Biomedical subjects

H Itoh

Publications and source records attributed to H Itoh.

At least 721 records · Page 40Linked to original sources

PubMed1995

Molecular biology and biochemistry of natriuretic peptide family.

The natriuretic peptide family consists of three endogenous ligands; atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP), and is involved in the regulation of cardiovascular homeostasis. Both ANP and BNP act mainly as cardiac hormones and are produced predominantly by the atrium and ventricle, respectively. Expression of the BNP and ANP genes is greatly augmented in patients with congestive heart failure and animal models of ventricular hypertrophy or cardiomyopathy. In the heart, the BNP gene expression is regulated differently from the ANP gene expression both at transcriptional and post-transcriptional levels. Transgenic technology has provided the direct evidence that BNP as well as ANP is involved in the chronic blood pressure control. Contrasting with ANP and BNP, CNP does not act as a cardiac hormone but as a neuropeptide or an endothelium-derived autocrine/paracrine regulator. Endothelial production of CNP is remarkably augmented by various cytokines and growth factors such as transforming growth factor-beta and tumour necrosis factor-alpha, suggesting the pathophysiological significance of CNP in the process of various vascular disorders. Chromosomal mapping of natriuretic peptides has revealed that the CNP gene is localized on mouse chromosome 1, while ANP and BNP are tightly linked on mouse chromosome 4, suggesting that CNP, a local regulator, is functionally and evolutionarily distinct from ANP and BNP, both of which are cardiac hormones. Understanding the molecular biology and biochemistry of the natriuretic peptide family will lead to the better understanding of its physiological and pathophysiological implication, and the clinical application in cardiorenal regulation.

Amino Acid Sequence↗

PubMed1995

Role of nitric oxide in impaired coronary circulation and improvement by angiotensin II receptor antagonist in spontaneously hypertensive rats.

1. To determine whether coronary flow regulation by nitric oxide (NO) is impaired in the hypertensive heart (HTH), coronary perfusion was measured in isolated rat hearts using NO synthesis inhibitor L-NG-monomethyl arginine (L-NMMA) in Wistar-Kyoto (WKY) rat and spontaneously hypertensive rat (SHR) with and without chronic Nomega-nitro-L-arginine-methylester (L-NAME) treatment. Moreover, the effect of angiotensin II receptor antagonist (AT1 receptor antagonist) (TCV-116) on the impaired coronary circulation in HTH was examined. 2. Coronary flow (CF) was decreased in HTH accompanied with cardiac hypertrophy. The decreased response of CF to L-NMMA infusion was diminished in HTH. It is suggested that NO production was reduced in coronary vasculature in HTH. 3. In chronic L-NAME treated SHR, blood pressure and cardiac hypertrophy were accelerated. Although coronary flow resistance (CFR) was increased, the increased response of CFR to L-NMMA infusion was not altered. 4. The AT1 antagonist improved total minimal coronary flow resistance (MCFR) restoring CFR response in SHR, although it did not recover CFR response in chronic L-NAME treated SHR. 5. Taken together the findings suggest that NO production was exhausted in the coronary artery even in the developing stage of hypertension and this exhaustion could contribute to the impairment of coronary circulation of HTH.

Angiotensin II↗

PubMed1995

Altered gene expression of natriuretic peptide receptor subtypes in the kidney of stroke-prone spontaneously hypertensive rats.

1. To elucidate the physiological and pathophysiological role of the natriuretic peptide system in the progression of hypertensive renal disease, we examined the gene expression of natriuretic peptide receptor subtypes, guanylate cyclase-A (GC-A), guanylate cyclase-B (GC-B) and clearance receptor (C receptor), in the kidney of stroke-prone spontaneously hypertensive rats (SHRSP) at 8 and 20 weeks of age, and compared them with their gene expression in age-matched Wistar-Kyoto (WKY) rats. 2. Northern blot analyses revealed that messages for three natriuretic peptide receptor subtypes were expressed in the kidney, and their expressions were higher in the glomeruli than in the whole kidney in each strain. 3. In 20 week old rats with established hypertension, the glomerular concentration of GC-A mRNA was significantly higher in SHRSP than in WKY. The concentrations of GC-B and C receptor mRNA in the glomeruli tended to increase and decrease, respectively, but they were not statistically significant in SHRSP. 4. In 8 week old rats, the glomerular concentrations of GC-A, GC-B and C receptor mRNA were not significantly different between SHRSP and WKY. 5. This study demonstrates that in the progression of hypertension, the expression of GC-A, which mediates biological actions of natriuretic peptides, is enhanced in the kidney of SHRSP compared to that of WKY. Together with the augmented secretion of the ligands previously revealed, altered expression of natriuretic peptide receptor subtypes in SHRSP may have a deterrent role in the development of hypertension and its renal complications.

