Serum adiponectin, bone mineral density and bone turnover markers in post-menopausal women with newly diagnosed Type 2 diabetes: a 12-month follow-up.

OBJECTIVE: During a period of 12 months, we evaluated the longitudinal impact of metabolic control of diabetes on selected bone turnover markers, bone mineral density and serum adiponectin concentrations in post-menopausal women with newly diagnosed Type 2 diabetes. METHODS: Serum total adiponectin, bone alkaline phosphatase, HbA(1c), urinary deoxypyridinoline excretion, bone mineral density of the total body, lumbar spine and total hip were measured in 57 women aged 50-78 years with newly diagnosed Type 2 diabetes. RESULTS: At baseline, women had normal bone-specific alkaline phosphatase, deoxypyridinoline and bone mineral density, as evaluated by t- and z-scores. After 12 months of treatment, a significant decrease in body weight, waist circumference and HbA(1c) was observed. Bone mineral density of the total body, lumbar spine and total hip decreased by 0.4, 0.2 and 1.0% (P = 0.018) per year, respectively. Adiponectin was inversely correlated with bone mineral density at three sites (R = -0.28, -0.24 and -0.19, respectively). There was a transient increase (P < 0.05) in serum adiponectin within the first 6 months, followed by a slow decrease toward the baseline value during the next 6 months. An improvement in diabetes control had no impact on bone turnover marker levels, which did not change significantly during the entire study period. CONCLUSIONS: Bone turnover markers, bone mineral density and the rate of bone loss are within normal ranges in post-menopausal women with newly diagnosed Type 2 diabetes. Bone mineral density of the total body, lumbar spine and total hip is inversely correlated with total adiponectin.

Can we talk about CD4+CD28- lymphocytes as a risk factor for ischemic stroke?

BACKGROUND: CD4+CD28- lymphocytes are implicated in the destabilization of atheromatous plaque, leading to acute coronary episodes. One may ask whether these cells play a similar role in ischemic stroke pathogenesis with an atherosclerotic background. METHODS: Flow cytometry was applied to determine the percentage of CD4+CD28- lymphocytes in the peripheral blood of patients during the acute phase of their first ischemic stroke (group I) and in patients without a history of stroke but with two of the most important risk factors (hypertension, diabetes) for atherosclerosis-related ischemic stroke (group II). The results were compared with healthy controls. RESULTS: The median percentages of CD4+CD28- lymphocytes in groups I and II did not differ significantly, but for each of these groups the percentage was higher than in the control group. The time of blood sampling from onset of stroke, presence of the ischemic focus in the CT brain scan and severity of neurological deficits did not correlate with the percentage of CD4+CD28- lymphocytes. CONCLUSIONS: We conclude that CD4+CD28- lymphocytes are implicated in mechanisms enhancing the risk of acute ischemic stroke and not a consequence of stroke.

Effects of perindopril treatment on hemostatic function in patients with essential hypertension in relation to angiotensin converting enzyme (ACE) and plasminogen activator inhibitor-1 (PAI-1) gene polymorphisms.

BACKGROUND AND AIM: An imbalance in the hemostatic system is a frequent finding in untreated essential hypertension (HT), and it has been shown that treatment with angiotensin converting entyme (ACE) inhibitors improves hemostatic function. In order to elucidate the role of genetic factors, we studied hemostasis in patients with untreated and treated HT and correlated the results with ACE I/D and plasminogen activator enhibitor-1 (PAI-1) 4G/5G gene polymorphisms. METHODS AND RESULTS: Forty-three males with HT (mean age 31.7 +/- 6.8 years) were compared with 34 age and gender-matched controls. All of the patients were treated with perindopril (4 mg/day) and, after one and six months of therapy, their levels of plasma fibrinogen (Fb), t-PA antigen, PAI-1 antigen, von Willebrand factor (vWF), ACE activity and blood pressure were measured. ACE and PAI-1 genotypes were identified by means of the polymerase chain reaction on DNA isolated from peripheral blood lymphocytes. Untreated patients had significantly higher levels of Fb, PAI-1 (p < 0.01) and t-PA (p < 0.05) regardless of their ACE or PAI-1 genotypes. Perindopril reduced blood pressure regardless of ACE or PAI-1 genotype (p < 0.001). ACE II homozygotes showed the greatest decrease in ACE activity (p < 0.01) and a significant reduction in Fb levels (p < 0.05) after just one month of treatment. Analysis of the group as a whole revealed an increase in t-PA antigen levels after six months of treatment, regardless of ACE or PAI-1 genotype (p < 0.01). CONCLUSIONS: Our results show that essential hypertension predisposes to the procoagulant state characterized by hyperfibrinogenemia and hypofibrinolysis. Perindopril reduced fibrinogen levels in ACE II homozygotes due to its more potent inhibitory action on the renin-angiotensin system in such patients. It improved fibrinolysis by increasing t-PA levels regardless of ACE and PAI-1 genotype.

