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)

PGE2 concentration (pg/ml + SEM) was measured in canine renal lymph (394 +/- 115), renal venous plasma (276 +/- 55), arterial plasma (172 +/- 34) and urine (1290 +/- 934). Control periods were followed by an infusion of the sodium salt of arachidonic acid (AA) (40 micrograms/kg min) into the renal artery to stimulate prostaglandin synthesis. During infusion of AA PGE2 concentrations increased significantly in renal lymph (672 +/- 155) renal venous plasma (549 +/- 123), and urine (6768 +/- 1420), but not in the arterial plasma (176 +/- 31). Concentrations in renal lymph and renal venous plasma were not significantly different under either condition. These findings indicate that PGE2 concentration in renal venous plasma is, by and large, representative of mean PGE2 concentrations in the cortical renal interstitium, although focal inhomogeneities in PGE2 concentration in the different areas of the renal interstitium cannot be excluded. Since flow rate of renal lymph is insignificant in comparison with renal venous plasma flow rate total renal PGE2 output can be estimated from measurements in renal venous plasma and urine.
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PMID:PGE2 concentrations in renal venous plasma and renal lymph during basal and stimulated conditions in the dog. 272 30

Large doses of atrial natriuretic peptide (ANP) inhibit renin and aldosterone secretion in normal man, but the effect of physiological levels is unknown. We, therefore, studied the effect of a low infusion rate of alpha-human ANP (alpha hANP; 0.5 microgram/min for 180 min) on the plasma corticosteroid response to graded physiological doses of angiotensin II (0.5, 1.0, 2.0, and 4.0 ng/kg X min, each for 30 min) and ACTH (6.25, 12.5, 25, and 50 mIU, each for 30 min) in six normal men eating a low salt diet (10 mmol sodium and 100 mmol potassium daily). The angiotensin II and ACTH infusions were given from 0900-1100 h on separate days, during which randomized infusions of placebo or alpha hANP were given from 0800-1100 h according to a single blind protocol. Plasma immunoreactive ANP levels were less than 10 pmol/L on the placebo day compared to 30-50 pmol/L during the alpha hANP infusions, and were not altered by either ACTH or angiotensin II. Compared with the control observations, there was no significant change in arterial pressure or heart rate during either the alpha hANP or angiotensin II infusions. ACTH infusions evoked an incremental response in plasma aldosterone and cortisol, and the dose-response relationship was unaltered by alpha hANP. In contrast, while an incremental and significant increase in plasma aldosterone in response to angiotensin II occurred with the placebo infusion, no significant increase occurred in response to angiotensin during the alpha hANP infusion. The slope of the angiotensin II/aldosterone regression line was significantly less during all alpha hANP infusions compared to that during the placebo infusion (P less than 0.02). In addition, on the ACTH infusion day significant suppression of both PRA (P less than 0.05) and plasma angiotensin II (P less than 0.008) occurred during the alpha hANP infusion compared to that during the placebo infusion, whereas PRA was equally suppressed by angiotensin II in the presence or absence of alpha hANP. alpha hANP also increased urine volume [176 +/- 31 (+/- SEM) vs. 113 +/- 19 mL/mmol creatinine with placebo; P less than 0.03] and sodium excretion (2.14 +/- 0.48 vs. 0.58 +/- 0.22 mmol/mmol creatinine with placebo; P less than 0.004) on the ACTH infusion days. With angiotensin II, urine volume was also significantly increased by alpha hANP (150 +/- 27 vs. 81 +/- 15 mL/mmol creatinine with placebo; P less than 0.03), and urine sodium excretion doubled.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effect of physiological levels of atrial natriuretic peptide on hormone secretion: inhibition of angiotensin-induced aldosterone secretion and renin release in normal man. 282 Oct 56