Animals↗

PubMed1995

Gene regulation of brain natriuretic peptide in cardiocyte hypertrophy by alpha1-adrenergic stimulation.

1. We previously demonstrated that brain natriuretic peptide (BNP) is a cardiac hormone mainly produced in the ventricle, while the major production site of atrial natriuretic peptide (ANP) is the atrium. The production and secretion of BNP and ANP in the hypertrophied ventricles were markedly augmented, serving as a compensation mechanism against ventricular overload by their natriuretic, diuretic and vasodilatory actions. 2. In the present study, we prepared an in vitro model of cardiocyte hypertrophy using cultured neonatal rat ventricular cardiocytes and alpha1-adrenergic stimulation, and examined the gene expressions of BNP and ANP during the process of cardiocyte hypertrophy. 3. The treatment of cultured ventricular cardiocytes with phenylephrine evoked cardiocyte hypertrophy around 24 h after the treatment, which was characterized by augmented expression of the myosin light chain-2 gene and increase in cell size. 4. In this model of cardiocyte hypertrophy, the steady-state level of BNP mRNA rapidly increased to the maximal level within 1 h after the treatment. In contrast, ANP mRNA began to increase at 3 h, and accumulated during the course of cardiocyte hypertrophy. The secretion of BNP from ventricular cardiocytes was also stimulated more rapidly than the ANP secretion. 5. These results indicate that the gene expression of BNP is distinctly regulated from that of ANP in cardiocyte hypertrophy, and suggest a discrete pathophysiological role of BNP as an 'emergency' cardiac hormone against ventricular overload.

Adrenergic alpha-1 Receptor Agonists↗

PubMed1995

Preparation of a monoclonal antibody against mouse brain natriuretic peptide (BNP) and tissue distribution of BNP in mice.

1. In order to explore the significance of brain natriuretic peptide (BNP), a cardiac hormone secreted from the ventricle, in mice, we prepared a monoclonal antibody against mouse BNP (mBNP) and established a specific radioimmunoassay (RIA) for mBNP. 2. A monoclonal antibody, KY-mBNP-I, was prepared by the fusion of mouse myeloma cells X63-Ag8.653 with spleen cells of the BALB/c mouse immunized with synthetic mBNP[108-121] conjugated to bovine thyroglobulin. KY-mBNP-I belonged to an IgG2a subclass and showed a high affinity for mBNP (Ka = 1.8 x 10(11) mol/L-1). 3. The RIA established that using KY-mBNP-I was highly sensitive and specific for mBNP, with an IC50 value of 3 fmol/tube and cross-reactivities of less than 0.003% with related natriuretic peptides. mBNP-like immunoreactivity (mBNP-LI) was detected in the mouse atrium (0.35 +/- 0.02 nmol/g), ventricle (20.5 +/- 0.5 pmol/g) and kidney (0.50 +/- 0.05 pmol/g), but not in other tissues including brain. 4. Gel filtration analysis revealed that the major component of tissue mBNP-LI was co-eluted with synthetic mBNP[77-121], a 45-amino acid mature peptide. 5. The monoclonal antibody and RIA for mBNP established here will provide useful tools to investigate the functional significance of BNP in mice, coupled with the genetic engineering approach.

Animals↗

PubMed1995

Augmented expression of the endothelin-A receptor gene in cultured mesangial cells from stroke-prone spontaneously hypertensive rats.

1. To elucidate the role of endothelin (ET) receptor in hypertension, we studied the expression of the ET-A receptor (ET-AR) gene and the ET-B receptor (ET-BR) gene in cultured mesangial cells isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats. 2. The mesangial cells from both SHRSP and WKY expressed ET-AR predominantly. The level of the ET-AR mRNA in mesangial cells from SHRSP was 5-fold higher than that in the cells from WKY. The ET-BR mRNA in the mesangial cells from both strains was hardly detectable by northern blot analysis. 3. These results demonstrate that the expression of the ET-AR gene was markedly augmented in mesangial cells from SHRSP.

