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M Jankowski

Publications and source records attributed to M Jankowski.

At least 55 records · Page 3Linked to original sources
PubMed1998

[Computer program "PANCREAS"].

Contemporary computer technology allows precise and fast large database analysis. Widespread and common use depends on appropriate, user friendly software, usually lacking in special medical applications. The aim of this work was to develop an integrated system designed to store, explore and analyze data of patients treated for pancreatic cancer. For that purpose the database administration system MS Visual Fox Pro 3.0 was used and special application, according to ISO 9000 series has been developed. The system works under MS Windows 95 with possibility of easy adaptation to MS Windows 3.11 or MS Windows NT by graphic user's interface. The system stores personal data, laboratory results, visual and histological analyses and information on treatment course and complications. However the system archives them and enables the preparation reports of according to individual and statistical needs. Help and security settings allow to work also for one not familiar with computer science.

Data Display↗
PubMed1997

Oxytocin releases atrial natriuretic peptide by combining with oxytocin receptors in the heart.

Previous studies indicated that the central nervous system induces release of the cardiac hormone atrial natriuretic peptide (ANP) by release of oxytocin from the neurohypophysis. The presence of specific transcripts for the oxytocin receptor was demonstrated in all chambers of the heart by amplification of cDNA by the PCR using specific oligonucleotide primers. Oxytocin receptor mRNA content in the heart is 10 times lower than in the uterus of female rats. Oxytocin receptor transcripts were demonstrated by in situ hybridization in atrial and ventricular sections and confirmed by competitive binding assay using frozen heart sections. Perfusion of female rat hearts for 25 min with Krebs-Henseleit buffer resulted in nearly constant release of ANP. Addition of oxytocin (10(-6) M) significantly stimulated ANP release, and an oxytocin receptor antagonist (10(-7) and 10(-6) M) caused dose-related inhibition of oxytocin-induced ANP release and in the last few minutes of perfusion decreased ANP release below that in control hearts, suggesting that intracardiac oxytocin stimulates ANP release. In contrast, brain natriuretic peptide release was unaltered by oxytocin. During perfusion, heart rate decreased gradually and it was further decreased significantly by oxytocin (10(-6) M). This decrease was totally reversed by the oxytocin antagonist (10(-6) M) indicating that oxytocin released ANP that directly slowed the heart, probably by release of cyclic GMP. The results indicate that oxytocin receptors mediate the action of oxytocin to release ANP, which slows the heart and reduces its force of contraction to produce a rapid reduction in circulating blood volume.

Animals↗
PubMed1997

Elevated levels of natriuretic peptides in lungs of hamsters with genetic cardiomyopathy.

Various alterations in the natriuretic peptide system have been observed in heart and plasma in humans and animals with heart failure. However, there is limited information about these hormones in hamster lung especially in those with genetic cardiomyopathy, a model of human congestive heart failure. Therefore, the aim of the present study was to investigate the content of the three natriuretic peptides (atrial natriuretic peptide (ANP); brain natriuretic peptide (BNP); C-type natriuretic peptide (CNP) and their gene expression in lungs of normal and cardiomyopathic hamsters. The presence of mRNA coding for ANP and BNP in lungs and heart was investigated by Northern blot and confirmed by reverse transcription polymerase chain reaction (RT-PCR). The peptide contents and plasma concentrations were determined by specific radioimmunoassays. Plasma ANP increased in hamsters with moderate to severe cardiomyopathy (aged 230 days) from control levels of 71.8+/-15.8 to 243.1+/-44.0 pg/ml (P < 0.01). Plasma BNP also increased from 79.7+/-23.5 to 227.9+/-51.6 pg/ml (P < 0.01). The levels of the three peptides in lungs of 30- and 120-day-old cardiomyopathic (CMO) hamsters were not different from their corresponding age-matched controls. However, lung ANP increased in 230-day-old CMO from 589+/-63 to 1624+/-219 pg/mg protein (P < 0.01). Lung BNP and CNP also increased from 332+/-35 to 531+/-55 pg/mg protein (P < 0.01) and from 118+/-21 to 224+/-29 pg/mg protein (P < 0.01), respectively. Lung ANP mRNA and BNP mRNA were significantly (P < 0.05) higher in 230-day-old hamsters than those detected in age-matched normal controls. Our data demonstrate that the hamster lungs produce ANP, BNP and CNP, and that this production is enhanced in moderate to severe cardiomyopathy. These findings imply that the lung natriuretic peptide system may participate in pulmonary function especially during cardiac dysfunction.

