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Biomedical subjects

D L Vesely

Publications and source records attributed to D L Vesely.

At least 73 records · Page 4Linked to original sources
PubMed1995

Kaliuretic peptide and long acting natriuretic peptide as well as atrial natriuretic factor inhibit aldosterone secretion.

The present investigation was designed to determine whether atrial natriuretic peptides consisting of amino acids 1-30 (long acting natriuretic peptide), 31-67 (vessel dilator) and 79-98 (kaliuretic peptide) as well as 99-126 (atrial natriuretic factor (ANF)) of the 126 amino acid ANF prohormone inhibit aldosterone secretion. Thirty healthy human subjects were studied following infusion of 100 ng/kg body weight/min for 60 min of each of the respective peptides. Kaliuretic peptide decreased plasma aldosterone concentration by the greatest amount (6-fold) and plasma aldosterone was still significantly decreased (P < 0.001) three hours after stopping the infusion. In contrast, within 30 min of cessation of the ANF infusion, plasma aldosterone levels had returned to pre-infusion values. Long acting natriuretic peptide also significantly (P < 0.01) decreased plasma aldosterone levels which remained significantly (P < 0.001) decreased 3 h after cessation of infusion. Vessel dilator did not decrease plasma aldosterone levels. Kaliuretic peptide, ANF and long acting natriuretic peptide also decreased (P < 0.01) urinary aldosterone concentrations. None of these peptides changed the plasma potassium concentration. We conclude that two new peptide hormones (long acting natriuretic peptide and kaliuretic peptide) inhibit aldosterone secretion. The length of time that aldosterone secretion is inhibited following kaliuretic peptide and long acting natriuretic peptide infusion is significantly longer (P < 0.001) than following ANF infusion.

Adrenal Glands↗
PubMed1995

Temporal (circadian) and functional relationship between atrial natriuretic peptides and blood pressure.

Long-acting natriuretic peptide, vessel dilator, and atrial natriuretic factor consisting of amino acids (a.a.) 1 to 30, 31 to 67, and 99 to 126 of the 126-a.a. atrial natriuretic factor (ANF) prohormone, respectively, circulate in humans and have potent vasodilatory properties. To determine if these atrial natriuretic peptides are directly related to blood pressure in clinically healthy normotensive humans, we obtained 24-h profiles of vessel dilator, long-acting natriuretic peptide, ANF, and blood pressure in 10 men in 1988 and 11 men in 1993 (seven men were studied twice) to compare circulating concentrations of atrial natriuretic peptides with naturally occurring changes in blood pressure. Overall, vessel dilator, long-acting natriuretic peptide, and ANF each had significant (p<0.001) circadian rhythms, with peak concentrations late during sleep (at 04:00 h) being nearly twice their concentrations in the afternoon and evening. This high-amplitude circadian change allowed for the refinement of normal limits for ANF peptides by computing 3-hourly tolerance intervals (chronodesms) against which to compare time-specified single samples for normality. Systolic, diastolic, and mean arterial blood pressure also had significant circadian rhythms (p<0.001) with peaks and troughs that were exactly opposite those of the ANF peptides. In addition to this inverse temporal relationship, there was a significant inverse correlation between absolute values for blood pressure and each ANF peptide (p<0.001), implying a functional relationship. These data suggest that in addition to other well-established neurochemical factors, the ANF peptides (vessel dilator, long-acting natriuretic peptide, and ANF) are important for the maintenance of blood pressure and modulation of its circadian rhythm.

Adult↗
PubMed1995

Release of kaliuretic peptide during immersion-induced central hypervolemia in healthy humans.

