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Biomedical subjects

A Miyata

Publications and source records attributed to A Miyata.

At least 163 records · Page 9Linked to original sources
PubMed1988

Plasma and atrial levels of atrial natriuretic peptide (ANP) in pulmonary hypertensive rats.

Immunoreactive atrial natriuretic peptide (IR-ANP) was measured in plasma and atrium of normal and monocrotaline induced pulmonary hypertensive rats (PH rats). In these animals, there was right ventricular hypertrophy and right ventricular systolic pressure was elevated. Fourteen days after a single dose of monocrotaline (40 mg/kg), plasma IR-ANP concentrations were significantly elevated (964.3 +/- 63.0 pg/ml vs. 521.0 +/- 81.9 pg/ml in controls, p less than 0.001). Tissue levels of IR-ANP in the right atrium in PH rats was significantly lower than those in the controls (45.1 +/- 3.9 ng/mg vs. 240.5 +/- 10.4 ng/mg, p less than 0.001), while there was no significant difference in tissue levels of atrial IR-ANP in the left atrium between the two groups. Thus, development of pulmonary hypertension led to an increase in release of ANP from the right atrium.

Animals↗
PubMed1988

Effect of rapid sodium load on circulating atrial natriuretic polypeptide.

The hypothesis that an increase in plasma sodium concentration (PNa) causes an increase in circulating atrial natriuretic polypeptide (ANP) was examined in conscious dogs. NaCl solution in small volume (0.3 ml/kg body wt) and at high concentration (20%) was injected intravenously within 2 s to rapidly increase PNa. PNa rapidly increased to 5.1 +/- 0.3 meq/l. Urinary excretion of sodium and water increased to 4.1 and 2.5 times the control levels, respectively. Plasma vasopressin level increased to 3.7 times the control level. Plasma ANP level (PANP) did not change significantly. PANP corrected for sodium-induced hemodilution did not change either. On a different day, a double amount of sodium (0.6 ml/kg body wt of 20% NaCl solution) was intravenously injected into the dogs. PNa increased by 7.3 +/- 0.4 meq/l, which was significantly more than the increase after the 0.3 ml/kg injection. PANP with or without correction for hemodilution again did not change. These results indicate that a rapid increase in PNa within the physiological range does not cause elevation of circulating ANP. This suggests that ANP does not contribute to the regulation of plasma sodium concentration.

Animals↗
PubMed1988

Hormonal and renal effects of atrial natriuretic peptide in patients with secondary hypertension.

To investigate the involvement of atrial natriuretic peptide (ANP) in secondary hypertension, we examined hormonal and renal responses to ANP infusion (0.025 microgram/kg/min) in 27 patients with renal parenchymal hypertension, 10 with primary aldosteronism, 8 with renovascular hypertension, and 15 normotensive subjects. The preinfusion plasma concentration of ANP was significantly higher in patients with renal parenchymal hypertension (120 pg/ml, p less than 0.01) and in patients with primary aldosteronism (98 pg/ml, p less than 0.05) than in the normotensive subjects (40 pg/ml), but it was not greater than in the patients with renovascular hypertension (73 pg/ml, NS). In the patients with renal parenchymal hypertension, plasma ANP correlated negatively with creatinine clearance (r = -0.76, p less than 0.001). Mean blood pressure (-5%, p less than 0.01) and plasma aldosterone (-40%, p less than 0.001) decreased to a similar degree in the four groups during ANP infusion. However, an increase in urinary sodium excretion caused by ANP was higher in the hypertensive than in the normotensive patients (+250% vs. +70%, p less than 0.01) and correlated positively with mean blood pressure during ANP infusion (r = 0.47, p less than 0.001). The removal of adenomas in the patients with primary aldosteronism significantly lowered both plasma levels of ANP and cyclic guanosine 2',3'-monophosphate and reduced an increase in sodium excretion during ANP infusion, whereas the responses of blood pressure and plasma aldosterone to ANP infusion were not altered by the operation. Thus, these results suggest that elevated ANP secretion and increased natriuretic responses to ANP may modify the blood pressure and body fluid volume status in some types of secondary hypertension.

Adrenal Gland Neoplasms↗
PubMed1988

Molecular forms of atrial natriuretic peptide in the atrium of patients with cardiovascular disease.

