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)

The nature of plasma cardiodilatin, the amino-terminal product of the human pro-atrial natriuretic peptide, was investigated by two separate radioimmunoassays directed against the N-terminal and the putative C-terminal of the cardiodilatin molecule: ANP-[Asn1-Lys16] and ANP-[Lys87-Arg98], respectively. Serial dilutions of normal and cardiac failure plasma exhibited parallelism with the synthetic peptide standard curves in both assays. The concentrations of N- and C-terminal cardiodilatin-immunoreactivity equivalents (-IE) were significantly higher in cardiac failure patients. N-terminal-IE: 912 +/- 87, normal subjects 129 +/- 13 (mean +/- SEM); C-terminal-IE: 7979 +/- 1784, normal subjects 895 +/- 213 (both p less than 0.001). Although the concentrations determined by the two assays were not identical, significant correlations were found between them in both normal subjects (r = .69, p less than 0.001) and cardiac failure patients (r = .72, p less than 0.01). Characterisation by gel permeation and fast protein liquid chromatography demonstrated coelution of the N- and C-terminal cardiodilatin immunoreactivities in a single chromatographic peak. These results suggest that the circulating cardiodilatin in normal subjects and patients with cardiac failure contains the entire prohormone amino-terminal sequence ANP-[Asn1-Arg98].
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PMID:Pro-atrial natriuretic peptide (1-98): the circulating cardiodilatin in man. 252 25

Atrial natriuretic factor (ANF) is a peptide released from the heart in response to atrial distension. This peptide causes diuresis, vasodilatation, decreased blood pressure, and antagonizes the renin-aldosterone and antidiuretic hormone neuraxes. The influence of cardiopulmonary bypass and cardiac surgery on the circulation and release of ANF is unknown. Plasma ANF concentrations were therefore determined in patients undergoing coronary artery revascularization (CABG) and mitral valve replacement (MVR). Peptide levels were unchanged following anaesthetic induction. Plasma ANF concentrations decreased significantly during hypothermic (less than or equal to 28 degrees C) cardiopulmonary bypass in both patient groups. After 60 minutes of cardiac bypass, ANF declined from (mean +/- SEM) 512 +/- 132 to 20 +/- 6 pg.ml-1 (P less than 0.05) during MVR, and from 178 +/- 41 to 110 +/- 48 pg.ml-1 during CABG (P less than 0.05). Rewarming during bypass was associated with an increase in ANF concentration in both groups. Heparin anticoagulation and protamine reversal had no effect on immunoreactive ANF levels. In patients undergoing CABG, there was a linear relationship between plasma ANF concentration (pg.ml-1) and right atrial pressure (mmHg) prior to cardiopulmonary bypass (r = 0.86, P less than 0.005). However, one and three hours after cardiopulmonary bypass there was no significant relationship between right atrial pressure and ANF plasma levels. These results suggest that reduction in plasma ANF concentration occurs during hypothermic cardiopulmonary bypass. Furthermore, the proportional relationship between atrial distension and circulating ANF concentration was altered following cardiac surgery.
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PMID:Influence of hypothermic cardiopulmonary bypass on atrial natriuretic factor levels. 214 Mar

In order to determine the relationships between allograft function and the recipient's plasma concentrations of atrial natriuretic factor (ANF), plasma ANF was measured by radioimmunoassay for 14 days after cadaveric renal transplantation in 9 patients aged 19-64 years. All received immunosuppression with prednisolone, azathioprine, and cyclosporine. No patient was in heart failure. During the study period, six grafts functioned, and three were nonfunctioning--two due to rejection and one to acute tubular necrosis. Plasma ANF concentration at the time of transplantation was 48 +/- 16 pmol/L (mean +/- SEM) range 15-145 pmol/L. In the six patients with functioning grafts, ANF declined in parallel with the fall in serum creatinine (658 +/- 35 to 210 +/- 34 mumol/L). In the three with nonfunctioning grafts, serum creatinine and plasma ANF concentration both increased. There was overall a significant linear relation between serum creatinine and plasma ANF (r = 0.527, P less than 0.001). The changes in plasma ANF after renal transplantation bore no relationship to changes in body weight or blood pressure. However, plasma ANF concentration was related to allograft fractional sodium excretion (r = 0.687, p less than 0.001). We conclude that elevated plasma ANF concentrations in end-stage renal disease are restored to normal by successful renal transplantation, implying that renal function is a determinant of plasma ANF concentration. Circulating plasma ANF may also have a direct effect on allograft sodium excretion.
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PMID:Plasma atrial natriuretic factor and graft function in renal transplant recipients. 253 Jun 66

