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Biomedical subjects

U Ackermann

Publications and source records attributed to U Ackermann.

At least 19 recordsLinked to original sources
PubMed1992

Beta 1- and beta 3-subunits can associate with presynthesized alpha-subunits of Xenopus oocyte Na,K-ATPase.

Oligomerization of newly synthesized alpha- and beta-subunits is a prerequisite for the structural and functional maturation of Na,K-ATPase. In this study, we have tested the competence of presynthesized alpha- and beta-subunits to assemble into functional enzyme complexes. Antisense oligonucleotides complementary to alpha-mRNA were used to inhibit alpha-subunit synthesis in Xenopus oocytes leaving a presynthesized trypsin-sensitive alpha-subunit pool. beta-Subunits expressed in these oocytes from injected cRNA assembled with the preexisting alpha-subunits, rendered them trypsin-resistant, and permitted the expression of more ouabain binding sites at the plasma membrane. Similarly, presynthesized beta 1- or beta 3-subunits produced in Xenopus oocytes by injection of beta-cRNA and later of specific antisense oligonucleotides were stabilized and transported out of the endoplasmic reticulum when alpha-cRNA was injected into oocytes. These data indicate that alpha- and beta-subunits can insert into endoplasmic reticulum membranes independent of each other in an assembly-competent form and retain their ability for oligomerization after synthesis.

Animals↗
PubMed1992

Atrial natriuretic peptide inhibits compensatory responses when cardiac performance is depressed.

We tested the hypothesis that the atrial natriuretic peptide (ANP) mediated decrease in baroreceptor sensitivity that is seen in normal rats is more pronounced in a state of depressed cardiac performance. Holtzman rats (n = 15) were injected with Adriamycin (1 mg/kg i.p. 3 times/week for 8-10 weeks). Control rats (n = 17) were injected with 0.9% saline. Experiments were done in conscious animals that had been catheterized for i.v. infusions and for measurement of arterial blood pressure (ABP) and heart rate (HR). ANP (250 ng.kg-1.min-1) or saline vehicle was infused i.v. Graded periodic bolus injections of phenylephrine or sodium nitroprusside were given to assess baroreceptor sensitivity (beats.min-1.mmHg-1) up to 60 mmHg (1 mmHg = 133.3 Pa) above and below resting ABP. The following day the experiment was repeated with the ANP-vehicle regimen reversed. Finally, the rats were anesthetized and the rate of left ventricular pressure increase (dP/dt) was measured. Data evaluation included calculation of least squares linear regression slopes of peak delta HR vs. peak delta ABP, applying corrections for experimental errors in both the dependent and independent variables. Adriamycin rats (A) did not differ significantly from control rats (C) with respect to either initial ABP (A = 105 +/- 5; C = 100 +/- 3; mean mmHg +/- SEM) or initial HR (335 +/- 9 vs. 312 +/- 13 beats.min-1). However, their indices of cardiac performance were significantly depressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Modulation of Na,K-ATPase expression during early development of Xenopus laevis.

In amphibian and mammalian systems, regulation of Na+ transport via the Na,K-ATPase plays an important role in distinct developmental processes such as blastocoele formation and neurulation. In this study, we have followed the Na,K-ATPase activity, the biosynthesis, and the cellular accumulation of catalytic alpha-subunits after fertilization of Xenopus laevis eggs up to neurula formation. Our data show that Na,K-ATPase activity increases significantly between stages 4 and 6 and again between stages 13 and 24. The four-fold rise in Na,K-ATPase activity during blastocoele formation is not mediated by an increased cellular pool of alpha-subunits. On the other hand, a five-fold increase of the biosynthesis rate around midblastula precedes a progressive accumulation up to neurula stage mainly of alpha 1-subunits and to a lesser extent of a second alpha-immunoreactive species. In contrast, newly synthesized glycoproteinic beta 1-subunits of Na,K-ATPase cannot be detected up to late neurula. These data indicate that (1) upregulation of Na,K-ATPase activity during blastocoele and neurula formation are mediated by different regulation mechanisms and (2) alpha- and possibly beta-isoforms are expressed in a developmentally regulated fashion during early Xenopus development.

Animals↗
PubMed1991

[Correlation between respiratory tract symptoms in young children and NO2 concentration of outside air].

The aim of a one year study was to ascertain whether air pollution measured as NO2-concentration has an measurable influence on the health of infants in Switzerland. Measurements of NO2-concentration were carried out by means of passive collectors in ambient air, living room and at the child itself. The results of 1225 children printed to a significant coherence between respiratory symptoms per day and child and the NO2 load of ambient air as an guide pollutant. Even in consideration of other childish, familiar and environmental factors the coherence remains. Although no causal relation thereby proved this factor supports the observation of parents and physicians that children more often fall ill of respiratory diseases in polluted air being in accordance with similar investigations abroad.

Air Pollutants↗
PubMed1990

Mutual dependence of Na,K-ATPase alpha- and beta-subunits for correct posttranslational processing and intracellular transport.

In this study, we have followed the fate of newly synthesized alpha- and beta-subunits of Na,K-ATPase in Xenopus oocytes injected with alpha and/or beta cRNA to examine whether assembly of the two subunits is needed for a correct folding and/or for intracellular transport of Na,K-ATPase. Our data indicate that (1) assembly of alpha- and beta-subunits occurs at the level of the ER, (2) beta-subunits are needed for the newly synthesized alpha-subunit to adopt a stable configuration and (3) alpha- and beta-subunits mutually depend on each other to be transported out of the ER.

Animals↗
PubMed1990

Significant association between outdoor NO2 and respiratory symptoms in preschool children.

