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)

1. Plasma human brain natriuretic peptide-like immunoreactivity (hBNP-li) was measured in ten patients with chronic renal failure before and after 4 h of haemodialysis. 2. Plasma hBNP-li was elevated in all patients before dialysis (mean +/- SEM 21.0 +/- 3.8 pmol/l) compared with healthy control subjects (1.3 +/- 0.2 pmol/l, n = 11), but showed considerable inter-patient variability. Before dialysis plasma hBNP-li bore no relationship to the serum creatinine level or to the mean blood pressure. 3. Plasma hBNP-li fell significantly (P = 0.04) during 4 h of haemodialysis. The fall in plasma hBNP-li correlated significantly with the degree of postural blood pressure drop (r2 = 0.44, P = 0.05) and with the fall in body weight (r2 = 0.64, P less than 0.01) after haemodialysis. In all patients, plasma hBNP-li at the end of treatment remained above that in healthy subjects. 4. There was no significant correlation between the fall in plasma hBNP-li and the fall in serum creatinine level, and between the fall in plasma hBNP-li and the fall in supine systolic or diastolic blood pressure, during haemodialysis. 5. We have shown that plasma hBNP-li is elevated in patients with chronic renal failure and is decreased during haemodialysis. The fact that the plasma hBNP-li was not reduced to normal by haemodialysis despite restoration to normovolaemia gives tentative support to the view that, in addition to hypervolaemia, another factor may also be responsible for the elevated plasma hBNP-li seen in these patients.
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PMID:Effect of haemodialysis on plasma levels of brain natriuretic peptide in patients with chronic renal failure. 131 49

1. Brain natriuretic peptide is a new natriuretic hormone with striking similarity to atrial natriuretic peptide, but there are no previous data concerning its clearance in man. Two pathways of clearance for atrial natriuretic peptide are recognized: degradation by neutral endopeptidase and binding to atrial natriuretic peptide clearance receptors. We have examined the effect of candoxatril, an inhibitor of neutral endopeptidase (dose range 10-200 mg), and the effect of an infusion of a pharmacological dose [45 micrograms (90 micrograms in two patients)] of synthetic human atrial natriuretic peptide on plasma human brain natriuretic peptide-like immunoreactivity levels in seven patients with mild to moderate chronic heart failure. 2. Plasma human brain natriuretic peptide-like immunoreactivity levels were elevated in all patients (mean +/- SEM 22.0 +/- 6.2 pmol/l) compared with healthy control subjects (1.3 +/- 0.2 pmol/l, n = 11). 3. In all patients, candoxatril increased both plasma atrial natriuretic peptide (P less than 0.05) and plasma human brain natriuretic peptide-like immunoreactivity (P less than 0.05) levels. 4. By contrast, an exogenous infusion of atrial natriuretic peptide had no effect on plasma human brain natriuretic peptide-like immunoreactivity levels despite increasing the plasma atrial natriuretic peptide concentration to 424 +/- 74 pmol/l, which is a level of atrial natriuretic peptide which would have 'swamped' all atrial natriuretic peptide clearance receptors. 5. We have therefore shown that plasma human brain natriuretic peptide-like immunoreactivity levels in chronic heart failure are increased by a neutral endopeptidase inhibitor, but are unchanged by an exogenous infusion of atrial natriuretic peptide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clearance of brain natriuretic peptide in patients with chronic heart failure: indirect evidence for a neutral endopeptidase mechanism but against an atrial natriuretic peptide clearance receptor mechanism. 132 May 40