To determine the molecular forms of atrial natriuretic peptide (ANP) in patients with cardiovascular disease, we analyzed the ANP content in the right atrium using reverse phase high performance liquid chromatography and RIA. Tissue from 35 patients, ranging in age from 1 month to 64 yr, was studied. The right atrial ANP content was high in patients with congestive heart failure regardless of age. We found three ANP components (alpha-, beta-, and gamma ANP), as previously found in tissue obtained at autopsy. In patients younger than 20 yr old, the major component was gamma ANP. In older patients, the frequency and content of the two low mol wt forms, especially beta ANP, were increased. The differences in the content and molecular forms of ANP in atrial tissue reflect the pathological state in patients with cardiovascular diseases, as well as the patient's age.

Adolescent↗
PubMed1988

Physiological factors of atrial natriuretic polypeptide release and its neural regulation in conscious dogs.

We have examined physiological factors in atrial natriuretic polypeptide (ANP) release and whether or not the cardiac nerves control release of ANP. Two possible factors were tested, an increase in plasma sodium level (PNa) and an increase in atrial pressure. Injection of 1.0 or 2.0 mEq/kg of sodium ions elevated PNa by 5.3 +/- 0.3 or 7.3 +/- 0.4 mEq/L, respectively, but plasma ANP level (PANP) did not change. Infusion of 18 ml/kg of 3% Dextran-40 over 5 min increased mean left atrial pressure (MLAP) by 7.6 +/- 0.9 mmHg. PANP increased from 206 +/- 17 pg/ml to 260 +/- 25 pg/ml, which was not significant. PANP, corrected for hemodilution, significantly increased to 348 +/- 34 pg/ml. These results suggest that PNa increase does not promote ANP release, but that an atrial pressure increase does. This transient volume load did not induce full response of the ANP releasing system. A prolonged volume load for 45 min increased corrected PANP to 435 +/- 73 pg/ml. A close linear correlation was found between the increases in MLAP and PANP. These facts indicate that prolonged volume expansion is necessary to induce full response of the ANP releasing system. Complete cardiac denervation did not affect the tonic level of plasma ANP, volume expansion-induced increase in PANP, or the sensitivity of the ANP releasing system. Thus we conclude that the cardiac nerves do not control ANP release caused by volume expansion.

Animals↗
PubMed1988

Plasma concentration of alpha-hANP and renal responses to alpha-hANP infusion in patients with congestive heart failure and those with chronic renal failure.

To study the role of alpha-human atrial natriuretic polypeptide (alpha-hANP) in body fluid regulation, we measured the plasma concentration of alpha-hANP and renal function in 9 patients with congestive heart failure (CHF), 10 with chronic renal failure (CRF) and 8 normotensives (NT) before and during alpha-hANP infusion at 0.025 microgram/kg.min. The plasma concentration of alpha-hANP was significantly higher in the CHFs and CRFs than in the NTs (319, 168 and 72 pg/ml, respectively). Alpha-hANP infusion decreased mean blood pressure in a similar manner in the 3 groups (-5%, p less than 0.01 each). Increases in urinary sodium excretion and glomerular filtration rate during alpha-hANP infusion, however, were greater in the CHFs and CRFs than in the NTs. Furthermore, the higher the preinfusion level of renal vascular resistance (RVR), the greater was the reduction in RVR by alpha-hANP (r = -0.80, p less than 0.001). The metabolic clearance rate (MCR) of alpha-hANP was significantly smaller in the CHFs and CRFs than in the NTs (38, 35 and 67 ml/min.kg, respectively). These results suggest that the renal vasodilatory actions of alpha-hANP seem to be enhanced in patients with increased RVR and that the elevation of the basal plasma concentration of alpha-hANP in CHFs and CRFs may be in part due to the low MCR.

Adult↗
PubMed1987

Molecular forms of atrial natriuretic polypeptides circulating in human plasma.

Molecular forms of atrial natriuretic polypeptides circulating in human plasma were analyzed by chromatographic separation, coupled with radioimmunoassay. Analyses were done with human plasma samples taken from 24 human subjects, divided into groups of healthy volunteers, patients with renal disease, and patients with heart disease, with 8 subjects in each group. Although alpha-hANP was found as a major circulating form in most of the plasma specimens (16 cases), beta-hANP accompanied by alpha-hANP was found in 6 cases including 2 healthy volunteers. In addition, hANP-immunoreactive macromolecule, which is likely a bound form of hANP, was found to some extent in all the specimens tested. Diversity of human plasma in ANP molecular distribution was discussed in connection with a radioimmunoassay for plasma ANP.

Atrial Natriuretic Factor↗
PubMed1987

Relationship between the renin-aldosterone system and atrial natriuretic polypeptide in rats.