Lack of association between Gly460Trp polymorphism of alpha-adducin gene and salt sensitivity of blood pressure in Polish hypertensives.

BACKGROUND: Previous studies have suggested that alpha-adducin (alpha-ADD) polymorphism may identify patients with a salt-sensitive form of hypertension. AIM: To investigate the association between Gly460Trp polymorphism of alpha-ADD and the pattern of blood pressure response to subacute (1 week) salt loading and depletion in young adult thin Polish hypertensives. METHODS: The study group consisted of 44 subjects with salt-sensitive hypertension (SS) and 24 subjects with non-salt-sensitive hypertension (SR). Genomic DNA isolated from peripheral blood leukocytes was amplified by PCR method with primers flanking the polymorphic region. The mismatch near to 3'-end of the upstream primer was introduced to create a Nla III restriction site in Trp 460 allele. In addition, excreted fraction of filtered sodium (FENa), plasma renin activity (PRA) and plasma concentrations of aldosterone (ALDO) were determined on normal, low and high salt diets. RESULTS: FENa on normal or high salt diets were significantly lower in the SS hypertensives as compared with the SR patients. PRA in SS group was also significantly lower as compared with results in SR group, but only on high salt diet. No significant difference was detected in frequencies of genotypes and alleles of alpha-ADD gene between SS and SR subjects. An additional analysis with regard to genotype (Gly/Gly vs. Gly/Trp+Trp/Trp) showed no significant difference in changes of blood pressure as well as in results of laboratory investigations. CONCLUSION: Our results suggest lack of association between Gly460Trp polymorphism of alpha-adducin gene and salt sensitivity of blood pressure in Polish hypertensives.

[Analysis of polymorphisms Sma (Hpa II) and Sca I gene precursors of atrial natriuretic peptide (ANP) in patients with essential hypertension]. / Analiza polimorfizmów Sma (Hpa II) i Sca I genu prekursora przedsionkowego peptydu natriuretycznego (ANP) u chorych z samoistnym nadcisnieniem tetniczym.

Both environmental and genetic factors are implicated in the pathogenesis of essential hypertension. The defect of the ANP precursor gene leading to the decrease of ANP synthesis are a cause of the development of sodium-sensitive hypertension in animals. Recent findings in African-Americans who are a model of sodium-sensitive population, reveal a strong association between Sma I polymorphism at intron 2 (the polymorphic site is identical for Hpa II restriction enzyme) or both Sma I and Sca I polymorphism at exon 3 of ANP precursor gene and essential hypertension. The aim of our study was to optimize the methods for Sma I and Sca I analysis in the ANP precursor gene (PCR followed by digestion with restriction enzymes) and to determine the frequencies of Sma I or Sca I genotypes and alleles in patients with sodium-sensitive (SS) or sodium-nonsensitive (SR) hypertension. The Sma I heterozygous mutation (WM genotype) were detected in 4 (8.9%) SS patients and in 2 (10%) patients in SR group. The frequency of Sca I M allele (allele with mutation) was significantly higher in SS group as compared to sodium-nonsensitive hypertensives. Our results suggest that, in contrast to Black hypertensives, in Caucasians with essential hypertension the Sma I polymorphism is very rare and the Sca I polymorphism of ANP precursor gene is associated with sodium-sensitivity of blood pressure.

[Mutation T-->C of nucleotide 2238 in the gene of atrial natriuretic peptide (ANP) precursor and heterogeneity of sodium-sensitive hypertension. Preliminary report]. / Mutacja T-->C nukleotydu 2238 genu prekursora przedsionkowego peptydu natriuretycznego (ANP) i niejednorodnosc sodowrazliwego nadcisnienia tetniczego. Doniesienie wstepne.