1. We have developed a radioimmunoassay for the measurement of immunoreactive brain natriuretic peptide (1-32) in human plasma. Simultaneous measurements of atrial natriuretic peptide have also been carried out to allow for direct comparison between circulating brain natriuretic peptide and atrial natriuretic peptide. Plasma levels of immunoreactive brain natriuretic peptide (means +/- SEM) were 1.1 +/- 0.1 pmol/l in 36 normal healthy subjects and were significantly elevated in cardiac transplant recipients (18.8 +/- 3.9 pmol/l, n = 12) and in patients with dialysis-independent (8.8 +/- 1.5 pmol/l, n = 11) or dialysis-dependent (41.6 +/- 8.8 pmol/l, n = 14) chronic renal failure. Similarly, in these groups of patients plasma levels of atrial natriuretic peptide were also significantly raised when compared with those in the group of normal healthy subjects. 2. The plasma level of atrial natriuretic peptide was significantly higher than that of brain natriuretic peptide in normal subjects and in patients with dialysis-independent chronic renal failure, with ratios (atrial natriuretic peptide/brain natriuretic peptide) of 2.8 +/- 0.2 and 2.2 +/- 0.3, respectively. However, in both cardiac transplant recipients and patients on dialysis plasma levels of atrial natriuretic peptide and brain natriuretic peptide were similar, with ratios of 1.3 +/- 0.2 and 1.0 +/- 0.1, respectively, in these two groups. 3. Plasma levels of brain natriuretic peptide and atrial natriuretic peptide were significantly correlated in the healthy subjects and within each group of patients. When all groups were taken together, there was an overall correlation of 0.90 (P < 0.001, n = 73).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma concentrations and comparisons of brain natriuretic peptide and atrial natriuretic peptide in normal subjects, cardiac transplant recipients and patients with dialysis-independent or dialysis-dependent chronic renal failure. 133 Apr 6

Epithelial cell height was measured in order to estimate the cell volume of dark cells from the ampullae of the semicircular canal of the gerbil. Under control conditions, addition of 10(-4) mol/l piretanide, 10(-5) mol/l 5-nitro-2(3-phenylpropylamino)-benzoic acid (NPPB), 5 mmol/l barium or 10(-3) mol/l quinidine had no significant effect on cell height. Addition of 10(-4) mol/l NPPB or 10(-3) mol/l ouabain led to a small significant decrease in cell height which was not reversible. Substitution of Na+ by N-methyl-D-glucamine or of Cl- by gluconate led to a significant and reversible reduction in cell height. Isotonic elevation of [K+] from 3.6 to 25 mmol/l in a PO4-buffered, HCO3-free solution led to an increase in cell height from 5.8 +/- 0.1 (SEM) to 8.7 +/- 0.2 microns (n = 62) during the first 40 s. During prolonged exposure to elevated [K+] (3-5 min; n = 19), some tissue samples underwent a regulatory volume decrease. K(+)-induced swelling was absent in both isotonic Cl(-)-free and isotonic Na(+)-free solutions and was inhibited by the loop diuretic piretanide (10(-5) and 10(-4) mol/l) or by the (Na+ + K+) ATPase inhibitor ouabain (10(-3) mol/l) or by 10(-4) mol/l NPPB. After the removal of ouabain or 10(-4) mol/l NPPB, K(+)-induced swelling under control conditions was enhanced and was less reversible as compared to control conditions before the experiment. K(+)-induced swelling was not altered by NPPB (10(-5) mol/l) or barium (5 mmol/l); however, barium slowed shrinking upon return of [K+] to control level. In the presence of 10(-3) mol/l quinidine, K(+)-induced swelling was enhanced and not reversible. These data suggest that dark cells from the semicircular canal possess an Na+2Cl-K+ cotransporter as a solute uptake mechanism and a solute efflux mechanism which is sensitive to barium and inhibited by quinidine.
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PMID:K(+)-induced swelling of vestibular dark cells is dependent on Na+ and Cl- and inhibited by piretanide. 169 72

The presence of immunoreactive porcine brain natriuretic peptide in rat tissues was studied with a specific radioimmunoassay for porcine brain natriuretic peptide-26. The cross-reactivity of the antiserum used was less than 0.001% with rat atrial natriuretic peptide, rat brain natriuretic peptide-32 and rat brain natriuretic peptide-45. Immunoreactive porcine brain natriuretic peptide was detectable in various tissues of the rat, and high concentrations of immunoreactive porcine brain natriuretic peptide were found in the brain and cardiac atrium, with the highest level in the hypothalamus (159 +/- 30 fmol/gram wet tissue, mean +/- SEM, n = 4). Reverse phase high performance liquid chromatography showed that the immunoreactive porcine brain natriuretic peptide of the whole brain and heart extracts eluted mainly at an identical position to synthetic porcine brain natriuretic peptide-26. These findings indicate that porcine brain natriuretic peptide-like substance, distinct from rat brain natriuretic peptide, is present in high concentrations in the rat brain and cardiac atrium.
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PMID:Porcine brain natriuretic peptide-like immunoreactivity in rat tissues. 181 20