In order to examine the relationship between the renin-aldosterone system and atrial natriuretic polypeptide (ANP), we investigated the effects of alpha-human atrial natriuretic polypeptide (alpha-hANP) on the plasma concentrations of renin (PRC) and aldosterone (PAC), as well as the effects of captopril pretreatment on the natriuresis and blood pressure reduction induced by alpha-hANP in rats. Although alpha-hANP infused into conscious rats at 0.67 microgram min-1 kg-1 markedly increased the urinary excretion of sodium and decreased mean arterial pressure, its infusion did not change PRC; however, it significantly lowered PAC. Frusemide infusion at 20.8 micrograms min-1 kg-1 induced natriuresis comparable with that of alpha-hANP and it elevated both PRC and PAC, but mean arterial pressure was not altered. Pretreatment of rats with captopril did not have any significant influence on the acute natriuretic and hypotensive effects of alpha-hANP. Although the inhibitory effect of ANP on the renin-aldosterone system may be involved in the chronic modulation of body fluid volume and blood pressure, this effect does not seem to be directly involved in the acute natriuretic and hypotensive effects of the peptide.

Aldosterone↗
PubMed1987

Lack of neural control of atrial natriuretic peptide release in conscious dogs.

To determine whether or not cardiac nerves control the release of atrial natriuretic polypeptide (ANP), we examined the effects of intrapericardial cardiac denervation on circulating ANP in conscious dogs. Base-line level of circulating ANP in six cardiac-denervated (CD) dogs (191 +/- 24 pg/ml) was not significantly different from that in seven intact (INT) dogs (196 +/- 18 pg/ml). Three percent dextran-40 in saline (18 ml/kg, 20% of estimated blood volume) was infused over 5 min, and the elevated left atrial pressure (LAP; approximately 8 mmHg) was maintained by supplemental infusion over 40 min. The increase in circulating ANP after infusion in the CD dogs (462 +/- 61 pg/ml) was not significantly different from that in the INT dogs (435 +/- 73 pg/ml). The regression line relating circulating ANP (normalized with regard to the control value) with the change in LAP in the INT dogs was not significantly different from that in the CD dogs. These results suggest that the cardiac nerves do not control the tonic release of ANP or the volume expansion-induced release of ANP.

Animals↗
PubMed1987

Effects of antiserum against alpha-rat atrial natriuretic peptide in anesthetized rats.

Although synthetic atrial natriuretic peptide is known to increase urinary volume and sodium excretion and to reduce arterial blood pressure, the physiological role of endogenous atrial natriuretic peptide is still unclear. We investigated the effects of specific rabbit antiserum against alpha-rat atrial natriuretic peptide on hemodynamics, diuresis, and natriuresis in anesthetized rats. A significant rise in mean blood pressure lasted for about 60 minutes after intravenous administration of the antiserum, with the maximal increment being approximately 7%. Similarly, a significant increase in cardiac output was obtained 20 minutes after injection at an increment of approximately 11%. Heart rate, however, remained unchanged. On the other hand, significant reductions in urine output and urinary sodium and potassium excretion lasted for about 20 minutes after administration of the antiserum, with maximal decrements being 63%, 63%, and 60%, respectively. No significant effects on hemodynamics, diuresis, and natriuresis were observed following injection of normal rabbit serum. These results indicate that endogenous atrial natriuretic peptide has an important physiological role in the regulation of hemodynamics and water-electrolyte balance.

Anesthesia↗
PubMed1987

Plasma concentration of atrial natriuretic polypeptide in patients with atrial tachycardia.

To investigate the mechanisms of polyuria associated with tachycardia, we measured plasma concentrations of alpha-human atrial natriuretic polypeptide (alpha-hANP) and cGMP in 6 patients with paroxysmal tachycardia. Plasma concentrations of immunoreactive alpha-hANP and cGMP increased by +69% (p less than 0.05) and +100% (p less than 0.05), respectively, during both paroxysmal atrial tachycardia and atrial fibrillation. To examine whether tachycardia per se raises the secretion of alpha-hANP, we also determined plasma concentrations of alpha-hANP and cGMP in 5 patients during rapid atrial pacing. The pacing-induced tachycardia also increased both of the plasma concentrations. Further, the examinations of cardiac and renal functions in patients with complete atrioventricular block during rapid pacing revealed that each of the increases in atrial pressures, urinary sodium excretion and creatinine clearance were in parallel with the change in plasma concentration of alpha-hANP. These results suggest that an increase in plasma concentration of alpha-hANP during paroxysmal tachycardia is mainly due to elevation of atrial pressure and that this increase in alpha-hANP contributes to tachycardia polyuria.