Plasma immunoreactive atrial natriuretic factor (irANF) levels and the effects of alpha-human ANF (alpha-hANF) infusion were investigated in 7 patients with liver cirrhosis and ascites. Under basal conditions, supine blood pressure (BP) averaged 136/76 +/- 9/4 mm Hg (mean +/- SEM). Plasma irANF concentrations (124 +/- 33 pg/ml) were higher (p less than 0.01) than those in age-matched normal subjects (47 +/- 5 pg/ml). Plasma renin activity (PRA 5.9 +/- 2.2 ng/ml/h), aldosterone (18 +/- 7 ng/dl) and norepinephrine (NE, 66 +/- 5 ng/dl) levels were also elevated compared to the age-related normal range. Alpha-hANF infusion for 60 min at 0.036 micrograms/kg/min decreased the mean BP (-14%; p less than 0.05), increased PRA (+179%; p less than 0.05) and plasma NE (+24%; p less than 0.05). Glomerular filtration rate (GFR), effective renal plasma flow (ERPF), diuresis and natriuresis were not modified. A subsequent 60-min infusion of alpha-hANF at 0.067 micrograms/kg/min produced a marked fall in mean BP (-26%; p less than 0.001), hemoconcentration (hematocrit +6%; p less than 0.001) despite stable body fluid balance and a further increase in PRA (+350%, p less than 0.005). GFR and ERPF were severely reduced (-55 and -56%, respectively; p less than 0.001), while diuresis and natriuresis were not modified. Plasma aldosterone was unaltered during, but rose (+72%; p less than 0.01) after the cessation of alpha-hANF infusion. Variations in natriuresis during alpha-hANF infusion correlated positively with BP (r = 0.47; p less than 0.01), ERPF (r = 0.53; p less than 0.01) or GFR (r = 0.51; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypotension and renal impairment during infusion of atrial natriuretic factor in liver cirrhosis with ascites. 253 Sep 3

This two-site immunoradiometric assay (IRMA) for human atrial natriuretic factor (ANF)99-126 in plasma utilizes a mouse monoclonal antibody raised against rat (r) ANF103-125 with specificity directed towards the ring structure of ANF, and a rabbit antiserum to human (h) ANF99-126. The monoclonal antibody is radioiodinated, and the IgG fraction of the antiserum is coated onto wells of a microtiter plate. Plasma or standard hANF99-126 (150 microL) is incubated with the radioligand in coated wells for 24 h. The detection limit is 0.9 pg per well, corresponding to 2 pmol/L, with a working range (CV less than 10%) from 4.5 to 540 pmol/L. Intra- and interassay precision are 7% and 9%, respectively, and the assay is unaffected by plasma matrix. In humans, the IRMA is specific for hANF99-126, the major circulating form of ANF, and does not cross-react with metabolites having deletions at the carboxy terminus. Plasma IRMA values in normal seated subjects were 6.6 +/- 1.5 (SEM) pmol/L and results correlated with those of an extraction RIA (r = 0.81, P less than 0.001).
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PMID:Development and validation of a two-site immunoradiometric assay for human atrial natriuretic factor in unextracted plasma. 254 18