Animals↗

PubMed1995

Gene expression of prostacyclin receptor in the hypertrophied heart of spontaneously hypertensive rats.

1. Prostacyclin elicits potent vasodilation and inhibition of platelet aggregation through binding to its membrane receptor. The impairment of prostacyclin receptor activity is implicated in various human cardiovascular diseases. We recently succeeded in molecular cloning of cDNA for the mouse, rat, and human prostacyclin receptors. 2. In the present study, we examined the mRNA expression of the prostacyclin receptor in various rat tissues, and further investigated its gene expression in the hypertrophied cardiac ventricles of stroke-prone spontaneously hypertensive rats (SHRSP). 3. In rat tissues, a single RNA band of approximately 3.7 kb was detected by northern blotting analysis using rat prostacyclin receptor cDNA as a probe. In adult Wistar rats, abundant mRNA expression was observed in the aorta, lung and spleen. Substantial amounts of transcript were expressed in the heart, pancreas, thymus and stomach. In contrast, no mRNA expression was detected in the brain. 4. We further examined the mRNA expression of the prostacyclin receptor in the ventricles of 21 week old SHRSP. The ventricles of SHRSP showed remarkable hypertrophy, compared with those of age-matched Wistar-Kyoto (WKY) rats. The expression of prostacyclin receptor mRNA in the hypertrophied ventricles of SHRSP was almost equivalent to that in the ventricles of WKY. 5. The present study revealed the gene expression of the prostacyclin receptor in various rat tissues, and further demonstrated the receptor mRNA expression in hypertensive cardiac hypertrophy. The present study will give a clue to investigate the clinical implication of prostacyclin and its receptor.

Animals↗

PubMed1995

Effects of gamma-linolenic and eicosapentaenoic acids on blood pressure in SHR.

1. The present study was performed to determine whether chronic treatments with gamma linolenic acid (n-6, GLA) or eicosapentaenoic acid (n-3, EPA) would alter serum and red blood cell (RBC) unsaturated fatty acid composition, and to determine whether these treatments would affect blood pressure (BP), serum lipid metabolism and the development of atherosclerosis in spontaneously hypertensive rats (SHR). 2. To compare the effects on atherosclerosis, some SHR were denuded of aortic endothelium so that the development of atherosclerosis would be accelerated. Olive oil (control), GLA or EPA (low dose: 5 mg/day per rat, high dose: 50 mg/day per kg, respectively) was administered intraperitoneally for 6 weeks in SHR. 3. GLA treatments increased GLA and its metabolite, dihomo-GLA, levels in serum but not in RBC, while EPA treatments increased EPA level both in serum and in RBC. 4. The BP of control SHR was further elevated. EPA significantly reduced this elevation of systolic, mean and diastolic pressure within the first week and thereafter, whereas GLA did not affect BP elevation. Neither heart rate or bodyweight gain was affected by these treatments. 5. Serum total cholesterol (TC), triglyceride (TG), and glucose (G) levels and the development of atherosclerosis were unaffected by either GLA or EPA treatment. 6. In summary, chronic EPA but not GLA treatment slightly reduced BP elevation in SHR. Although chronic GLA or EPA treatment increased the respective serum level, these treatments unaltered serum TC, TG and G levels, and could not prevent the development of aortic atherosclerosis in SHR.

Animals↗

PubMed1995

Hypothalamic and medullary GABAA and GABAB-ergic systems differently regulate sympathetic and cardiovascular systems.