The rat cortical collecting duct (CCD) exhibits high rates of NaCl reabsorption when stimulated by mineralocorticoid and antidiuretic hormone (ADH). The present study was undertaken to determine if there is significant transcellular Cl- movement across the principal cells of the rat CCD. CCDs were dissected from kidneys of rats that had been injected with deoxycorticosterone (5 mg, i.m.) 2-9 days prior to the experiment. The ducts were perfused in vitro with identical perfusing and bathing solutions, except that 200 pmol.l-1 ADH was added to the bathing solutions. The basolateral membrane voltage (PDbl) of principal cells was -77 +/- 1 mV and the luminal membrane voltage (PD1) was -68 +/- 1 mV (mean +/- SEM, n = 124). Separate impalements with single-barrelled Cl(-)-selective microelectrodes gave an apparent intracellular Cl- activity of principal cells of 17 +/- 2 mmol.l-1. Transepithelial PD and PDbl were unaffected by luminal furosemide, hydrochlorothiazide (HCT), 4-acetamido-4-isothiocyanostilbene2,2-disulphonic acid, (SITS), or the Cl- channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB); bath addition of SITS or the Cl- channel blocker diphenylamino-2-carboxylic acid; or replacement of bath HCO3- by Cl-. The intracellular Cl- activity (a(cell)Cl) also remained unchanged with the addition of HCT, SITS or the Cl- channel blockers to either the perfusing or bathing solutions, or with replacement of the bathing solution HCO3-.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Principal cells of cortical collecting ducts of the rat are not a route of transepithelial Cl- transport. 227 16

There exist conflicting data regarding the inhibitory effect of atrial natriuretic peptide on aldosterone production from aldosterone-producing adenoma (APA). Natriuretic peptides mediate their actions through natriuretic peptide receptors (NPRs). Whether or not NPRs are present in the tumors remains controversial. To elucidate this paradox, gene expression of NPRs was examined by Northern blot analysis and competitive polymerase chain reaction in tumorous and non-tumorous portions of APA, and in normal adrenal gland from patients with renal cell carcinoma. The results of Northern blot analysis showed the presence of messenger ribonucleic acid (mRNA) of three NPRs in all adrenal tissues, including APA. The proportional expression of NPR gene transcripts in APA was type A (0.6%), type B (18.7%), and type C (80.7%). The levels, but not the proportions, of type C and possibly type B NPR mRNAs were lower in tumorous and non-tumorous portions of APA compared to those in normal adrenal gland (type C 190.2 +/- 24.5 [means +/- SEM, normal adrenal gland] > 168.1 +/- 20.8 [non-tumorous portion] > 112.2 +/- 15.5 [tumorous portion] pg/10 micrograms total RNA, F = 3.82, P < 0.05; type B 45.2 +/- 8.5 [normal adrenal gland] > 30.0 +/- 5.2 [non-tumorous portion] > 25.1 +/- 4.1 [tumorous portion] pg/10 micrograms total RNA, F = 3.03, P = 0.065). The mRNA levels of type C, rather than type A or type B, NPR were correlated with the percentage of zona fasciculata-like cells in APA (r = 0.90, P < 0.05). In conclusion we have demonstrated the presence of mRNA encoding the three NPRs in APA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitative analysis of messenger ribonucleic acid encoding natriuretic peptide receptors in aldosterone-producing adenoma. 755 75