Animals↗
PubMed1997

Modulation by low sodium intake of glomerular response to cicletanine and atrial natriuretic factor.

1. The aim of the study was to investigate whether cicletanine (CIC), as a potential inhibitor of cyclic GMP phosphodiesterase, is able to restore glomerular response to atrial natriuretic factor (ANF) in rats under conditions of diet deprived of sodium. We examined the effects of CIC on glomerular filtration rate (GFR), natriuresis and nephrogenous cyclic GMP excretion in response to ANF and the effects of both agents on intracapillary volume and cyclic GMP accumulation in isolated glomeruli of rats on normal and low sodium diets. 2. CIC (0.25 mg min-1 kg-1 BW) of ANF (0.5 microgram min-1 BW) alone, given in pharmacological doses, increased Cin significantly in normal sodium rats, whereas the effect of each agent was blunted in low sodium diet rats. Pretreatment with CIC restored the increase in C(in) in response to ANF infusion in low sodium diet rats. In rats on either diet, there were no differences in the extent of diuresis and natriuresis induced by CIC or ANF alone. In contrast to FENa, combined effects of both agents on V and UNa V in rats on normal and low sodium diets were observed. 3. In normal sodium diet rats, CIC 10(-4) M or ANF 10(-6) M alone inhibited angiotensin II 10(-6) M (AII)-induced decrease in intracapillary volume reflected by the glomerular [3H]-inulin space (GIS). In contrast, CIC or ANF alone did not inhibit AII-induced decrease in GIS in low sodium diet rats. Both agents given together inhibited AII-induced decrease in GIS in low sodium diet rats. 4. CIC both alone and in combination with ANF increased nephrogenous cyclic GMP excretion and cyclic GMP accumulation in isolated glomeruli of rats on normal and low sodium diets. In rats on either diet, CIC abolished the difference in ANF-stimulated increase in nephrogenous cyclic GMP excretion and cyclic GMP accumulation in glomeruli. 5. These results suggest that CIC and ANF alone induce relaxation of glomeruli and a resultant increase in glomerular filtration rate in normal sodium diet rats; in contrast, these effects are blunted in the low sodium diet rats. CIC restores glomerular response to ANF in low sodium diet rats, apparently involving inhibition of the cyclic GMP phosphodiesterase.

Animals↗
PubMed1997

C-type natriuretic peptide and the guanylyl cyclase receptors in the rat ovary are modulated by the estrous cycle.

We have previously shown that rat ovaries synthesize atrial natriuretic peptide (ANP) and express the cognate guanylyl cyclase (GC-A and GC-B) receptors for ANP. Since another natriuretic peptide, termed the C-type natriuretic peptide (CNP), can also interact with these receptors, we have investigated whether rat ovaries express CNP and if so, whether the concentration of this natriuretic peptide and the guanylyl-cyclase receptors are influenced by the estrous cycle. CNP mRNA was detected in rat ovaries using a reverse transcription (RT) polymerase chain reaction (PCR) strategy. RIA of ovarian extracts, obtained at the individual days of the estrous cycle, revealed the presence of immunoreactive CNP. The highest levels of CNP were detected at proestrus and were approximately 4-fold higher than the levels seen at any other stage of the cycle. GC-A and GC-B receptors were detected using quantitative autoradiography after application of either [125I]ANP or [125I]-tyr0CNP to sections of frozen ovaries. The highest specific binding of each radiolabeled ligand was seen in ovaries from proestrous animals. The GC-B receptors were localized to the membrana granulosa of developing ovarian follicles. Using quantitative PCR, we determined that levels of GC-A and GC-B mRNAs were highest in the ovaries of proestrous animals and were approximately 2- to 3-fold higher than the levels seen at diestrus. These findings demonstrate that a natriuretic peptide system, consisting of ligands and receptors, is present in the rat ovary. Since CNP and the GC receptors show coordinate estrous cycle-dependent variation with maximal expression at proestrus, we speculate that the natriuretic peptides may play an important role in either the development of ovulatory follicles or in the ovulatory process.