1. To determine whether hypothalamic and medullary GABA (gamma-aminobutyric acid)B stimulation would affect the sympathetic and cardiovascular activities, and to determine whether these effects would be altered in hypertension, baclofen (a GABAB agonist) was injected into a hypothalamic pressor area (ventromedial hypothalamus, VMH), a depressor area (anterior hypothalamus, AH), or a nucleus tractus solitarius (NTS) in normotensive and spontaneously hypertensive rats (SHR). 2. Intracerebroventricular (ICV) injections of a GABAA agonist (muscimol, 1 mu g) decreased blood pressure (BP) and heart rate (HR). ICV injections of baclofen (2 mu g) elicited biphasic depressor and pressor effects, and these effects were abolished by a pretreatment with saclofen (GABAB antagonist, 100 mu g, icv). 3. Muscimol (400 ng) and baclofen (800 ng) injected into VMH decreased sympathetic nerve activity (SNA), BP and HR to almost similar levels, while saclofen injected into VMH increased HR without affecting BP levels. 4. The same dose of baclofen injected into AH increased BP, but muscimol (AH) did not alter BP. 5. Both muscimol and baclofen injected into NTS increased BP, but its magnitude was larger in baclofen injections. 6. Depressor and sympatho-inhibitory effects of baclofen (VMH) in SHR were larger than those in normotensive Wistar-Kyoto (WKY) rats, while pressor responses elicited by baclofen (AH) did not differ between SHR and WKY. 7. In summary, GABA reduces SNA, BP and HR through both GABAA and GABAB receptors in VMH. In addition, the GABAB system acts on AH and NTS to further regulate the cardiovascular activities. In SHR, GABAB-ergic dysfunction in VMH but not in AH might contribute to the development of hypertension.

Animals↗

PubMed1995

Role of baroreflex and central alpha2-adrenergic receptor systems in the diurnal variation of blood pressure and heart rate in normotensive and hypertensive rats.

1. To elucidate whether baroreflex could contribute to manifest the diurnal blood pressure variations (DBPV) in normotension and hypertension, DBPV were recorded continuously via a femoral artery in awake normotensive (NT) rats and spontaneously hypertensive rats (SHR) with and without sinoaortic denervation (SAD). To determine the role of central alpha2-adrenergic receptor system in DBPV in hypertension, guanabentz (0.5-1.0 mu g/kg per min) was infused in SHR. 2. There were no differences in mean arterial pressure (MAP) variability (SD) of MAP of 24 h (MAP -- SD/MAP) and SD of 24 h heart rate (HR -- SD/HR) between SHR and NT. SAD did not elevate MAP and HR in both SHR and NT. 3. However, in SAD rats, MAP -- SD/MAP was significantly greater than those in sham-operated rats in both SHR and NT, while MAP -- SD/MAP and HR -- SD/HR did not show any difference between the two groups even after SAD. On the other hand, SAD did not augment HR -- SD/HR in either strain. 4. During guanabentz infusion, MAP was significantly lowered in sham-operated and SAD -- SHR. Moreover, MAP -- SD/MAP was significantly reduced in sham-operated, but it was not in SAD -- SHR. 5. These findings suggest that baroreflex could suppress tonically the diurnal change of blood pressure in NT and SHR. The regulation of diurnal blood pressure by baroreflex via a central alpha-adrenergic receptor system may be altered in SHR.

Adrenergic alpha-2 Receptor Antagonists↗

PubMed1995

Primary malignant lymphoma of the intestine: clinicopathologic and immunohistochemical studies of 39 cases.

Clinicopathologic and immunohistochemical features in 39 cases of primary intestinal non-Hodgkin's lymphoma (NHL) in Japanese patients were studied. Only resection materials in state IE and IIE-1 were included in this study because of the certainty that the intestine was the primary site of the lymphoma. The updated Kiel classification was used to classify NHL. Histologically, only two cases (5.1%) were follicular lymphomas, and the others were diffuse lymphomas. Twenty-eight patients (71.8%) had high-grade NHL and 11 (28.2%) had low-grade NHL. Twenty (71.4%) of the 28 high-grade NHL were centroblastic lymphomas, and 14 (70.0%) of these 20 cases of centroblastic lymphoma were the polymorphic variant. Ten (90.9%) of the 11 low-grade NHL were low-grade mucosa-associated lymphoid tissue (MALT) lymphomas. Macroscopically, 18 patients had polypoid masses, 17 ulcerative tumors and four had diffusely infiltrating NHL. Seven of the 10 low-grade MALT lymphomas were polypoid masses. Immunohistochemically, 35 lesions (89.7%) were of the B cell phenotype and three (7.7%) were of the T cell phenotype. In the remaining case, the cell lineage could not be determined. No lesions were considered to be of histiocytic origin. The 5 year survival rate for high-grade B cell lymphomas was poorer than for low-grade B cell lymphomas, and the present study indicated that the histological grade of the intestinal B cell lymphomas was a prognostically significant factor.