Kaliuretic peptide, a new peptide hormone consisting of amino acids 79-98 of the 126 amino acid atrial natriuretic factor (ANF) prohormone, is synthesized in the heart and is a potent stimulator of potassium excretion. The mechanism(s) controlling the release of kaliuretic peptide heretofore has not been defined. Because water immersion to the neck provides an acute central volume expansion identical to that produced by 2 liters of saline but without the plasma compositional change, immersion to the neck (NI) was utilized to assess kaliuretic peptide responses to acute central blood volume expansion in seven seated sodium-replete normal subjects. Since atrial natriuretic factor (ANF; amino acids 99-126 of the prohormone) originates from the amino acids adjacent to kaliuretic peptide in the ANF prohormone but is proteolytically cleaved from the rest of the prohormone before release, measurement of ANF was incorporated into this study to determine if there are differences with respect to release of these two portions of the ANF prohormone. Both kaliuretic peptide and ANF increased promptly with NI, with ANF peaking at 1 hr of immersion, whereas kaliuretic peptide peaked at the 3rd hr of immersion. With cessation of immersion, ANF decreased to preimmersion levels within 0.5 hr while kaliuretic peptide was still significantly (P < 0.05) elevated at 1 hr postimmersion. These findings indicate that kaliuretic peptide and ANF are released simultaneously but that kaliuretic peptide peak circulating concentration and its return to preimmersion values are prolonged compared with ANF. These last findings suggest a slower clearance from the circulation for kaliuretic peptide. The diuretic peak response to NI corresponded in a temporal manner to the peak circulating concentration of kaliuretic peptide, suggesting a possible physiologic role for kaliuretic peptide in modulating volume homeostasis in humans.

Adult↗
PubMed1994

Atrial natriuretic peptide gene expression in the rat gastrointestinal tract.

The presence of ANP prohormone immunoreactivity in rat GI tract suggests that it may be an extracardiac site of ANP synthesis. The aim of this study was to investigate the expression of ANP mRNA in the adult rat GI tract. ANP mRNA was detected by ribonuclease protection analysis in stomach, small and large intestines, and rectum/anus. The highest concentrations of ANP transcripts were found in the proximal stomach, antrum, proximal colon, and rectum/anus at levels that ranged from 1 to 10% of that found in cardiac ventricle. Northern blot analysis of total RNA from these tissues identified a single 0.9 kb ANP transcript similar to that detected in heart. Gel filtration chromatography of tissue extracts provided evidence for the presence of the complete ANP prohormone in proximal stomach, antrum, proximal colon and rectum/anus. These results demonstrate that the gene for ANP is expressed in specific regions of the rat GI tract, suggesting that tissue-specific differential regulation of ANP synthesis occurs within the GI tract.

Animals↗
PubMed1994

Ozone increases amino- and carboxy-terminal atrial natriuretic factor prohormone peptides in lung, heart, and circulation.

Ozone can cause pulmonary edema and simultaneously decrease blood pressure. Atrial natriuretic peptides may mediate both of these effects in that they increase pulmonary capillary permeability resulting in edema formation and are potent vasodilating peptides. To examine this possibility, the lungs of Fischer 344 rats were exposed to ozone (0.5 ppm) for 8 hours which resulted in a three- to fourfold increase in atrial natriuretic peptides. Ozone also increased atrial natriuretic peptides in the heart two- to fivefold from 266 +/- 25, 226 +/- 22, and 288 +/- 40 ng/g (room air) to 716 +/- 26, 471 +/- 14, and 1473 +/- 235 ng/g recognized by the proANFs 1-30 and 31-67 and atrial natriuretic factor radioimmunoassays, respectively. Ozone also doubled the concentrations of pro-ANFs 1-30, 31-67, and 1-98 and ANF in the circulation. This study demonstrates that ozone increases atrial natriuretic peptides within the heart, lung, and circulation, suggesting that atrial natriuretic peptides may mediate the decreased blood pressure and pulmonary edema observed with ozone exposure. Since the proANF 31-67 radioimmunoassay exclusively recognizes the ANF prohormone within the heart, this study further indicates that ozone can increase the synthesis of the ANF prohormone.

Animals↗
PubMed1994

Normalization of circulating atrial natriuretic peptides in cardiac transplant recipients.

To assess whether heart transplantation (Htx) alters the marked elevation of circulating atrial natriuretic peptides usually found in patients with congestive heart failure (CHF), 14 subjects (nine with compensated and five with decompensated CHF), each with an ejection fraction < or = 28%, were evaluated. Immediately before and hourly for the first 12 hours after Htx, then daily for 21 days and every 1 to 4 weeks for 6 months, the circulating concentrations of the N-terminus (pro atrial natriuretic factor [ANF] 1-98), midportion of the N-terminus (pro ANF 31-67), and C-terminus (that is, ANF) of the 126 amino acid prohormone were measured. Increased (p < 0.001) levels of these peptides were found in superior vena cava, right atrial, and peripheral venous samples 1 hour after Htx in all subjects except one. The atrial natriuretic peptide levels correlated only with right atrial pressure (p < 0.01) in the first 24 hours. Circulating concentrations of these peptides returned to those of healthy adults between 5 and 12 days after Htx in 11 out of 14 Htx recipients. Thus successful Htx can restore the elevated circulating concentrations of atrial natriuretic peptides to those of healthy adults.