The actions of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] are thought to be mediated through receptor proteins which have been described in a variety of avian and mammalian tissues, but not in the liver. To determine if a binding protein for 1,25-(OH)2D3 is present in this tissue, rat liver was homogenized in a low ionic strength buffer containing 10 mM Tris (pH 7.4), 2.2 m sucrose, 3 mM calcium chloride, 0.2% Triton X-100, and 0.04% Trasylol (sucrose buffer) and centrifuged over a 10-ml cushion of sucrose buffer at 61,000 x g for 80 min at 4 C. The resultant nuclear pellet was extracted in a 26 mM Tris (pH 7.4) buffer containing 0.3 M potassium chloride, 5 mM dithiothreitol, 1 mM EDTA, and 10 mM sodium molybdate. Saturable 1,25-(OH)2D3 binding was identified in high salt extracts of rat liver nuclei and was eliminated by treatment with trypsin. This liver binding protein cosediments on high salt 5-20% sucrose density gradients with the 1,25-(OH)2D3 receptor protein from intestine and is distinct from the 6.OS tissue binding protein for 25-hydroxyvitamin D3. Perfusion of rat liver with PBS to remove receptor-positive blood cells before isolation of the nuclei did not change 1,25-(OH)2D3 binding. The nuclear protein bound 1,25-(OH)2D3 more avidly than either 24,25-(OH)2 D3 or 25-hydroxyvitamin D3. Saturation analysis of 1,25-(OH)2D3 binding revealed an apparent equilibrium dissociation constant of 20.6 +/- 2.2 pM (mean +/- SEM) at 4 C and a maximum binding capacity of 49.0 +/- 14.6 fmol/extract from 1.0 mg DNA. The 1,25-(OH)2D3-binding binding protein was present in liver nuclei isolated from mice, rabbits, and chicks and in nuclei isolated from cultured rat hepatocytes. The ligand specificity, sedimentation coefficient, limited binding capacity, trypsin sensitivity, and nuclear location of the hepatic 1,25-(OH)2D3-binding protein are similar to those of 1,25-(OH)2D3 receptors described in other tissues and suggest that the liver may be a target organ for [1,25-(OH)2D3] action.
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PMID:A 1,25-dihydroxyvitamin D3 receptor-like protein in mammalian and avian liver nuclei. 283 67

This study was undertaken to determine the systemic and regional hemodynamic effects of long-term dietary calcium supplementation in mineralocorticoid (DOC)-salt hypertension. Systemic and regional hemodynamic measurements were determined by the radioactive microsphere technique in conscious and unrestrained rats (kidneys intact) with DOC-salt-induced hypertension that were pair-fed either a normal calcium (0.6% by weight, n = 12) or a calcium-supplemented (high-calcium) diet (2.5% by weight, n = 12). After 7 to 8 weeks, there were no differences in weight, heart rate, or cardiac output between the two groups. In contrast, the high-calcium rats had a significantly lower mean blood pressure (125 +/- 4 mm Hg, mean +/- SEM) than the normal calcium rats (143 +/- 5 mm Hg); this finding appeared to result predominantly from a reduction in total peripheral resistance. The high-calcium rats had a higher renal blood flow (7.8 +/- 0.5% vs. 6.2 +/- 0.4% cardiac output; p less than 0.05) and lower renal (14.3 +/- 1 vs. 19.3 +/- 2 mm Hg/min/ml/g tissue; p less than 0.05) and jejunal vascular resistance than did the normal calcium rats. Two additional identical groups of normal calcium-and high-calcium-DOC-salt rats (n = 12 each) were also studied. In these rats, serum-ionized calcium decreased significantly (p less than 0.05) from baseline in both groups. Urinary sodium increased in both groups but did not differ significantly. In conclusion, dietary calcium supplementation attenuates the rise in peripheral vascular resistance that accompanies DOC-salt hypertension. This attenuated resistance appears to be relatively selective and is noted particularly in the renal vasculature.
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PMID:Systemic and regional hemodynamic effects of dietary calcium supplementation in mineralocorticoid hypertension. 291 Aug 16