Adolescent↗

PubMed1995

Immunohistochemical expression of glutathione S-transferase pi (GST-pi) and chemotherapy response in malignant ovarian tumors.

OBJECTIVES: To clarify the relationship between the expression of GST-pi and the therapeutic effects of high-dose combination chemotherapy with support by autologous bone-marrow transplantation (ABMT). METHODS: Expression of GST-pi in tissue specimen were analyzed by indirect immunoperoxidase methods using anti-GST-pi polyclonal antibody. RESULTS: (1) Eighteen of 36 cases (50%) tested prior to administration of any chemotherapeutic agents were found to be positive in terms of immunohistochemical expression of GST-pi in the cancer cells. (2) The rate of GST-pi expression was elevated following administration of cisplatin, adriamycin, and cyclophosphamide, which suggests that administration of such anti-cancer agents is capable of inducing expression of GST-pi in cancer cells. (3) GST-pi negative patients exhibit better survival rates than do GST-pi positive patients (Kaplan Meier method: p < 0.001). CONCLUSIONS: Analysis of GST-pi obtained at primary surgery can serve as a valid marker in anticipating chemotherapeutic effects and long-term prognoses.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1995

Salivary and blood lactate after supramaximal exercise in sprinters and long-distance runners.

This investigation examined the reproducibility of salivary lactate measurement in long-distance runners following a 3000-m run and compared the salivary and blood lactate concentrations in sprinters and long-distance runners following a 400-m run. There was no significant difference in salivary and blood lactate between the first and second 3000-m run test. The peak salivary and blood lactate following a 400-m run was higher in sprinters than in long-distance runners. There was a significant relationship between the peak lactate of saliva and that of blood following a 400-m run. The results showed that the salivary lactate following exercise was reproducible and the salivary lactate concentration may serve as a relevant indicator in determining which have a higher lactate production.

Humans↗

PubMed1995

Different effects of traditional Chinese medicines containing similar herbal constituents on prednisolone pharmacokinetics.

Three major traditional Chinese medicines (TCM), Sho-saiko-To, Saiboku-To, and Sairei-To, consist of similar herbal prescriptions containing glycyrrhizin, which is a strong inhibitor of 11 beta-hydroxysteroid dehydrogenase. We performed cross-over open trials in healthy subjects to clarify prednisolone pharmacokinetics on co-administration of these preparations. All subjects received a single oral dose of 10 mg prednisolone before oral treatment with one of the test preparations. After a 2-week wash-out interval, they received one of the test preparations for three days at daily doses of 7.5 or 9.0 g. On the third study day, 10mg prednisolone was administered orally in combination with the test preparation. Area under the curves (AUC) of prednisolone before and after the treatment decreased from 0.94 to 0.78 mg h L-1 (P < 0.05) in the Sho-saiko-To group, increased from 0.92 to 1.06 mg h L-1 (P < 0.01) in the Saiboku-To group, and did not change in the Sairei-To group. AUC ratios of prednisone and prednisolone, which reflect the 11 beta-hydroxysteroid dehydrogenase activity, increased in the Sho-saiko-To group (P < 0.01), decreased in the Saiboku-To group (P < 0.01), and did not change in the Sairei-To group after the treatments. Similar results were observed in ratios of endogenous cortisone to cortisol. Because of the equal glycyrrhizin content in all three preparations, it was unexpected that the 11 beta-hydroxysteroid dehydrogenase effect was different amongst the three groups. These observations suggest that some unknown metabolic enzyme modifiers, promoters or inhibitors, may be involved in these traditional treatments.

Administration, Oral↗

PubMed1995

Quantitation of hepatitis C viral RNA in liver and serum samples using competitive polymerase chain reaction.