Atrial natriuretic peptide (ANP) is involved in the pathogenesis of sodium-sensitive hypertension. The loss of Sca I restriction site in the ANP precursor gene abolishes the regular stop codon. The aim of our study was the analysis of the Sca I gene polymorphism in 23 patients with sodium-sensitive hypertension, the molecular characteristic of the mutation and the comparison of the blood pressure values, plasma renin activity, plasma ANP and aldosterone concentration between patients with or without mutation. Applying the polymerase chain reaction (PCR), followed by digestion with Sca I, the heterozygous mutation has been found in 9 (39%) patients. The sequencing of PCR products indicated that the loss of Sca I restriction site is caused by T2238-->C transition leading to the translation of ANP with two additional arginines. The higher concentration of ANP in plasma has been found in T2238-->C transition patients on normal and high sodium diet as compared with patients without mutation. These preliminary results suggest that the heterogeneity of sodium-sensitive hypertension is associated with the T2238-->C mutation of the ANP precursor gene.

[Comparison of treatment effects with an angiotensin converting enzyme inhibitor--lisinopril and a calcium blocker--nifedipine retard on urinary albumin excretion in patients with non-complicated essential hypertension]. / Porównanie wplywu leczenia inhibitorem enzymu konwertujacego--lizynoprylem i blokerem wapnia--nifedypina retard na wydalanie albumin z moczem u chorych z samoistnym niepowiklanym nadcisnieniem tetniczym.

The purpose of the study was to compare the effect of treatment with an angiotensin converting enzyme inhibitor (Lisinopril, MSD) or calcium blocker (Nifedipine retard, MSD) treatment during three months on blood pressure (measured with sphygmomanometric method and ambulatory blood pressure monitoring--ABPM) and urinary albumin excretion in essential hypertension class I acc. to WHO. Fifteen untreated patients aged 38 +/- 5 years with essential hypertension participated in the study and received diet with normal sodium content. Urinary albumin excretion was measured by RIA method in two 24 hour urine collections and mean value was calculated. ABPM was measured with Spacelabs monitor. After first examination 8 patients were randomly selected for the treatment with lisinopril and 7 patients to the treatment with nifedipine. The doses of both drugs were gradually adjusted to reach diastolic blood pressure below 90 mmHg. After 3 months of treatment urinary albumin excretion and blood pressure was found in both after treatment in patients treated with lisinopril but not in those receiving nifedipine. In patients treated with lisinopril a correlation between the decrease in systolic and diastolic blood pressure (measured by ABPM) and decrease of urinary albumin excretion was demonstrated. It was concluded that the normalization of blood pressure induced by lisinopril treatment in patients with uncomplicated essential hypertension and normoalbuminuria is accompanied with significant diminution of urinary albumin excretion which suggests preventive action of the drug in the development of microalbuminuria. Diminution of urinary albumin excretion caused by lisinopril is probably due to both the decrease of blood pressure and the specific renal action of the drug.

Atrial natriuretic peptide and cyclic guanosine monophosphate plasma concentrations in patients with thyrotoxicosis and atrial fibrillation. Effect of short-term methimazole therapy.

Plasma immunoreactive atrial natriuretic peptide (ANP) and cyclic guanosine monophosphate (cGMP), serum thyroxine (T4), triiodothyronine (T3), and thyrotropin (TSH) concentrations were measured in 11 patients with thyrotoxicosis and atrial fibrillation (group 1), in 5 patients with thyrotoxicosis and sinus cardiac rhythm (group 2) and in 8 healthy subjects in comparable age. Patients with thyrotoxicosis were studied before and after treatment with methimazole (3 x 20 mg daily) during 10 days. During treatment sinus cardiac rhythm returned in 6 patients with initial fibrillation (group 1a) while 5 patients still presented atrial fibrillation at the end of the study (group 1b). All patients from group 2 maintained a sinus cardiac rhythm throughout the study. Median plasma concentrations of ANP and cGMP before treatment in patients from group 1 were higher: 43.8 pmol/l and 11.0 nmol/l, respectively than in patients from group 2: 20.0 pmol/l (p < 0.005) and 6.5 nmol/l (p < 0.01), respectively. In all groups of patients methimazole treatment resulted in a significant decrease of plasma ANP and cGMP concentrations in parallel to a reduction of serum T3 and T4 levels. After therapy, plasma ANP and cGMP levels in patients from group 1a were not significantly different from those in patients from group 2, while in patients from group 1b remained slightly elevated. Presented results suggest that atrial fibrillation in patients with thyrotoxicosis represents an important factor augmenting plasma ANP and cGMP levels, in addition to the stimulatory effect exerted by thyroid hormones. However, the marked reduction of serum thyroid hormones produced by short-term methimazole treatment in patients with thyrotoxicosis was associated with parallel decrease of plasma ANP and cGMP levels toward normal values. Therefore, the influence of thyroid hormones on plasma ANP and cGMP concentrations seems relatively more important than the effect of atrial fibrillation.

