +/- 6 pg/ml to 67 +/- 14 pg/ml in the nonpregnant group 10 ml/kg, 25 ml/kg, and 40 ml/kg experiments, respectively. In the pregnant groups, plasma atrial natriuretic factor levels rose from 50 +/- 2 pg/ml to 75 +/- 20 pg/ml, 43 +/- 5 pg/ml to 57 +/- 5 pg/ml, and 46 +/- 4 pg/ml to 67 +/- 7 pg/ml, respectively. Differences in atrial natriuretic factor responses were not seen between pregnant and nonpregnant groups at any volume expansion level. As expected, atrial pressure and urine flow significantly increased after all volume expansion experiments. Pregnant and nonpregnant groups were similar with respect to atrial pressure and urine flow responses. Over various volume expansion levels significant associations were seen between atrial pressure, atrial natriuretic factor, and urine flow. These relationships were unaltered by pregnancy. In summary, atrial natriuretic factor responses to volume expansion do not appear to differ between pregnant and nonpregnant sheep.
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PMID:Atrial natriuretic factor responses to volume expansion in pregnant and nonpregnant sheep. 183 2

Plasma atrial natriuretic factor and angiotensin II have opposing actions in the regulation of body fluid homeostasis and systemic blood pressure. Angiotensin II infusions stimulate atrial natriuretic factor release in some, but not all, studies in adult mammals. To examine the response during the perinatal period, graded intravenous angiotensin II infusions were administered to four chronically instrumented pregnant ewes and fetuses (132 +/- 1 days of gestation). Fetuses received successive 20-minute intravenous angiotensin II infusions at 25, 50, and 100 ng/kg/min. After a 90-minute recovery, maternal ewes received successive 20-minute angiotensin II infusions (5, 10, and 25 ng/kg/min). During the fetal infusions, mean (+/- SEM) fetal arterial blood pressure (47 +/- 2 to 61 +/- 2 mm Hg, p less than 0.05) and heart rate (155 +/- 16 to 196 +/- 36 beats/min, p less than 0.05) increased, although there was no change in maternal measured parameters. In response to the maternal infusion, maternal mean arterial blood pressure increased (92 +/- 7 to 110 +/- 8 mm Hg, p less than 0.05) and maternal heart rate decreased (136 +/- 4 to 125 +/- 2 beats/min, p less than 0.05) without change in fetal parameters. Fetal plasma atrial natriuretic factor levels (210 +/- 27 to 664 +/- 250 pg/ml, p less than 0.05) significantly increased during the fetal angiotensin II infusions in spite of no change in maternal plasma atrial natriuretic factor (85 +/- 21 to 124 +/- 22 pg/ml) during the maternal angiotensin II infusions. These findings indicate that similar increases in systemic blood pressure in response to angiotensin II infusions stimulate increased fetal, but not maternal, plasma atrial natriuretic factor.
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PMID:Fetal and maternal plasma atrial natriuretic factor responses to angiotensin II infusion. 183 3

Surprisingly inappropriately high levels of plasma atrial natriuretic factor (ANF) in subjects with Bartter's syndrome are lowered by indomethacin therapy. Indomethacin in normal man causes sodium retention. One might therefore expect plasma ANF to increase in subjects taking indomethacin as a secondary phenomenon. On the other hand a decrease of plasma ANF in normal man similar to that reported in Bartter's subjects may explain the sodium retention caused by the drug in normals. We have studied plasma ANF before and during a two litre, four hour normal saline infusion in eight healthy male subjects both before and following five days of oral indomethacin. Plasma ANF basally was 4.2 +/- 0.9 pmol/l (mean +/- SEM) on no drug and 5.2 +/- 0.6 pmol/l on indomethacin (NS). It increased in response to saline in both studies (7.8 +/- 1.5 pmol/l after two litres of saline on control day; 10.6 +/- 1.5 pmol/l on the drug at the equivalent time, both p less than 0.05 vs basal value). Overall response to saline as assessed by the area under the curve above the basal value of hourly measurements, was not different in the two studies. Basal serum aldosterone and plasma renin activity were reduced by indomethacin. Urinary sodium excretion was not different between groups during the 12 hours before, four hours during and eight hours after the infusion. We have shown that indomethacin does not alter basal or saline stimulated plasma ANF in normal man, a finding in contrast to that reported in subjects with Bartter's syndrome. The sodium retention caused by indomethacin in normal man is not therefore due to a decrease of plasma ANF.
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PMID:The effect of indomethacin on basal and saline-stimulated plasma atrial natriuretic factor levels in normal man. 183 82

To investigate the release of atrial natriuretic factor (ANF) in mitral stenosis and the influence of the increase on the frequency of atrial contraction or atrial distention on ANF secretion, we studied 10 patients with symptoms of congestive heart failure (New York Heart Association classes II and III) in sinus rhythm, who were undergoing cardiac catheterization as part of an evaluation workup for mitral stenosis. Echocardiographic tracings, repeat determinations of mean pulmonary artery wedge pressure (MPAWP) and mean right atrial pressure, and blood sampling from the pulmonary artery for measurements of ANF were performed at baseline, during atrial pacing (pacing rate of 125 beats/min for 5 minutes), and 5 minutes after the pacing protocol was completed. Baseline ANF levels were closely related to right atrial pressure (r = 0.89; p less than 0.001) and increased markedly after atrial pacing from 205.6 +/- 39.8 (SEM) to 343.9 +/- 57.9 (SEM) pg/ml. A similar pacing-induced increase was shown for MPAWP and left atrial size. Our data indicate that pacing-induced increases in atrial distention and intracavitary pressure further stimulate release of ANF. However, an independent effect of frequency of atrial pacing on plasma ANF in humans could not be identified.
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PMID:Baseline and post-atrial pacing release of atrial natriuretic factor in mitral stenosis. 213 67


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