Adult↗
PubMed1994

Molecular forms of circulating atrial natriuretic peptides in human plasma and their metabolites.

High performance gel permeation chromatography (HP-GPC) followed by four radioimmunoassays (RIAs) devised to amino acids (a.a.) 1-30, 31-67, 79-98, and 99-126 of the 126 a.a. atrial natriuretic factor (ANF) prohormone revealed that the proANF(1-30) assay immunoreactivity in plasma is 50% proANF(1-30) and 50% proANF(1-98). The HP-GPC evaluation of plasma followed by proANF(31-67) and ANF [i.e., proANF(99-126)] assays revealed that proANF(31-67) and ANF circulate as distinct peptides. the HP-GPC plasma examination followed by proANF(79-98) assay immunologically recognized three peaks in plasma consistent with proANF(1-98), -(68-98), and -(79-98). Similar HP-GPC evaluation of urine followed by these RIAs indicated that the proANF(1-30), -(79-98), and ANF assays only recognize 500 mol.wt. or less peptides, and the proANF(31-67) RIA recognizes a nearly intact proANF(31-67) with only two to three amino acids removed during processing of this peptide.

Adult↗
PubMed1994

Dome-shaped lesion on chest radiograph: retroperitoneal abscess dissecting through the posterior chest wall.

A 50-year-old man with an 8 x 4 cm mass on the posterior chest was found to have a large retroperitoneal abscess due to Klebsiella pneumoniae. The abscess dissected through the right lower lobe of the lung and the posterior chest wall to produce a subcutaneous mass. The source of the posterior chest wall mass appeared to be a perinephric abscess. A dome-shaped lesion above the right hemidiaphragm on chest radiograph resolved immediately with surgical drainage, suggesting that an abscess should be a prime consideration when one observes such a lesion on a chest film.

Abscess↗
PubMed1994

Possible mechanisms involved in the natriuretic response to atrial natriuretic factor (ANF) and proANF 31-67 in the rat.

1. The present study was conducted to compare the mechanisms involved in the natriuretic response to atrial natriuretic factor (ANF) and proANF 31-67. The peptides were infused intravenously into anaesthetized rats at 10 pmol/min for 40 min. 2. Only ANF produced a significant decrease in arterial pressure; the maximum decrease was 11 mmHg (P < 0.05). 3. Both peptides produced significant increases in sodium excretion (P < 0.05) but only ANF increased the cyclic GMP (cGMP) excretion rate (P < 0.01) and neither peptide had a significant effect on plasma renin activity or glomerular filtration rate (GFR). ProANF 31-67 did not increase the plasma levels of ANF. 4. These results demonstrate that both ANF and proANF 31-67 have natriuretic effects via a tubular mechanism and suggest that the natriuretic effects of ANF are mediated by cGMP while the excretion, changes in GFR or a reduction in renin secretion.

Analysis of Variance↗
PubMed1994

Ozone increases atrial natriuretic peptides in heart, lung and circulation of aged vs. adult animals.