[Churg-Strauss syndrome: two cases histories]. / Zespól Churga-Straussa: opis dwóch przypadków.

Two cases of Churg-Strauss syndrome with severe polyneuropathy have been diagnosed according to clinical and histopathologic criteria. Perforation of small intestine, successfully treated with surgery, was observed in one of two cases. The resected part of gut presented specific histologic picture of Churg-Strauss syndrome.

[Comparison of the effect of short-term treatment with nifedipine and verapamil on blood pressure, plasma atrial natriuretic peptide (ANP) and cyclic guanosine monophosphate (cGMP) in patients with primary arterial hypertension I degree according to WHO]. / Porównanie wplywu krótkotrwalego leczenia nifedypina i werapamilem na cisnienie tetnicze oraz stezenie przedsionkowego peptydu natriuretycznego (ANP) i cyklicznego guanozynomonofosforanu (cGMP) w osoczu chorych na pierwotne nadcisnienie tetnicze I stopnia wg WHO.

The aim of the study was the comparison of the effect of seven day treatment with nifedipine (2 x 10 mg daily) and subsequently with verapamil (3 x 40 mg daily) on blood pressure, heart rate, plasma ANP, cGMP, renin activity (PRA), aldosterone (ALDO) concentrations in patients with primary hypertension. The material consisted of 12 untreated patients with primary arterial hypertension Io WHO. These results suggest that short-term treatment with nifedipine and subsequently with verapamil in patients with primary hypertension Io WHO not influence on plasma ANP, cGMP, PRA and ALDO in spite of blood pressure reduction and the changes in heart rate. It seems that ANP did not participate in hypotensive action of nifedipine and verapamil. No augmentation of urinary sodium excretion was found after short-term treatment with nifedipine or verapamil.

[Effect of different amounts of dietary sodium on plasma atrial natriuretic peptide (ANP)in essential salt sensitive hypertension]. / Wplyw róznej ilosci sodu w diecie na stezenie w osoczu przedsionkowego peptydu natriuretycznego (ANP) w pierwotnym nadcisnieniu tetniczym sodowrazliwym.

The aim of the study was an evaluation of the effect of different dietary sodium intake on: blood pressure, plasma concentration of atrial natriuretic peptide (ANP), cyclic guanosine monophosphate (cGMP), aldosterone (ALDO) and plasma renin activity (PRA) in patients with primary sodium sensitive arterial hypertension class I acc. to WHO criteria. Thirteen patients, non treated, with sodium sensitive arterial hypertension aged 30 +/- 8 years participated in the study. Blood samples were taken three times: in 5th day of normal sodium intake (100-120 mmol Na per 24 h); in 5th day of low sodium diet (10-20 mmol Na per 24 h); in 5th day of high sodium diet (200-220 mmol Na per 24 h). During 24 hours before each blood sampling the urine was collected and sodium and potassium excretions were evaluated. Concentrations of ANP, cGMP, ALDO in plasma and PRA were determined by radioimmunoassays and serum sodium and potassium concentration by flame photometry. Significant (p < 0.05) diminution of blood pressure, plasma ANP and cGMP concentrations and the increase of plasma ALDO and PRA after sodium restriction when compared to normal sodium diet were found. High sodium diet resulted in significant increase of blood pressure, plasma ANP and cGMP concentrations to the values comparable with these on normal sodium diet. On the contrary PRA and plasma ALDO concentration decreased (p < 0.001) below the values during normal sodium diet. Urinary sodium excretion corresponded to dietary sodium intake during all diets.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effect of intravenous sodium chloride load on levels of atrial natriuretic peptide (ANP) and 3'5' guanosine monophosphate (cGMP) in plasma of patients with uncomplicated sodium-sensitive arterial hypertension maintained on different dietary sodium intake]. / Wplyw dozylnego obciazenia ladunkiem sodu na stezenie przedsionkowego peptydu natriuretycznego (ANP) i 3'5' guanozynomonofosforanu (cGMP) w osoczu chorych z niepowiklanym samoistnym nadcisnieniem tetniczym sodowrazliwym zywionych dieta o róznej zawartosci sodu.