Human oocytes were stored (25 degrees C) in 1.5 M MgCl2 for 6-30 days, then utilized in the new hemizona assay (HZA) for tight binding of human spermatozoa [Burkman et al.: Fertil Steril 49:688-697, 1988]. We have compared 1) the ability of matching salt-treated hemizonae or dimethylsulfoxide (DMSO)-treated hemizonae to distinguish between sperm from semen having normal versus subnormal characteristics and, 2) the kinetics of fertile sperm binding to salt-treated or DMSO-treated hemizonae. After sperm preparation one salt-treated hemizona was incubated with normal spermatozoa and the matching hemizona was placed with sperm from the subnormal group. As a control, DMSO-treated hemizonae were incubated in additional sperm droplets. After 4 hours, the number of sperm tightly bound to each hemizona was counted. Within the normal semen group, there was equivalent binding to salt- or DMSO-treated hemizonae (54.0 +/- 12 and 49 +/- 14, respectively, mean +/- SEM). Similarly, tight binding of sperm from the subnormal group was not affected by the zona storage method (21 +/- 8 and 17 +/- 5, respectively). For either storage approach, binding of subnormal sperm was significantly less (P less than 0.01) compared with the number of normal sperm attached to the matching hemizona. For the kinetics study, the hemizona binding of proven fertile spermatozoa was followed throughout 8.5 hours. The shape of the binding curve was the same for zonae stored by either method and was consistent with our published kinetics data. Salt storage offers a simple and inexpensive means for accumulating and transporting human zonae pellucida; the resulting hemizonae function effectively in the HZA for estimating sperm binding potential.
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PMID:Hemizona assay using salt-stored human oocytes: evaluation of zona pellucida capacity for binding human spermatozoa. 291 26

Plasma concentrations of immunoreactive (IR)-atrial natriuretic polypeptide (hANP) were measured by radioimmunoassay in 9 essential hypertensive patients after alteration of salt intake and acute saline infusion. Daily salt intake was altered every one week in the order of 15g/day, 3g/day, and 7g/day. On the last day of the first week, 1500 ml of 0.9% saline was infused intravenously over one hour. Plasma concentrations of IR-hANP tended to decrease, although not significant, by salt restriction. Further, there were significant positive correlations between changes in plasma concentrations of IR-hANP and those of several variables such as body weight, systolic blood pressure, and creatinine clearance. Plasma concentrations of IR-hANP rose significantly (p less than 0.05) from 50.7 +/- 20.1 (Mean +/- SEM) pg/ml to 119.0 +/- 48.8 after acute saline infusion. Although there was significant correlation between mean blood pressure and the increase in sodium excretion by saline infusion, this increase was unrelated to the rise in plasma concentrations of IR-hANP. These results suggest that the release of ANP is stimulated mainly by expansion of extracellular fluid volume in hypertensive patients. However, natriuretic and hypotensive effects attributable to the changes of ANP release could not be elucidated.
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PMID:Effects of changes in dietary sodium intake and saline infusion on plasma atrial natriuretic peptide in hypertensive patients. 295 26

Hyponatremia is common following aneurysmal subarachnoid hemorrhage and has been linked to the syndrome of inappropriate secretion of antidiuretic hormone. However, the demonstration of volume depletion and natriuresis in some patients has suggested that salt wasting is a more likely etiology. Atrial natriuretic factor appears to play a role in both central and peripheral regulation of sodium homeostasis. To investigate the behavior of circulating atrial natriuretic factor following subarachnoid hemorrhage, we studied 25 patients with intracranial aneurysms: 21 after acute subarachnoid hemorrhage and four without evidence of recent rupture. Atrial natriuretic factor was measured by radioimmunoassay of extracted plasma (normal value, 20.8 +/- 24.6, mean +/- 3 SD). Mean +/- SEM plasma atrial natriuretic factor concentration was elevated to 84 +/- 25 pg/ml on Day 1, rose to 134 +/- 29 pg/ml on Day 3, and fell to 86 +/- 17 pg/ml by Day 7 after subarachnoid hemorrhage (p less than 0.01). In two patients (9.5%) who developed hyponatremia after aneurysm rupture, plasma concentrations were no different from that in the group as a whole; concentrations in patients with no evidence of recent subarachnoid hemorrhage were not elevated. Neither fluid administration nor timing of surgery could account for the elevated concentrations. We conclude that concentrations of circulating atrial natriuretic factor are elevated after subarachnoid hemorrhage but do not solely account for the accompanying hyponatremia.
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PMID:Plasma atrial natriuretic factor and subarachnoid hemorrhage. 297 Jul 2

