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 relationship between kidney function and plasma immunoreactive atrial natriuretic factor (irANF) levels as well as the effects of synthetic human ANF-(99-126) were investigated in 13 patients with mild to moderate chronic renal failure. Under basal conditions, glomerular filtration rate averaged 39 +/- 5 (SEM) ml/min/1.73 m2 and blood pressure (BP) averaged 166/107 +/- 7/2 mm Hg; 12 patients were hypertensive. Plasma irANF levels were significantly increased (98 +/- 16 vs 42 +/- 4 pg/ml in healthy control subjects; p less than 0.001) and correlated (p less than 0.05-0.005) inversely with hematocrit (r = -0.65) and positively with systolic BP (r = 0.75) or fractional sodium excretion (r = 0.75). Human ANF-(99-126) infusion for 45 minutes at 0.034 microgram/kg/min augmented (p less than 0.05-0.01) diuresis and urinary sodium, chloride, calcium, phosphate, and magnesium excretion. During the subsequent 45 minutes of human ANF-(99-126) infusion at a rate of 0.077 microgram/kg/min, diuresis and electrolyte excretion remained elevated (p less than 0.05-0.01). Glomerular filtration rate and effective renal plasma flow were not significantly modified, but filtration fraction rose progressively (p less than 0.01). Human ANF-(99-126) infusion decreased BP (p less than 0.05-0.01), produced hemoconcentration (hematocrit + 7%; p less than 0.01) without negative body fluid balance, and increased (p less than 0.01-0.001) plasma norepinephrine, insulin, and serum free fatty acids; plasma aldosterone and renin activity were unaltered during but rose after cessation of human ANF-(99-126) infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor in mild to moderate chronic renal failure. 296 70

Clonidine, an alpha 2-adrenergic agonist, induced a marked, dose-related increase of plasma IR-ANF in normally-hydrated rats. Maximal ANF release was observed at 10 min after injection of 50 micrograms clonidine, rising from 40.5 +/- 4.6 pg/ml (X +/- SEM) to 1064.4 +/- 22.4 pg/ml. This effect on plasma IR-ANF was partially blocked by pretreatment with 0.8 mg naloxone, whereas synthetic Arg8-vasopressin (AVP) did not inhibit clonidine's action. These findings indicate that increased ANF release may be involved in the mechanism of clonidine-induced diuresis. The clonidine's effect on ANF release may be mediated via activation of opioid receptors besides stimulation of alpha 2-adrenergic receptors.
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PMID:Plasma immunoreactive atrial natriuretic factor (IR-ANF) increases markedly after alpha 2-adrenergic stimulation with clonidine in normally-hydrated rats. 303 Mar 13

Specific binding sites for ANF have been identified on human platelets. To determine maximal binding (Bmax) and dissociation constant (Kd), we adapted the only original method by developing a specific sequence of platelet preparation. From venous blood collected on citrated anticoagulant, platelets were prepared by successive centrifugations at 20 degrees C (blood centrifugated at 1500 rpm for 10 min., supernatant centrifugated at 3000 rpm for 1 min., supernatant centrifugated at 2800 rpm for 10 min, the inner platelet-rich layer resuspended in citrated solution) and aliquoted (200 microliters at 5.10(5) platelets/microliters). Competition experiments [incubation of platelets with fixed concentration (20-25 pM) of labeledhuman ANF (125Ih ANF) and increasing concentrations (10(-12) to 10(-6) pM) of unlabeled hANF] led to the drawing of a mean displacement curve (n = 8), usable as reference, and to verification of the specificity of binding assay (cross-reactivity with ratANF, no cross-reactivity with arginine-vasopressine). From saturation experiments [incubation of platelets with increasing concentrations (3.5 to 63.7 pM) of labeled hANF and with (10(-8) M) or without unlabeled hANF], we determined (n = 11): Bmax (m +/- SEM) = 4.5 +/- 0.7 pM or 5.4 +/- 0.8 sites per cell and Kd (m +/- SEM) = 10.84 +/- 1.70 pM.
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PMID:Atrial natriuretic factor receptors on human platelets. 792 Jan 77