AIMS: To investigate whether the amount of hepatitis C viral RNA (HCV-RNA) in liver and serum can predict the effectiveness of interferon treatment in patients with chronic hepatitis C. METHODS: The amount of HCV-RNA in frozen liver tissues and sera of 22 patients with chronic hepatitis C was determined before and after interferon alfa treatment by the competitive reverse transcriptional polymerase chain reaction method. RESULTS: Patients with small amounts of HCV-RNA in serum before treatment showed a significantly more effective response to interferon treatment. After treatment, HCV-RNA disappeared from both the liver and serum of all patients who sustained complete response (n = 11); in contrast, HCV-RNA decreased but persisted in the liver of all those who relapsed after cessation of treatment (n = 11). CONCLUSIONS: The elimination of hepatitis C virus from the liver as well as from the serum seems to be essential for sustained remission. The quantitation of HCV-RNA in liver biopsy specimens obtained after treatment would be a highly accurate predictor of whether relapse is likely to occur.

Base Sequence↗

PubMed1995

Inhibition of hepatic regeneration after 70% partial hepatectomy by simultaneous resection of the bowel in rats.

This study was aimed to evaluate bow simultaneous resection of the bowel influences hepatic regeneration after partial hepatectomy (HTX). Two hundred and sixty-four rats underwent 70% partial HTX, ileocecal resection (ICR), transverse colon resection (TR), colon amputation and simulatenous resection of the liver and the bowel (HTX+ICR, HTX+TR). Hepatic DNA synthesis was remarkably suppressed by simultaneous resection compared with the 70% HTX group (p < 0.01). In simultaneous resection groups, delayed enhanced hepatic protein synthesis (HPS) was observed after the operation as compared with the 70% HTX group, which showed an early postoperative peak of HPS. Postoperative anastomosis leakage occurred more frequently and survival rates were significantly lower in simultaneous resection groups. Higher plasma endotoxin levels of the portal and the peripheral veins were found in simultaneous resection groups as compared with other groups (p < 0.01-0.001). This study suggested that simultaneous resection of the bowel with partial HTX might inhibit hepatic regeneration and result in the increased risk of anastomosis leakage and high surgical mortality rate by increased plasma endotoxin levels and delayed enhanced HPS.

Animals↗

PubMed1995

A high-resolution cytogenetic map of human chromosome 2: localization of 434 cosmid markers by direct R-banding fluorescence in situ hybridization.

We have constructed a high-resolution cytogenetic map of human chromosome 2 with 434 newly isolated cosmid markers by means of direct R-banding fluorescence in situ hybridization. Two markers were mapped to the centromeric region, 173 to the short arm, and 259 to the long arm. The clones were evenly distributed along the entire chromosome, although a tendency toward clustering in R-positive bands was observed. The mapped cosmids provide useful landmarks for construction of a contig map and for positional cloning of cancer-associated genes, as well as genes responsible for hereditary diseases.

Animals↗

PubMed1995

Lipoproteins regulate C-type natriuretic peptide secretion from cultured vascular endothelial cells.

We have shown that oxidized low-density lipoprotein (Ox-LDL) modulates various endothelial cell (EC) functions. C-type natriuretic peptide (CNP), the third member of the natriuretic peptide family to be discovered, is secreted from peripheral vascular ECs and regulates body fluid homeostasis, vascular tone, and vascular growth. This study was designed to investigate the effects of lipoproteins on CNP secretion from cultured ECs. Treatment of bovine carotid ECs with OX-LDL and its extracted lipids resulted in a concentration-dependent suppression of the spontaneous and transforming growth factor-beta 1-stimulated secretion CNP. Native LDL, its extracted lipids, and acetylated LDL were inactive. OX-LDL depleted of its amphiphilic lipids, which was prepared by incubation with defatted albumin, lost its suppressive effect on CNP secretion. 7-Ketocholesterol, one of the amphiphilic lipids in OX-LDL that is transferable from OX-LDL to defatted albumin, suppressed CNP secretion by ECs, thus mimicking the effect of OX-LDL. Coincubation with high-density lipoprotein (HDL), which alone had no effect on CNP release, significantly prevented OX-LDL-induced inhibition of CNP secretion by ECs. Analysis by thin-layer chromatography demonstrated that oxysterols, including 7-ketocholesterol, in OX-LDL were transferred from OX-LDL to HDL during coincubation of these two lipoproteins. These results indicate that OX-LDL suppresses CNP secretion from ECs by 7-ketocholesterol or other transferable hydrophilic lipids in OX-LDL, and the suppressive effect of OX-LDL is reversed by HDL. Lipoproteins thus may regulate CNP secretion from the endothelium of atherosclerotic arteries.

Animals↗