Ozone can cause pulmonary edema and simultaneously decrease blood pressure. Atrial natriuretic peptides may mediate both of these affects since they increase pulmonary capillary permeability and are potent vasodilating peptides. To examine this possibility and determine if aged animals respond differently to ozone, adult (4-6 months old) and aged (24-26 months old) Fischer 344 rats were exposed to ozone (0.5 parts per million) for 8 h. Ozone increased atrial natriuretic peptides recognized by the proANF 1-30, proANF 31-67, and atrial natriuretic factor (ANF) radioimmunoassays in lung from 3.7 +/- 0.2, 3.5 +/- 0.1, and 3.0 +/- 0.2 ng/g of lung, respectively, to 9.7 +/- 1.0, 9.2 +/- 0.4, and 13.3 +/- 2.7 ng/g in adult rats (n = 6) and from 3.6 +/- 0.1, 3.5 +/- 0.1, and 3.2 +/- 0.1 ng/g of lung of aged rats (n = 6) to 10.2 +/- 0.3, 10.0 +/- 0.2, and 12.6 +/- 0.2 ng/g. Ozone increased the content of these peptides in the heart 2- to 5-fold from 266 +/- 25, 226 +/- 22, and 288 +/- 40 ng/g of heart to 716 +/- 26, 471 +/- 14, and 1,473 +/- 235 ng/g in the same adult animals and from 495 +/- 17, 483 +/- 22, and 501 +/- 18 ng/g to 903 +/- 16,879 +/- 21, and 1,489 +/- 31 ng/g of heart in the aged animals. Ozone also doubled the concentration of these atrial natriuretic peptides in the circulatory system. This study demonstrates that ozone increases atrial natriuretic peptides in the lung, heart, and circulation of equal magnitude in aged versus adult animals, indicating an equal response to ozone with aging. This study further suggests that atrial natriuretic peptides may mediate the decreased blood pressure and pulmonary edema observed with ozone exposure.

Aging↗
PubMed1994

Three peptides from the atrial natriuretic factor prohormone amino terminus lower blood pressure and produce diuresis, natriuresis, and/or kaliuresis in humans.

BACKGROUND: Three peptides consisting of amino acids 1-30, 31-67, and 79-98 of the 126-amino acid atrial natriuretic factor prohormone (proANF), which have blood pressure-lowering, diuretic, natriuretic, and/or kaliuretic properties in animals, were investigated to determine if they have similar properties in humans. METHODS AND RESULTS: Thirty-six healthy, normotensive human volunteers (18 men and 18 women, ages 20 to 58 years) were divided into six similar groups based on age, sex, weight, blood pressure, and heart rate. After a 60-minute baseline period, 100 ng of proANFs 1-30, 31-67, 79-98, or ANF/kg body wt per minute was given intravenously for 60 minutes followed by a 3-hour postinfusion data collection period. Each of the atrial natriuretic peptides decreased systolic and diastolic blood pressures (P < .05), with proANF 31-67 causing the largest decrease. Urine flow increased 4- to 12-fold and was still significantly increased (P < .01) for 2 to 3 hours after stopping the respective infusions of proANFs 1-30, 31-67, and 79-98. Atrial natriuretic factor (ANF) increased urine flow 4- to 11-fold but by 2 hours after infusion was significantly increased in only 1 of 6 subjects. Sodium excretion increased 3- to 8-fold, 3- to 6-fold, 0- to 2-fold (NS), and 3- to 11-fold, respectively, with proANFs 1-30, 31-67, 79-98, and ANF. Natriuretic effects of proANFs 1-30 and 31-67 were significantly prolonged (P < .001) compared with ANF. ProANFs 1-30, 31-67, 79-98, and ANF increased potassium excretion 2- to 3-fold, 0-fold, 3- to 4-fold, and 2-fold, respectively. High-performance gel permeation chromatography followed by the respective radioimmunoassays revealed that proANFs 1-30, 31-67, 79-98, and 68-98, as well as ANF circulate as distinct peptides. CONCLUSIONS: ProANFs 1-30, 31-67, and 79-98, as well as ANF have significant blood pressure-lowering and diuretic properties. ProANFs 1-30 and 31-67 also have natriuretic properties in humans that are significantly (P < .001) prolonged compared with ANF. ProANF 79-98, although not possessing any natriuretic property, is the strongest stimulator of potassium excretion of the four atrial natriuretic peptides.

Adult↗
PubMed1994

Negative feedback of atrial natriuretic peptides.