Brush-border membrane vesicles were prepared from superficial rat renal cortex by a Mg(2+)-precipitation technique. The initial (20 s) [14C]glucose uptake rate from solutions containing 100 mmol/l Na (salt) was found to be dependent upon the anion composition of the medium; in comparison to gluconate-containing medium (0.46 +/- 0.05 nmol/mg protein), Cl- accelerated the initial rate to 1.47 +/- 0.21 nmol/mg protein (n = 4 preparations, +/- SEM). This enhancement was reduced by 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB, 0.5 mmol/l), but was unaffected by 4,4'-diisothiocyanatostilbene 2,2'-disulphonate (DIDS, 0.5 mmol/l). When membrane vesicles were pre-equilibrated with 100 mmol/l K (salt) and 100 mmol/l mannitol and glucose uptake was measured from a solution containing 100 mmol/l Na gluconate and 100 mmol/l mannitol in the presence of 80 mumol/l valinomycin (to generate an outward K+ diffusion electrical p. d.), it was found that intravesicular KCl depressed the initial glucose uptake compared to K gluconate. NPPB (0.5 mmol/l) increased the initial glucose uptake with intravesicular KCl towards values seen in K gluconate vesicles. In conditions where the only driving force for glucose uptake was established by an inward anion gradient (Nao = Nai) it was found that inward Cl- gradients could drive uphill glucose transport and that this was sensitive to NPPB (0.5 mmol/l), but insensitive to DIDS. We conclude that a Cl- conductance co-exists with Na-cotransport in rat renal brush-border membrane vesicles prepared from superficial renal cortex and this may function to regulate the activity of electrogenic transport systems at this membrane.
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PMID:Co-expression of an anion conductance pathway with Na(+)-glucose cotransport in rat renal brush-border membrane vesicles. 768 90

To investigate the clinical significance of plasma brain natriuretic peptide (BNP) measurement in patients with acute myocardial infarction (MI), circulating levels of BNP, atrial natriuretic peptide, creatine kinase (CK), and hemodynamic parameters were serially determined in 24 patients with a first episode of acute MI. Plasma BNP (mean +/- SEM) gradually increased and peaked 21 h after the onset (from 13.7 +/- 2.2 to 23.0 +/- 3.3 fmol/ml; p < 0.001). A significant correlation was found between the increase in plasma BNP level and both the peak CK level (r = 0.83; p < 0.05) and the MI size (r = 0.74; p < 0.05). The increase in plasma BNP in the acute phase was found to be a significant predictor of left ventricular (LV) function evaluated in the convalescent phase (LV ejection fraction, r = -0.63; p < 0.05, LV end-diastolic pressure, r = 0.56; p < 0.05). In conclusion, in patients with acute MI, increases in plasma BNP concentration during the early phase reflect MI size, and thereby may predict later LV function.
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PMID:Relationship between plasma level of brain natriuretic peptide and myocardial infarct size. 785 Aug 23

In the present experiments we have made a new attempt to characterize the ion transport properties of H(+)-secreting cells of the gastric mucosa using electrophysiological techniques. Individual gastric glands of bullfrog fundus mucosa were manually dissected, mounted in holding pipettes and superfused with various test solutions while individual cells were punctured with conventional or H(+)-sensitive double-barrelled microelectrodes. All measurements were performed in the resting state (0.1 mmol/l cimetidine). In HCO3(-)-containing control Ringer solution the cell membrane potential (Vb) averaged -45.6 +/- 0.9 mV (+/- SEM, n = 54). From the fast initial Vb responses to changing bath K+, Na+, Cl- or HCO3- concentrations we deduced that the basolateral cell membrane contains conductances for K+, Na+, and Cl- but not for HCO3-, and that a Na(+)-HCO3- cotransporter is not present. The K+ conductance was inhibited by Ba2+ (3 mmol/l), but the Cl- conductance was not inhibited by 4,4' diisothiocyanato-stilbene-2,2' disulphonic acid (DIDS, 0.3 mmol/l), nor selectively inhibited by 5-nitro-2-(3)- phenylpropyl-aminobenzoate (NPPB, 10 mumol/l). In a great number of cells the Vb response to Cl- substitution revealed two components: an initial spiking depolarization which reflected conductive Cl- efflux and a secondary slow hyperpolarization, the origin of which was not immediately evident. Since the latter response could be mimicked by CO2-free perfusion, strongly depressed by Ba2+ and eliminated by DIDS, we conclude that it reflects HCO3- uptake into the cells via a DIDS sensitive Cl-/HCO3- exchanger which alkalinizes the cells and stimulates the basolateral K+ conductance. Our results confirm, revise and extend the results of previous, less direct, investigations of gastric cell ion transport.
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PMID:Electrophysiological investigation of microdissected gastric glands of bullfrog. I. Basolateral membrane properties in the resting state. 789 5


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