The aim of this work was an evaluation of the effect of the acute hypervolemia induced by 90 min intravenous infusion of 1500 ml 0.9% NaCl (16.7 ml/min) on blood pressure, plasma concentration of the atrial natriuretic peptide (ANP), cyclic guanosine monophosphate (cGMP), aldosterone (ALDO), plasma renin activity (PRA) in patients with essential hypertension on the normal, low and high sodium intake. Twelve patients with noncomplicated essential sodium-sensitive arterial hypertension participated in the study. Sodium chloride infusions were performed three times: first--on the fifth day of normal daily sodium u intake (110-120 mmol/day), second--on the fifth day of low sodium intake (10-20 mmol/day), third--on the fifth day of high sodium intake (200-220 mmol/day). Acute intravenous sodium chloride load induced a significant increase of the mean arterial pressure (MBP) only when the patients were on the high sodium diet. This increase of the MBP was associated with a significantly lower increment of plasma ANP, cGMP, lower decrement of ALDO and PRA when compared to normal- or low- sodium intake. The results suggest an impairment of the adaptive homeostatic mechanisms induced by an acute intravenous sodium load in patients with noncomplicated salt-sensitive essential hypertension ingesting high-sodium diet.

Plasma concentrations of atrial natriuretic peptide and cyclic guanosine monophosphate in patients with hyperthyroidism before and after short-term treatment with methimazole.

The aim of the study was to answer the question whether a rapid decrease in serum triiodothyronine (T3) and thyroxine (T4) levels resulting from the treatment with a full dose (3 x 20 mg daily) of methimazole applied in patients with thyrotoxicosis is associated with the parallel diminution of plasma atrial natriuretic peptide (ANP) and its second messenger-cyclic guanosine monophosphate (cGMP) concentrations. Sixteen patients with thyrotoxicosis of mean age 41.5 +/- 10.5 years participated in the study. Short-term (10 days) methimazole treatment resulted in a significant decrease in serum T3 and T4 concentrations to the values found in 14 healthy subjects serving as control group. Plasma ANP and cGMP levels also decreased significantly during the treatment attaining the normal range. A significant correlation was found between the decrease in serum T3 and T4 concentrations during the treatment and the decrease in plasma ANP level. The decrease in plasma ANP was not closely correlated with the reduction of cGMP levels. These results indicate that: 1) a steep decrease in serum thyroid hormone concentrations induced by a full methimazole treatment during ten days in patients with thyrotoxicosis due to Graves' disease was accompanied by the return of elevated plasma ANP levels to normal range; 2. diminution of serum concentrations of both T3 and T4 during the treatment was correlated with the decrease in plasma ANP; 3) reduction in plasma cGMP concentration associated with short-term methimazole treatment in thyrotoxicosis seems to depend not only on the diminution of plasma ANP level.

Iodized salt consumption, urinary iodine concentration and prevalence of goiter in children from four districts of north-western Poland (Szczecin coordinating center).

The study was aimed at evaluation of iodized salt consumption, urinary iodine concentration and incidence of goiter in children from four districts of north-western Poland: Szczecin, Koszalin, Slupsk and Gorzów Wlkp. The study was a part of the national programme: "Investigations of iodine deficite and iodine prophylaxis in Poland". The investigations were performed in ten schools randomly selected by Coordinating Centre in Kraków. Altogether 1793 children attending these schools (838 boys and 955 girls) of age between 6 ad 13 years, living in the cities and villages of coastal and lowland region were studied. The examination included interview in the form of a standard questionnaire, physical examination of the thyroid according to the WHO criteria, ultrasonographic evaluation of thyroid volume and determination of iodine concentration in single urine specimen. It appeared that only 11.2% of children used to consume iodized salt. Mean iodine concentration in urine was 76.2 micrograms/l both in children consuming and not consuming iodized salt, indicating dietary iodine deficiency. The incidence of goiter in country population of children (12.9%), indicated that the region of north-western Poland should be considered as an area of mild goiter endemy. These results suggest a need for iodine supplementation of edible salt in this region of Poland.