Based on oscillatory long-term blood pressure recordings and on biochemical findings in 62 normotensive and 54 untreated hypertensive subjects, who were investigated during their usual high sodium diet and after moderate salt restriction, we have developed a concept for the pathogenesis of essential hypertension, which differs from current concept proposed by others: We demonstrated that normotensive subjects with a positive family history of hypertension respond to sodium restriction from 200 to 50 mmol/day over 2 weeks with a minute fall of mean blood pressure of 2.9 +/- 0.7 mmHg (+/- SEM), whereas in subjects with a negative family history of hypertension blood pressure remained unchanged (-0.93 +/- 0.67 mmHg). This difference was only revealed by computing the "basal blood pressure average" from 240 heart beats, but not by conventional sphygmomanometric blood pressure measurements. Normotensives with heredity of hypertension or "salt sensitive" normotensive subjects were not different from subjects with a negative family history in the sodium pump, Na-K-cotransport or intracellular sodium and potassium of erythrocytes. In contrast, the former group had an increased sensitivity to infused noradrenaline, which might be responsible for enhanced tubular sodium reabsorption in subjects with a positive family history of hypertension (or "salt sensitive" subjects). We only found an increased K-permeability of red cells in established hypertension, which was compensated for by a an increased activity of the sodium pump. These cell membrane defects were more pronounced in more severe hypertension. In the course of essential hypertension a cell membrane defect may develop as a consequence rather than a cause of the disease.
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PMID:[Hereditary salt sensitivity as a cause of essential hypertension: studies of membrane transport and intracellular electrolytes]. 299 39

Radioimmunoassays have been used to detect digoxin-like immunoreactive factors (DLF) in the plasma and urine of hypertensive patients and rats with deoxycorticosterone acetate (DOCA)-salt hypertension. Uninephrectomized rats (n = 9), given 15 mg DOCA . kg-1 . wk-1, were fed a standard rat chow supplemented with 2% NaCl (DOCA-HS); control animals (n = 15) were given vehicle injection and a specially formulated low-salt diet (0.05% NaCl). At 4 wk, DOCA-HS rats were hypertensive (121.4 +/- 10.1 vs. 88 +/- 4.4 Torr, mean +/- SEM, P less than 0.05) and excreted more DLF (2.7 +/- 1.1 vs. 0.2 +/- 0.1 ng digoxin equivalents . day-1, P less than 0.001) compared with control rats. DLF, partially purified from DOCA-HS urine by antidigoxin antibody immunoaffinity chromatography, was found to have a molecular weight less than 2,000, was resistant to acid hydrolysis or proteases, and had many properties of the cardiac glycosides, including inhibition of Na+-K+-ATPase activity, displacement of ouabain from human erythrocyte membranes, and inhibition of 86Rb influx into red blood cells. When DOCA-HS rats were switched to the low-sodium chow, DLF excretion dropped precipitously. No measurable DLF (less than 10 pg/ml) was detected in the plasma of rats eating either chow. However, greater than 95% of the urinary DLF could be attributed to a contaminant in the standard laboratory chow; rats fed the low-salt chow supplemented with 2% NaCl excreted much less DLF, and DLF was isolated from the standard chow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Excretion of artifactual endogenous digitalis-like factors. 301 5

The primate-specific renin inhibitor CGP 29287 (30 mg/kg/d, n = 5) or the converting-enzyme inhibitor CGS 14831 (30 mg/kg/d, n = 8) were administered by continuous intraperitoneal infusion via osmotic minipumps to normotensive marmosets fed a low salt diet. CGP 29287 and CGS 14831 induced a similar reduction in blood pressure after 2 days of administration (-22 +/- 6, SEM and -24 +/- 6 mmHg respectively). The hypotensive response persisted at 7 days (-20 +/- 3 and -22 +/- 8 mmHg respectively). Despite the fall in blood pressure, heart rate was not changed after either inhibitor. Blood pressure and heart rate remained stable in control marmosets that received vehicle only (0.9% saline). Plasma renin activity was inhibited after CGP 29287 (100% at day 2 and 75% at day 7) and increased after CGS 14831 (4 and 3 fold on days 2 and 7 respectively). Total plasma immunoreactive renin was increased to a similar extent after both inhibitors (approximately 5 fold on days 2 and 7). These findings show that a similar hypotensive response is induced in sodium-depleted primates after chronic inhibition of renin or converting enzyme. Thus the fall in blood pressure after chronic treatment with either inhibitor appears to be mainly due to the blockade of the renin-angiotensin system and the consequent reduction in endogenous angiotensin II formation.
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PMID:Comparison of chronic inhibition of renin and converting enzyme in the marmoset. 303 92


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