In diabetic patients, several factors contribute to volume expansion and have to be counteracted by humoral and neuronal feedback control systems. We investigated N-terminal proatrial natriuretic factor (ANF1-98) and digoxin-like immunoreactive factor (DLIF), which are two counteracting hormones, and their interrelationship, with additional consideration given to autonomic nervous function in diabetic patients. ANF1-98 and DLIF were measured in 64 diabetic patients. Autonomic nervous function was assessed using nine autonomic nervous function tests. The patients were subdivided into two groups, one with four or more (group 1) and one with less than four abnormal results in autonomic function tests (group 2). Compared with group 2, group 1 demonstrated detectable DLIF levels less often (17.2 vs. 45.7, P = 0.0195) and increased levels of ANF1-98 (mean +/- SEM: 850.0 +/- 108.8 vs. 554.8 +/- 45.9 pmol/L, P = 0.0099). However, the groups did not differ in blood pressure, daily sodium, and daily potassium excretion. The number of abnormal autonomic function tests correlated significantly with ANF1-98 (P = 0.0002). In patients with detectable DLIF, DLIF correlated with ANF1-98 (P = 0.0080). These results demonstrate close interactions between the autonomic nervous system and the two natriuretic hormones. In patients with autonomic nervous dysfunction, higher levels of ANF may possibly compensate for the lack of the natriuretic DLIF to counteract hypertension and chronic volume expansion.
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PMID:Atrial natriuretic factor and digoxin-like immunoreactive factor in diabetic patients: their interrelation and the influence of the autonomic nervous system. 921 23

Developmental exposure to aryl hydrocarbon receptor (AhR) agonists in fish causes severe defects in the cardiovascular system. However, the effects of acute AhR agonist exposure on the adult fish cardiovascular system are not clear. We hypothesized that AhR-mediated changes in adult vascular tissue gene expression would differ from that of hepatic tissue. Therefore, zebrafish (Danio rerio) were intraperitoneally injected with the AhR agonists benzo-a-pyrene (BaP; 1mg/kg) or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; 20microg/kg) alone and in combination with the AhR antagonists resveratrol (Res; 10mg/kg) or alpha-naphthoflavone (ANF; 50mg/kg). Hepatic and mesenteric artery cytochrome P450 enzyme (subtypes 1A, 1B1, 1C1, and 1C2) and cyclooxygenase enzyme (subtypes 1, 2a, and 2b) mRNA expression was quantified using real-time reverse transcriptase PCR. TCDD exposure significantly increased (p<or=0.05 in Tukey's posteriori test after 1-way ANOVA; n=4-6/group) CYP1A, CYP1C1, and COX-2b mRNA expression in hepatic tissue (105+/-21, 12+/-2, and 2+/-0.3 fold-increase, mean+/-SEM respectively). TCDD also increased CYP1A, CYP1B1, CYP1C1, CYP1C2, and COX-1 mRNA expression in mesenteric artery (121+/-23, 5+/-1, 28+/-6, 7+/-1, and 3+/-0.3, respectively). Importantly, while BaP exposure elicited no significant alterations in hepatic CYP mRNA expression, it increased COX-1 and COX-2b in liver tissues (3+/-1 and 2+/-0.1, respectively), as well as CYP1A, CYP1B1, CYP1C1, CYP1C2, and COX-1 expression in mesenteric artery (2+/-0.3, 4+/-0.3, 5+/-1, 5+/-1, and 2+/-0.3, respectively). Resveratrol was able to antagonize TCDD-induced CYP1C2 in mesenteric artery but was without effect in all other treatments in both liver and mesenteric artery. In contrast, ANF antagonized TCDD and BaP-induced COX-2b and TCDD-induced CYP1C1 expression increases, as well as reduced baseline CYP1B1 and COX-2a expression in liver, while failing to affect BaP and TCDD-induced hepatic CYP1A increases. However, in mesenteric artery, ANF alone acted instead as an agonist to increase expression of CYP1A, CYP1B1, CYP1C1, CYP1C2, COX-2a and COX-2b. Thus, there are important differences in response to both AhR agonists and antagonists between liver and mesenteric artery in adult zebrafish. The vascular-specific changes in gene expression will be linked to future studies examining alterations in cardiovascular function produced by acute AhR agonist exposure in adult fish.
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PMID:Hepatic and vascular mRNA expression in adult zebrafish (Danio rerio) following exposure to benzo-a-pyrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin. 1940 81


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