[Effect of naloxone on beta-endorphin and insulin concentrations during glucose tolerance testing in patients with simple obesity]. / Wplyw naloksonu na stezenia beta-endorfiny i insuliny w czasie testu doustnej tolerancji glukozy w otylosci prostej.

The concentrations of beta-endorphin, ACTH, insulin (IRI), glucagon (IRG), cortisol and growth hormone were determined by radioimmunoassay during oral glucose tolerance test (OGTT) performed in 13 obese patients with normal glucose tolerance and without arterial hypertension. The test was performed in random, before and after intravenous administration of 0.8 mg of naloxone. Six persons with normal body weight served as controls. Higher basal concentrations of beta-endorphin and significant increase in beta-endorphin levels during OGTT, without concomitant increase in ACTH concentrations, have been found in obese patients. No effect of naloxone on beta-endorphin liberation during OGTT was observed, though the drug caused lowering in maximal increment of beta-endorphin and paradoxically lowered the concentrations of ACTH and cortisol. The basal concentrations of beta-endorphin did not correlate with the concentrations of insulin, ACTH, cortisol and growth hormone. Elevated concentrations of insulin, lowered concentration of growth hormone and normal levels of glucose and glucagon were observed in basal conditions, and excessive responses of insulin, glucose and glucagon were observed in obese patients during OGTT. Naloxone lowered insulin response and inhibited the fall of growth hormone during OGTT but did not influence the concentrations of glucose and glucagon. No correlation was found during OGTT after naloxone between insulin and beta-endorphin, ACTH or cortisol, whereas negative correlation was observed between insulin and growth hormone. The obtained results suggest that the elevated concentrations of beta-endorphin in simple obesity may be of both hypophyseal and peripheral origin. Hyper-beta-endorphinemia observed in obesity is probably not directly responsible for hyperinsulinemia, it may, however, be responsible for lower sensitivity of tissues to the action of insulin.

Exaggerated natriuresis induced by sodium chloride infusion in essential hypertension is accompanied by an exaggerated urinary 3' 5' guanosine monophosphate excretion.

The effects of an intravenous infusion of physiological saline on plasma atrial natriuretic peptide (ANP), guanosine 3' 5' monophosphate (cGMP) concentrations, and on urinary cGMP and sodium excretion were studied in 13 patients with essential hypertension, class I according to WHO criteria, and in 10 healthy subjects. It was found that the groups did not differ as to basal and infusion-induced plasma ANP and cGMP and basal urinary cGMP and sodium excretion, but the sodium chloride infusion resulted in a significantly greater urinary cGMP and sodium excretion and creatinine clearance in hypertensive than in control subjects. The results of this study demonstrate that patients with essential hypertension respond to an intravenous sodium chloride load not only with exaggerated natriuresis, but also with augmented urinary cGMP excretion. The latter finding may in part be due to a greater glomerular filtration of cGMP, but increased renal contribution cannot be excluded. Apart from the possible stronger intrarenal effect of ANP on cGMP production in patients with hypertension, independent direct effect of volume expansion on cGMP excretion and modified activity of other cGMP generating systems may all be responsible for the higher urinary cGMP excretion in essential hypertension.

Atrial natriuretic factor in untreated hyperthyroidism.

Increased plasma concentration of atrial natriuretic factor (ANF) in untreated hyperthyroid patients is reported. A significant positive correlation between the concentration of ANF and serum thyroid hormones (T4 and T3) has been found when hyperthyroid patients and healthy controls were pooled together. The mechanism by which thyroid hormones raise plasma ANF concentration and its relevance to the symptomatology of hyperthyroidism is discussed.

Low plasma concentrations of atrial natriuretic peptide in untreated hypothyroid patients.

A group of patients with primary hypothyroidism has been studied, and it is reported that low serum levels of thyroid hormones are accompanied by low plasma atrial natriuretic peptide (ANP) concentrations. While the correlation between ANP and thyroid hormone levels is strong, no correlation was found between ANP and heart rate or arterial blood pressure. It is suggested that thyroid hormones directly stimulate the release of ANP from atrial cardiocytes.