The effects of low bolus dose (70 +/- 6 micrograms [mean +/- SEM]) atrial natriuretic factor (ANF) administration was assessed in 16 patients with chronic congestive heart failure. Measurements were made for at least 60 minutes before and after the dose of ANF. There was a significant increase in urine flow rate (0.81 +/- 0.06 to 1.81 +/- 0.23 ml/min, p less than 0.01), sodium excretion rate (56 +/- 14 to 80 +/- 23 microEq/min, p less than 0.01), fractional excretion of sodium (1.23 +/- 0.49 to 1.63 +/- 0.60 percent, p less than 0.01) and potassium excretion rate (35 +/- 7 to 42 +/- 6 microEq/min, p less than 0.02). However, no significant alterations in renal plasma flow or glomerular filtration rate were observed. Furthermore, there was no significant correlation between the change in urine flow rate or sodium excretion rate and the change in renal plasma flow or glomerular filtration rate, respectively. In addition, there was no significant effect on cardiac index, mean aortic or left ventricular filling pressures, or systemic vascular resistance. There also was no discernible relationship between the response to ANF and the baseline concentrations of plasma ANF, aldosterone, or plasma renin activity. Thus, in patients with congestive heart failure, low dose ANF boluses may produce an increase in urine flow rate and sodium excretion rate that is independent of renal plasma flow or glomerular filtration rate. This suggests a meaningful direct renal tubular effect of exogenous ANF in this setting.
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PMID:Cardiorenal effects of atrial natriuretic factor administration in congestive heart failure: natriuresis and diuresis without hemodynamic alterations. 256 86

The natriuretic effects of atrial peptide hormones have been attributed, at least in part, to their stimulation of guanylate cyclase activity in renal cell membranes. The effects of atrial natriuretic factor (ANF) on stimulation of cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) accumulation were investigated in cloned human kidney tumor (hKT) cells and parent cells from a human renal tumor epithelial cell line (SK-NEP-1). Human ANF-(99-126) (10(-6)M) stimulated (p less than 0.001) cellular cGMP accumulation in a dose-dependent manner from a basal level of 0.26 +/- 0.04 to 3.73 +/- 0.81 pmol/mg protein/5 mi (mean +/- SEM, n = 13). ANF stimulation of cGMP accumulation was specific, in that high concentrations (10(-6)M) of atriopeptin I [rat ANF-(103-123)], angiotensin II, arginine vasopressin, and amiloride (10(-4)M) did not increase basal cGMP. Amiloride (10(-4)M) enhanced (p less than 0.01, n = 6) the ANF stimulation of cGMP accumulation (1.24 +/- 0.39 pmol/mg protein/5 min), particularly at low doses of ANF (10(-10)M) where stimulation by ANF without amiloride (0.34 +/- 0.08 pmol/mg protein/5 min) was barely distinguishable from a basal level (0.19 +/- 0.02 pmol/mg protein/5 min) of cGMP accumulation. The stimulatory effect of ANF (1.59 +/- 0.07 pmol/mg protein/5 min) was attenuated (0.75 +/- 0.06 pmol/mg protein/5 min, p less than 0.01, n = 6) by preincubation of the cells with pertussis toxin but not by cholera toxin. ANF (4.56 +/- 0.93 pmol/mg protein/5 min, n = 8) did not affect cAMP accumulation (4.32 +/- 0.98 pmol/mg protein/5 min) in hKT cells. This is the first report of an ANF responsive human renal cell line, and its use should facilitate investigation of ANF-receptor interactions.
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PMID:Atrial natriuretic factor effects on cyclic nucleotides in a human renal cell line. 256 5

The role of the atrial natriuretic factor (ANF), its second messenger cyclic guanosine monophosphate (cGMP), and the counteracting renin-aldosterone system in acute volume regulation was investigated in 25 healthy human subjects. Central volume stimulation by 1-h head-out water immersion (WI) into a thermoneutral water-bath increased plasma levels of ANF (mean +/- SEM) from 6.0 +/- 0.6 to 13.6 +/- 2.6 fmol ml-1. This was paralleled by a rise of plasma cGMP levels from 1.9 +/- 0.2 to 2.8 +/- 0.4 pmol ml-1, and an increase of urinary cGMP excretion from 340 +/- 64 to 692 +/- 103 pmol min-1. Water immersion reduced plasma aldosterone concentration (PAC) from 13.0 +/- 1.7 to 6.5 +/- 0.8 ng 100 ml-1 and plasma renin activity (PRA) from 5.3 +/- 0.9 to 2.4 +/- 0.3 ng AI ml-1 h-1. Volume stimulation markedly increased diuresis and natriuresis. Whereas the plasma cGMP increase correlated with plasma ANF stimulation, neither ANF nor PRA or PAC correlated with basal or stimulated renal parameters. Water immersion-induced changes in natriuresis and urinary cGMP excretion were correlated. These data suggest a role of ANF and cGMP in acute volume regulation of healthy human subjects.
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PMID:Role of atrial natriuretic factor, cyclic GMP and the renin-aldosterone system in acute volume regulation of healthy human subjects. 284 47