Atrial Fibrillation↗
PubMed1987

Isolation of complementary DNA clones for genes exhibiting reduced expression after treatment of mouse teratocarcinoma stem cells with a tumor-promoting phorbol ester.

For the study of the effects of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) on early mammalian cell differentiation, a complementary DNA (cDNA) library was constructed on the poly(A)+RNAs extracted from undifferentiated F9 cells derived from a 129/Sv mouse teratocarcinoma OTT6050, and screening was done for the cNDA sequences corresponding to the mRNAs, the levels of which decreased significantly in the F9 cells after the TPA treatment. From about 80,000 clones screened, 3 different cDNA clones, pFT27, pFT43, and pFT60, were isolated and characterized. Levels of the RNAs hybridizable to these clones were decreased by fourfold to more than fiftyfold within 1-10 hours in the presence of TPA. Northern blotting experiments identified transcripts corresponding to these clones: pFT27 hybridized to 3.0 kb RNA, pFT43 hybridized to 1.5 kb RNA, and pFT60 hybridized to 1.0 kb RNA. The levels of these 3 transcripts were also decreased after treatment of the undifferentiated F9 cells with retinoic acid (RA) and dibutyryl cyclic AMP (cAMP). The TPA-induced as well as the RA- and cAMP-induced decreases in the RNAs hybridizable to pFT27 were regulated at the transcriptional level, whereas similar decreases in the RNAs hybridizable to pFT43 and pFT60 were regulated at the post-transcriptional level. These findings show that TPA treatment shares common effects with RA and cAMP on the undifferentiated F9 cells.

Animals↗
PubMed1986

Increase in plasma atrial natriuretic polypeptide (ANP) following sodium load in anesthetized rats.

To investigate the releasing mechanisms of atrial natriuretic polypeptide (ANP), identical amounts of 5% glucose solution, isotonic (0.9%) or hypertonic (5%) saline were infused intravenously for 5 min (2 ml/min) in anesthetized rats. At the same time, plasma immunoreactive ANP (ir-ANP) was measured using a direct radioimmunoassay. Plasma ir-ANP increased after infusion of 5% glucose solution (P less than 0.01) and isotonic saline (P less than 0.05), and returned rapidly to the basal levels in the recovery period. Plasma ir-ANP increased to a greater degree in the group infused with hypertonic saline than in the other two groups. The major immunoreactive component of increased ir-ANP was identified as alpha-rat ANP, a 28 amino acid residue, by using reverse phase high-performance liquid chromatography. These results suggest that sodium ions may be a stimulating factor of ANP release as well as volume expansion.

Animals↗
PubMed1986

Increased release of atrial natriuretic polypeptides in rats with DOCA-salt hypertension.

This study compared atrial and plasma concentrations of immunoreactive alpha-rat atrial natriuretic polypeptide (i alpha-rANP) in rats given tap water (control), a 1% saline solution (salt), deoxycorticosterone acetate (DOCA) and DOCA plus 1% saline solution (DOCA-salt) after 1 and 8 weeks of treatment. DOCA (100 mg/kg) was given by implanting a piece of silicon rubber impregnated with DOCA subcutaneously. Atrial i alpha-rANP increased, while plasma i alpha-rANP decreased with time in all groups. Atrial concentration of i alpha-rANP was significantly lower in the DOCA-salt group than in the other groups at 1 week, and was reduced in the DOCA and DOCA-salt groups as compared to the control group at 8 weeks. On the other hand, plasma concentration of i alpha-rANP was significantly higher in the DOCA and the DOCA-salt groups than in the control group at 1 week; the DOCA and DOCA-salt group values were also higher than the control and salt group values at 8 weeks. Atrial concentration of i alpha-rANP was inversely correlated with systolic blood pressure in the all rats at 1 week (r = 0.48, p less than 0.001) and at 8 weeks (r = 0.33, p less than 0.05). Plasma concentration of i alpha-rANP was positively correlated with systolic blood pressure at 8 weeks (r = 0.37, p less than 0.05). In addition, there was a significant positive correlation between plasma/atrial ratio of i alpha-rANP concentration and systolic blood pressure at either stage (r = 0.41, p less than 0.01 at 1 week; r = 0.40, p less than 0.01 at 8 weeks). Thus, it seems likely that the release of ANPs is increased in response to expansion of extracellular fluid volume or elevation of blood pressure, modifying the development of hypertension in DOCA-salt rats.

Animals↗