Animals↗
PubMed1997

Regulation of the natriuretic peptide system in rat uterus during the estrous cycle.

Uterine natriuretic peptides may be involved in the alterations that occur in the uterus during the estrous cycle through its role in hydromineral balance. The following studies were performed to determine whether uterine natriuretic peptides and receptors follow a cyclic pattern during the estrous cycle. The results obtained show that atrial natriuretic peptide (ANP) content in rat uterine tissue was low in proestrus (8.5 +/- 2.6 pg/g) and significantly increased (P < 0.001) in estrus (71.5 +/- 16.6 pg/g), metestrus (82.6 +/- 19.7 pg/g) and diestrus (91.0 +/- 19.4 pg/g), whereas plasma ANP was not altered during the cycle. Similarly, measurement of uterine ANP mRNA by reverse transcribed polymerase chain reaction (RT-PCR) indicated lowest levels of ANP mRNA at proestrus. Measurement of C-type natriuretic peptide (CNP) by a specific and sensitive radioimmunoassay revealed that uterine CNP also varies with the estrous cycle. Uterine CNP was low in diestrus (143.2 +/- 22.4 pg/mg protein) as compared with proestrus, estrus and metestrus (305.3 +/- 51.5, 267.5 +/- 44.9, 291 +/- 41.2 pg/mg protein respectively, P < 0.05). Autoradiography performed on uterine tissue slices localized natriuretic peptide receptors to myometrial smooth muscle layers and to endometrial uterine glands. High binding of 125I-ANP was observed in proestrus and estrus with 60-75% decreases during metestrus and diestrus. Binding of 125I-tyr0CNP to uterine slices was also high during proestrus, but declined by 35% at estrus, metestrus and diestrus. The alterations in the receptors were also observed at the level of synthesis. RT-PCR detection of guanylyl cyclase A (GC-A) receptor mRNA and guanylyl cyclase B (GC-B) mRNA showed high signals at proestrus but 4- and 2-fold reductions respectively at metestrus and diestrus. In conclusion, variations in uterine ANP and CNP and their receptors during the rat estrous cycle imply the involvement of the natriuretic peptides in uterine hydromineral balance and myometrial motor activity.

Animals↗
PubMed1997

Anticardiolipin, anti-beta(2)-glycoprotein I, antiprothrombin antibodies, and lupus anticoagulant in patients with systemic lupus erythematosus with a history of thrombosis.

OBJECTIVE: To determine the clinical importance of anticardiolipin (aCL), anti-beta(2)-glycoprotein I (a beta(2)-GPI), antiprothrombin (aPT), and lupus anticoagulant (LAC) antibodies in patients with systemic lupus erythematosis (SLE) with and without a history of thrombosis. METHODS: We studied 100 patients with SLE (32 with a history of thrombosis), 27 patients with a lupus-like disease (9 with a history of thrombosis), and 41 healthy volunteers, IgG and IgM aCL, antibodies to the protein cofactors (a beta(2)-GPI and aPT) were determined by ELISA. Eighty-six of 127 patients were also tested for LAC. RESULTS: IgG aCL and LAC were associated with thrombosis but sensitivity (63 and 61%) and specificity (66 and 66%, respectively) of these tests were low. IgG and IgM a beta(2)-GPI were, respectively, 85 and 86% specific for a thrombotic history, but sensitivity was very low (32 and 29%). High IgG aCL were associated with the presence of a beta(2)-GPI and were 85% specific for thrombosis. There was no significant association between IgG or IgM aPT and thrombosis. CONCLUSION: Only high levels of IgG aCL and presence of LAC and/or a beta(2)-GPI are relevant in defining a thrombotic subset of patients with SLE. Longitudinal prospective studies are needed to investigate the predictive value of the different antiphospholipid and protein cofactor antibodies.