The present investigation was designed to determine whether atrial natriuretic peptides consisting of amino acids 1-30 [i.e. pro-ANF-(1-30)], 31-67 [i.e. pro-ANF(31-67)], 79-98 [i.e. pro-ANF-(79-98)], and 99-126 [i.e. atrial natriuretic factor (ANF)] of 126-amino acid ANF prohormone have a negative feedback on their own and each others' release. Thirty healthy human subjects were studied with infusion of 100 ng/kg BW.min for 60 min of each of the respective peptides. Pro-ANF-(1-30) decreased the circulating concentrations of pro-ANF-(31-67) and ANF 51% and 89%, respectively. Pro-ANF-(31-67) decreased the circulating concentration of ANF by 55% and the peptides immunologically recognized by the pro-ANF-(1-30) RIA by 58% [this assay recognizes pro-ANF-(1-30) (50%) and pro-ANF-(1-98) (50%)]. Pro-ANF-(79-98) decreased the circulating concentration of ANF by 40%, pro-ANF-(31-67) by 31%, and the peptides recognized by the pro-ANF-(1-30) RIA by 46%. ANF decreased the circulating concentration of pro-ANF-(31-67) by 40% and the peptides recognized by pro-ANF-(1-30) RIA by 38%. Infusion of pro-ANF-(1-30), -(31-67), -(79-98), and -(99-126) also decreased the excretion of the other atrial natriuretic peptides measured in the urine by 32-84%. Infusion of vehicle only did not result in any decrease in these atrial natriuretic peptides in either plasma or urine. These data taken together indicate that each of the respective atrial natriuretic peptides inhibits the release, rather than breakdown, of each other, as increased breakdown would have resulted in their urinary concentrations being increased. This study further indicates that because pro-ANF-(1-98) was decreased in the circulation secondary to pro-ANF-(31-67) and pro-ANF-(79-98) infusions, they inhibit their own release, as they are both derived from pro-ANF-(1-98).

Adult↗
PubMed1994

Increase in atrial natriuretic factor in the lungs, heart, and circulatory system owing to ozone.

Ozone can cause pulmonary edema and simultaneously decrease blood pressure. Atrial natriuretic factor (ANF) may mediate both of these effects in that it increases pulmonary capillary permeability resulting in edema formation and vasodilates the vascular system. The present investigation was designed to test directly the effect of ozone on the content of ANF in the lungs, heart, and the circulatory system. Ozone (0.5 ppm) exposure for 8 h increased ANF content in the lungs fourfold (13.33 +/- 2.7 ng/g tissue) in six Fischer 344 rats compared with ANF content (3.03 +/- 0.2 ng/g tissue) in six Fischer 344 rats exposed only to room air. Ozone increased ANF content in the heart fivefold in the same animals from 288 +/- 39.6 ng/g tissue in the rats exposed to room air to 1,473 +/- 234.8 ng/g tissue in those exposed to ozone. Ozone also doubled the concentration of ANF in the circulatory system. This study demonstrates that ozone does increase ANF in the lungs, heart, and circulatory system, suggesting that ANF may mediate the decreased blood pressure and pulmonary edema observed with ozone exposure.

Animals↗
PubMed1993

Atrial natriuretic peptides in the heart and hemolymph of the oyster, Crassostrea virginica: a comparison with vertebrates.

1. The content of atrial natriuretic peptides (ANPs) in the auricles of oysters, Crassostrea virginica, was significantly (P < 0.01) greater than in their ventricles. 2. High-performance gel permeation chromatography (HP-GPC) followed by ANF radioimmunoassay revealed two peaks in both oyster and vertebrate (rat) hearts--a major peak where the 12.6-14 kDa ANF prohormone elutes and a smaller peak where the pure human form of ANF elutes. 3. HP-GPC evaluation followed by proANF 31-67 radioimmunoassay revealed only an ANF-like prohormone while HP-GPC followed by proANF 1-30 radioimmunoassay revealed the ANF prohormone and a proANF 1-30-like peptide in oyster and rat hearts. 4. ANPs concentrations in hemolymph were 940 +/- 129, 225 +/- 25, and 100 +/- 10 pg/ml by the proANF 1-30, proANF 31-67, and ANF radioimmunoassays, respectively. 5. Atrial natriuretic-like peptides are present in the oyster heart in molecular species similar to vertebrate species and these peptides are also present in hemolymph.

Animals↗
PubMed1993

Atrial natriuretic peptides are present throughout the plant kingdom and enhance solute flow in plants.