1. The relationship between plasma immunoreactive atrial natriuretic factor (Ir-ANF) and the urinary excretion of sodium, guanosine 3':5'-cyclic monophosphate (cyclic GMP) and of tissue kallikrein was examined in seven healthy female volunteers. 2. Each volunteer attended on two occasions, a control and a saline infusion day. On the infusion day saline (2 litres, 0.9% NaCl) was administered over 60 min. Measurements of plasma Ir-ANF and urinary excretion of sodium, cyclic GMP and of tissue kallikrein were made at 30 min intervals during the infusion and for 3 h after the infusion. 3. Mean (+/- SEM) urinary sodium excretion increased from a basal value (time 0) of 102 +/- 15 mumo/min to 222 +/- 47 mumol/min 60-90 min from the start of the infusion and thereafter remained significantly elevated (P less than 0.01) above sodium excretion on the control day. 4. In response to saline infusion there was a transient rise in mean (+/- SEM) plasma Ir-ANF from 6.7 +/- 0.8 pmol/l to a peak of 22.5 +/- 3.7 pmol/l at 75 min, falling to 12.7 +/- 1.9 pmol/l at 135 min. The peak plasma Ir-ANF level on the infusion day was significantly elevated (P less than 0.05) above the time-matched measurement on the control day. 5. Similarly, there was a transient rise in mean (+/- SEM) urinary cyclic GMP excretion on the infusion day from 30.9 +/- 4.4 fmol/min to 64.6 +/- 11.4 fmol/min during the 60-90 min collection period, returning to 43.7 +/- 14.5 fmol/min at 210-240 min.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary guanosine 3':5'-cyclic monophosphate but not tissue kallikrein follows the plasma atrial natriuretic factor response to acute volume expansion with saline. 285 78

To determine the effect of clonidine, an alpha 2-adrenergic agonist, on atrial natriuretic factor (ANF) release during water deprivation, plasma immunoreactive ANF (IR-ANF) arginine vasopressin, diuresis and natriuresis were measured in rats which had been deprived of water for 24 and 48 hr after intravenous (IV) administration of 50 micrograms clonidine. In normally-hydrated rats clonidine produced a marked elevation of plasma IR-ANF from 40.5 +/- 4.6 pg/ml to 1064 +/- 22 pg/ml (mean +/- SEM) and sodium excretion from 73.3 +/- 6.8 microEq to 723.4 +/- 62.3 microEq. Clonidine evoked an increase in plasma IR-ANF from 16.6 +/- 5.9 pg/ml to 229.5 +/- 60 pg/ml (mean +/- SEM) after 24 hr water deprivation and from 13.6 +/- 7.4 pg/ml to 104.8 +/- 21 pg/ml (mean +/- SEM) after 48 hr water deprivation. Clonidine did not induce any significant changes in vasopressin levels. During 24 hr and 48 hr water deprivation vasopressin rose from 3.1 +/- 0.3 pg/ml to 7.3 +/- 1.3 pg/ml and 8.4 +/- 0.6 pg/ml (mean +/- SEM), respectively. In normally-hydrated rats clonidine produced a marked diuresis and natriuresis. These effects and urinary cGMP excretion were significantly inhibited by anti-ANF antibodies. Clonidine caused a significant increase in urine output in 24 hr water-deprived rats but the response was markedly lower than that seen in normally-hydrated rats. In conclusion, clonidine stimulates ANF release both in normally-hydrated and water-deprived rats. The diuretic effect of clonidine appears to be related to ANF release but not to inhibition of vasopressin.
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PMID:Clonidine stimulates atrial natriuretic factor (ANF) release in water-deprived rats. 285 43


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