Adult↗
PubMed1997

Thrombin generation measured ex vivo following microvascular injury is increased in SLE patients with antiphospholipid-protein antibodies.

Antiphospholipid-protein antibodies (APA) include lupus-type anticoagulant (LA) and antibodies recognizing complexes of anionic phospholipids (e.g. cardiolipin) and proteins (e.g. prothrombin and beta2-glycoprotein I). The presence of APA is associated with an increased risk of both arterial and venous thrombosis. However, the pathogenic mechanism leading to thrombosis in patients with APA remains unclear. We studied 32 patients with systemic lupus erythematosus (SLE) who were divided into two groups depending on the presence (n = 19) or absence (n = 13) of APA. Healthy volunteers (n = 12) matched by age and sex served as controls. In all subjects LA and IgG class anticardiolipin antibodies (ACA) were determined. Thrombin generation was monitored ex vivo measuring fibrinopeptide A (FPA) and prothrombin fragment F1 + 2 (F1 + 2) in blood emerging from a skin microvasculature injury, collected at 30 second intervals. In subjects with antiphospholipid antibodies mean FPA and F1 + 2 concentrations were significantly higher at most blood sampling times than in controls. In some SLE patients with APA the process of thrombin generation was clearly disturbed and very high concentrations of fibrinopeptide A were detected already in the first samples collected. Two minutes after skin incision SLE patients without APA produced slightly more FPA, but not F1 + 2, as compared to healthy subjects. Mathematical model applied to analyze the thrombin generation kinetics revealed that APA patients generated significantly greater amounts of thrombin than healthy controls (p = 0.02 for either marker). In contrast, in the same patients generation of thrombin in recalcified plasma in vitro was delayed pointing to the role of endothelium in the phenomenon studied. In summary, these data show for the first time that in SLE patients with antiphospholipid-protein antibodies thrombin generation after small blood vessel injury is markedly increased. Enhanced thrombin generation might explain thrombotic tendency observed in these patients.

Adult↗
PubMed1996

Effect of chronic moderate ethanol consumption on heart brain natriuretic peptide.

There is experimental evidence indicating that chronic moderate ethanol consumption delays the age-dependent increase in blood pressure. Since the brain natriuretic peptide (BNP) is a potent hypotensive hormone, the effect of chronic ethanol treatment on the heart BNP system was investigated, using spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. Chronic moderate ethanol consumption resulted in significantly lower circulating BNP levels for both SHR (206.9 +/- 18.5 vs. 306.9 +/- 28.1 pg/ml, n = 12, P < or = 0.05) and WKY rats (131.3 +/- 20.7 vs. 220.6 +/- 25.0 pg/ml, n = 12, P < or = 0.05). Left and right atrial BNP content and concentration in WKY rats and left atrial BNP content and concentration in SHR rats were augmented by the ethanol treatment, but not atrial BNP mRNA. In ventricular tissue, alcohol had no effect on total BNP content of either SHR or WKY rats, but it induced a significant elevation in ventricular BNP concentration (microgram/mg protein) and BNP mRNA in SHR, but not WKY rats. Thus, chronic ethanol treatment resulted in specific alterations in the activity of the heart BNP system.

Age Factors↗
PubMed1996

Natriuretic peptide system in the rat submaxillary gland.