The present investigation was designed to 1) determine if atrial natriuretic-like peptides are present throughout the plant kingdom and 2) to determine if these peptides increase the flow of solute and/or water upward to leaves and flowers of plants. The 126-amino acid prohormone of atrial natriuretic factor (proANF)-(1-30), proANF-(31-67), and atrial natriuretic factor (ANF)-like peptides were present in the roots, stems, leaves, and flower petals of the more highly developed plants (Tracheophyta), with their highest concentrations being: Florida beauty > buddhist pine > Boston fern > rose = geranium = resurrection plant or club moss > Moses-in-the-cradle > Florida coontie. These peptides were also present in Bryophata (plants without vascular tissue or roots) and even in Euglena, flagellated chlorophyll-containing plants without leaves, stems, or roots. proANF-(1-30), proANF-(31-67), and proANF-(79-98) but not ANF (each at < 5.9 pg/ml) significantly increased (P < 0.001) the flow of colored water up stems, coloring their flowers 15-35 min earlier than the other one-half of the same flowers without exogenous peptide addition. These same peptides increased the rate of transpiration (i.e., loss of water from the leaves) and the absorption of solutions. High-performance gel permeation chromatography revealed that proANF-(1-30), proANF-(31-67), and ANF extracted from plants are very similar to their pure synthetic human sequences, with elution profiles and molecular weights of the plant extracts duplicating those of the pure synthetic peptides.

Atrial Natriuretic Factor↗
PubMed1993

Immunocytochemical localization of ProANF 1-30, ProANF 31-67, atrial natriuretic factor and urodilatin in the human kidney.

Whether ProANF 1-30 [first 30 amino acids (a.a.) of the 126-a.a. atrial natriuretic factor (ANF) prohormone] and ProANF 31-67 (a.a. 31-67 of this prohormone) with their natriuretic and diuretic properties are present within the human kidney is unknown. In the present investigation, ProANFs 1-30 and 31-67 as well as ANF (a.a. 99-126) of the ANF prohormone localized to the subbrush border of the pars convoluta and pars recta of the proximal tubules of the human kidney with immunoperoxidase staining. Immunofluorescent studies revealed that each of these peptides had a strong inclination for the perinuclear region in the proximal and distal tubules. ProANFs 1-30, 31-67 and 99-126 (i.e. ANF) also localized with both immunoperoxidase and immunofluorescent staining to the coritcal collecting ducts, glomeruli, and peritubular and interstitial blood vessels. ANF immunoperoxidase staining was particularly striking in the endothelium of interstitial arteries and vasa recta. In the glomeruli, prominent staining was noted in the peripheral glomerular capillary wall and in some of the visceral epithelial cells. In contrast, urodilatin (i.e. a.a. 95-126 of the ANF prohormone) was not found in the proximal tubules, but weak staining was found in the distal tubules and interstitial vessels with some but not all glomeruli, peritubular vessels, cortical collecting tubules and outer medullary nephrons weakly staining by immunoperoxidase and immunofluorescent methods. The whole prohormone being present in the kidney was suggested by immunological recognition of both the N- and C-termini of the ANF prohormone by radioimmunoassays.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1993

Increased atrial natriuretic factor prohormone peptides with aging in the heart, but not in lung, liver, or intestine.

Atrial natriuretic factor (ANF) has been found to be increased in the circulation of aged rats. The present investigation was designed to determine if the N-terminal ANF prohormone peptides with blood pressure lowering properties are increased in the circulation of "aged" (24-26 months) versus "adult" (4-6 month old) Fisher 344 rats. We utilized two sensitive and specific radioimmunoassays that immunologically recognize the 98 amino acid (a.a.) N-terminus (proANF 1-98) and a.a. 31-67 (proANF 31-67, Vessel dilator) from the midportion of the N-terminus of the 126 a.a. ANF prohormone. ProANF 1-98, and proANF 31-67, as well as ANF, were found to be elevated in the circulation of aged versus adult animals with proANF 31-67 and ANF elevations being significant at p < 0.05. To determine the potential source of the increased atrial natriuretic peptides in aged animals four tissue sources (liver, lung, heart, and intestine) from both adult and aged animals were examined. Hearts of aged animals contained significantly (P < 0.05; ANOVA) more proANF 1-98, proANF 31-67, and ANF than hearts of adult animals. There was no significant difference in the concentration of proANF 1-98, proANF 31-67, or ANF in the lung, liver, or intestine of the aged versus the adult animals. These results indicate that aged animals contained increased N-terminal and C-terminal ANF prohormone peptides in the circulation. The source of these increased peptides appears to be the heart.

Aging↗