Natriuretic peptides and their receptors were characterized in rat submaxillary glands (SGs). Reverse phase-high performance liquid chromatography (HPLC) of rat SGs extracts revealed the presence of the 28-amino-acid (AA) circulating peptide ANP (Ser99-Tyr126) and the 126-AA prohormone (Asn1-Tyr126). The presence of ANP prohormone indicated that SGs are a site of ANP synthesis. Indeed, ANP mRNAs were demonstrated. ANP mRNA was 10 times lower than in the lung and only about 7 times lower than in the hypothalamus. ANP content in SG was determined as 30 +/- 8 ng/mg of protein (n = 7). In addition the presence of another member of the natriuretic peptide family, C-type natriuretic peptide (CNP), was found in SG. The CNP level of 293 +/- 38 pg/mg protein was significantly higher than in the lungs (44 +/- 6 pg/mg protein, P < 0.001, n = 5), but about 15 times lower than in hypothalamus (4.5 +/- 0.6 ng/mg protein, P < 0.001, n = 6). Both guanylyl cyclase and clearance receptors were expressed in SG. The presence of natriuretic peptide transcripts and their receptors suggests a role in rat SG functions.

Animals↗
PubMed1996

Effect of chronic ethanol consumption on the atrial natriuretic system of spontaneously hypertensive rats.

There is a lot of discussion on the effects of ethanol (ETOH) on blood pressure (BP). It has been suggested that chronic moderate ETOH consumption prevents the development of age-dependent hypertension in humans and spontaneously hypertensive rats (SHR). However, the mechanism mediating this effect is unknown. In the present studies, we hypothesized the implication of atrial natriuretic peptide (ANP), a BP-lowering hormone, on the antihypertensive effect of moderate ETOH consumption. A 20% v/v solution of alcohol was given as drinking fluid to SHR and normotensive Wistar-Kyoto (WKY) rats for up to 32 weeks. This treatment prevented, at least in part, the age-dependent increase of BP in SHR and WKY rats. The lower BP was associated with significantly lower levels of circulating atrial natriuretic peptide in both groups. After chronic ETOH administration, total ANP content and concentration were higher in the left and right atria of SHR and WKY rats than in water-treated controls. Despite the ETOH-induced increase in atrial ANP content, there was no significant change in atrial ANP mRNA, suggesting decreased atrial release. Chronic ETOH treatment significantly reduced ANP mRNA in the ventricles of SHR but not of WKY rats. Correspondingly, ventricular ANP content and concentration were lowered by ETOH in SHR only. Chronic ETOH administration induced a significant increase of plasma arginine vasopressin and a significant decrease of plasma aldosterone in SHR but not in WKY rats. Thus, chronic ETOH treatment prevented the age-dependent elevation of BP in both SHR and WKY rats and altered the activity of heart ANP as well as of the aldosterone and plasma arginine vasopressin systems.

Aging↗
PubMed1996

Alteration of lung atrial natriuretic peptide receptors in genetic cardiomyopathy.

These studies were designed to characterize the atrial natriuretic peptide (ANF) receptor subtypes [guanylyl cyclase natriuretic peptide receptors (NPR-A, NPR-B) and NPR-C] in lungs of normal hamsters and to evaluate alterations in receptor kinetics in genetic cardiomyopathy (CMO), a model of human congestive heart failure. Lung membranes were obtained from normal and CMO 200-to 230-day-old hamsters. Cross-linking and competitive binding receptor assays using 125I-labeled human ANF showed that lung membranes exhibit NPR, mainly guanylyl cyclase NPR-A and clearance NPR-C receptors. Stimulation of guanylyl cyclase by ANF and C-type natriuretic peptide (CNP) confirmed the presence of NPR-A and NPR-B. The maximum binding capacity of total ANF binding sites (442 +/- 68 vs. 271 +/- 57 fmol/mg protein, P < 0.05) was reduced, but dissociation constant (0.26 +/- 0.04 vs. 0.41 +/- 0.08 nM) was not altered in CMO animals. Similar reductions were observed in the binding sites for brain natriuretic peptide (BNP; 438 +/- 83 vs. 236 +/- 53 fmol/mg protein) and CNP (321 +/- 80 vs. 165 +/- 56 fmol/mg protein, P < 0.05) which may reflect a decline in NPR-A and NPR-B and/or NPR-C. Acid wash improved binding of 125I-labeled rat ANF to lung membranes of both normal and CMO hamsters, but the tendency towards reduced binding in CMO hamsters did not reach statistical significance, implying that downregulation may not have been due only to prior occupancy of the receptors. Transcripts of NPR-A, NPR-B, and NPR-C receptors in hamster lungs were detected by quantitative polymerase chain reaction. Compared with normal controls, the CMO hamster lung NPR-A mRNA was reduced by 50%, but NPR-B mRNA and NPR-C mRNA were not altered. Moreover, CMO hamster lungs showed less activation of guanylyl cyclase by ANF. These studies demonstrate that lung NPR are downregulated in hamster CMO.

Animals↗
PubMed1996

[Prevalence of thrombosis in secondary antiphospholipid-protein syndrome].

Antiphospholipid-protein syndrome (APS) comprises venous and arterial thrombosis, spontaneous abortion and thrombocytopenia in patients with antiphospholipid-protein antibodies (APA). Such antibodies are detected by immunoenzymatic (ELISA) methods (e.g. anticardiolipin antibodies-ACL) or coagulation assays (lupus anticoagulant-LA). APS in patients showing other symptoms of autoimmune disease is called secondary antiphospholipid-protein syndrome. The aim of the study was to find relation between history of thrombosis and APA in a group of patients with lupus erythematosus and lupus-like disease. Lupus anticoagulant was detected by a three step procedure using phospholipid dependent clotting assays and anticardiolipin antibodies were measured by ELISA. We studied 95 subjects (91 women, 4 men) suffering from lupus erythematosus (67 patients) and lupus-like-disease (28 patients). Lupus anticoagulant was found in 26, anticardiolipin antibodies IgG in 34 and IgM in 27 subjects. In a retrospective study 40 thrombotic events were detected in 36 patients; deep vein thrombosis in 19, pulmonary embolism in 7, ischaemic CNS events in 13 and myocardial infarction in one. Thrombosis was present more often in subjects with LA (61%) and ACL IgG (52%) than in subjects without these antibodies (24%) (p = 0.004 and 0.015, respectively). ACL IgM antibodies were not related to thrombotic episodes. The ACL IgG antibodies and LA are helpful in identifying subjects at risk factors of venous and arterial thrombosis among patients suffering from lupus erythematosus and lupus-like disease.

Adolescent↗
PubMed1996

[Evan's syndrome with antiphospholipid-protein antibodies].

This is a case report of a 34 years old man with Evans syndrome associated with antiphospholipid-protein antibodies. They include lupus anticoagulant and antibodies against cardiolipin, prothrombin and beta 2-glycoprotein I, detected by ELISA. No thrombotic events were observed. The presence of several antibodies directed against surface cell membrane structures in Evans syndrome suggests a common pathogenetic mechanism.

Adult↗
PubMed1996

[Laboratory diagnosis of lupus anticoagulant].

Lupus anticoagulant (LA) prolongs clotting times in vitro, but in vivo leads to an increased risk of thromboembolic complications. LA is detected in many patients with lupus erythematosus but also in subjects without any autoimmune disease (primary antiphospholipid syndrome). We determined LA in 133 patients, mostly with lupus erythematosus and other autoimmune diseases. Three screening and two confirmatory tests based on different mechanisms of clotting system activation were used. LA was found in 34 patients. DRVVT was the most useful test in detecting LA while kaolin clotting time was the least sensitive. Anticardiolipin antibodies (ACL) of IgG class were found in 41 patients studied (31%). They were most often detected in patient positive for LA (64%). ACL IgM were not associated with prolonged clotting times. Laboratory diagnosis of antiphospholipid syndrome is easy when the presence of LA is confirmed by two independent tests and in addition ACL would be detected. In other cases, when only single tests are positive, it is suggested to repeat diagnostic procedure at least once.

Adolescent↗
PubMed1995

Renal atrial natriuretic factor receptors in hamster cardiomyopathy.

Hamsters with cardiomyopathy (CMO), an experimental model of congestive heart failure, display stimulated renin-angiotensin-aldosterone and enhanced sympathetic nervous activity, all factors that lead to sodium retention, volume expansion and subsequent elevation of plasma atrial natriuretic factor (ANF) by the cardiac atria. However, sodium and water retention persist in CMO, indicating hyporesponsiveness to endogenous ANF. These studies were undertaken to fully characterize renal ANF receptor subtypes in normal hamsters and to evaluate whether alterations in renal ANF receptors may contribute to renal resistance to ANF in cardiomyopathy. Transcripts of the guanylyl cyclase-A (GC-A) and guanylyl cyclase B (GC-B) receptors were detected by quantitative polymerase chain reaction (PCR) in renal cortex, and outer and inner medullas. Compared to normal controls, the cardiomyopathic hamster's GC-A mRNA was similar in cortex but significantly increased in outer and inner medulla. Levels of GC-B mRNA were not altered by the disease. On the other hand, competitive binding studies, autoradiography, and affinity cross-linking demonstrated the absence of functional GC-B receptors in the kidney glomeruli and inner medulla. Also, C-type natriuretic peptide (CNP), the natural ligand for the GC-B receptors, failed to stimulate glomerular production of its second messenger cGMP. In CMO, sodium and water excretion were significantly reduced despite elevated plasma ANF (50.5 +/- 11.1 vs. 309.4 +/- 32.6 pg/ml, P < 0.001). Competitive binding studies of renal glomerular ANF receptors revealed no change in total receptor density, Bmax (369.6 +/- 27.4 vs. 282.8 +/- 26.2 fmol/mg protein), nor in dissociation constant, Kd (647.4 +/- 79.4 vs. 648.5 +/- 22.9 pM). Also, ANF-C receptor density (254.3 +/- 24.8 vs. 233.8 +/- 23.5 fmol/mg protein), nor affinity were affected by heart failure. Inner medullary receptors were exclusively of the GC-A subtype with Bmax (153.2 +/- 26.4 vs. 134.5 +/- 21.2 fmol/mg protein) and Kd (395.7 +/- 148.0 vs. 285.8 +/- 45.0 pM) not altered by cardiomyopathy. The increase in ANF-stimulated glomerular cGMP production was similar in normal and CMO hamsters (94- vs. 75-fold). These results demonstrate that renal ANF receptors do not contribute to the attenuated renal responses to ANF in hamster cardiomyopathy.

Animals↗
PubMed1995

Characterization and distribution of natriuretic peptide receptors in the rat uterus.

Atrial natriuretic peptide (ANP) receptors were characterized in rat uterus. The binding of [125I]ANP to uterine membranes was completely competed for by increasing concentrations of unlabeled ANP (Kd = 0.39 nM) and brain natriuretic peptide (Kd = 1.24 nM) and partially by C-type natriuretic peptide (CNP; Kd = 80.4 nM), but not by C-ANF. Also, [125I]Tyr-CNP bound to uterine membranes was completely competed by unlabeled CNP (Kd = 1.12 nM). Cross-linking of [125I]ANP to uterine membranes revealed the presence of one band of 130 kilodaltons, corresponding to the guanylyl cyclase (GC-A and/or GC-B) subtypes of natriuretic peptide receptors. The presence of messenger RNA coding for genes of both GC-A and GC-B receptors was shown by quantitative reverse transcriptase polymerase chain reaction. Furthermore, ANP and, to a lesser degree, CNP stimulated the production of cGMP in rat uterus. Autoradiographic studies localized the highest binding of [125I]ANP in the endometrium, whereas [125I]Tyr-CNP binding was distributed in the endometrium as well as in the myometrium. These results demonstrate that rat uterine ANP receptors are of the guanylyl cyclase-coupled subtypes. The uterus is a target of natriuretic peptides where ANP induces its biological effects through the production of cGMP.

Animals↗