A study of 1225 preschool children was conducted in four regions of Switzerland with different levels of air pollution to investigate the relationship between air pollution and respiratory symptoms. Daily symptoms were recorded by parents on a diary form and air pollution exposure assessed by personal NO2 samplers. Each family participated for 6 weeks and personal samplers were changed every week. The frequency of respiratory symptoms per child and day was found to increase with increasing levels of NO2 measured outdoors. This relationship remained significant in a multiple regression model in which the factors smoking, origin, indoor air pollution, age and sex, season, and parents appreciation of air pollution at the living site were taken into account.

Air Pollutants↗
PubMed1990

Influence of atrial natriuretic factor on autonomic control of heart rate.

Atrial natriuretic factor (ANF) may prevent reflex tachycardia. To determine whether this action occurs in the central or peripheral nervous system, Sprague-Dawley rats, anesthetized with Inactin (100 mg/kg ip), underwent surgical cardiac denervation and subsequent vagus nerve and stellate ganglion stimulation. We compared the change in heart rate (delta HR) in response to high- and low-frequency stimulation in a group receiving a vehicle infusion with a group receiving an ANF infusion (0.28 microgram.kg-1.min-1). We found that ANF had no effect on delta HR in the absence of all stimulation or during sympathetic stimulation at any frequency. There was no significant interaction between ANF enhancement of parasympathetic activity and the level of sympathetic stimulation. ANF acted peripherally to significantly (P less than 0.05) increase the magnitude of delta HR in response to parasympathetic stimulation at high (5 Hz) and low (2 Hz) frequencies. We speculate that a common step in mechanism of action of ANF and acetylcholine may be responsible for the enhancement of cardiac parasympathetic effects by ANF.

Animals↗
PubMed1990

[Correlation of respiratory tract symptoms in young children and NO2 concentrations of the outside air].

In four regions of Switzerland (2 towns, 1 municipal agglomerate, 1 rural area) the relationship between the degree of air pollution measured in terms of NO2 and the incidence of airway symptomatology was investigated in 1,225 young children. The airway symptoms were recorded by the parents in a diary; the NO2 loading was measured with the aid of personal collecting tubes at the place of residence of the child. A significant relationship was found to exist between the mean incidence of airway symptomatology per child and day, and the individually measured NO2 concentration in the outside air at the child's place of residence. This relationship remained significant even when, in a multiple regression analysis, account was also taken of other major factors, such as smoking, nationality, individual susceptibility to airway diseases, the season of the year, and the subjective assessment of the air pollution at the place of residence, were also taken into account.

Air Pollutants↗
PubMed1989

Angiotensin restores atrial natriuretic factor-induced decrease of baroreceptor sensitivity in normotensive rats, but not in spontaneously hypertensive rats.

The effect of atrial natriuretic factor (ANF) on baroreflex sensitivity was determined in unanesthetized normotensive (Wistar-Kyoto, WKY) or spontaneously hypertensive rats (SHR) during acute hypertensive stimuli (phenylephrine) or hypotensive stimuli (sodium nitroprusside). The i.v. dose of rat ANF [( Ser99,Tyr126]ANF) was 50 ng/min per rat, sufficient to decrease mean arterial blood pressure (ABP) by about 6 mmHg (1 mmHg = 133.3 Pa) in WKY. SHR showed no change in ABP with this ANF dose. During a control infusion of physiological saline, the mean heart rate (HR) response to increases in ABP was -1.30 +/- 0.27 beats/min (bpm)/mmHg in WKY and -0.37 +/- 0.22 in SHR (p less than 0.05). These values were not affected significantly by ANF. However, ANF blunted chronotropic responses to ABP decreases. The control values of the delta HR/delta ABP slope in WKY and SHR were -2.34 +/- 0.57 and -2.01 +/- 0.37 bpm/mmHg, respectively. In the presence of ANF, the slope changed to -0.36 +/- 0.43 (i.e., bradycardia in response to hypotension) in WKY and to +0.20 +/- 0.21 in SHR (p less than 0.005 for the difference from control for both). This ANF-induced loss of baroreflex sensitivity was reversed in WKY by the addition of angiotensin I (sufficient to increase ABP by 5 mmHg in control rats). Angiotensin did not restore baroreflex sensitivity in ANF-infused SHR, and ANF had no effect on the ABP increase caused by angiotensin in either group. The data suggest that ANF does not act on baroreceptor structures directly, but inhibits mechanisms involved in efferent sympathetic activation. Parasympathetic responses do not appear to be compromised.

Angiotensin I↗
PubMed1988

Atrial natriuretic factor alters autonomic interactions in the control of heart rate in conscious rats.

Regulation of heart rate was studied in rats receiving either i.v. saline at 64 microL/min or synthetic 28-residue rat atrial natriuretic peptide (ANF) at a dose sufficient to decrease mean arterial blood pressure by 10%. Autonomic influences were deduced from steady-state heart rate responses of each group to propranolol, atropine, or propranolol and atropine combined. A multiplicative model of heart rate control was used to derive quantitatively from the data the modulation of intrinsic heart rate by sympathetic and parasympathetic mechanisms. Animals receiving ANF showed a lower heart rate than control animals. This relative bradycardia was abolished by atropine. Blocking of sympathetic effects with propranolol had no effect on basal heart rate in either group, and atropinization led to significant increases in heart rate in both groups of rats. Mathematical analysis of the results showed that the bradycardia produced by ANF was due predominantly to a reduced intrinsic heart rate and to enhanced vagal inhibition of postganglionic sympathetic activity. Parasympathetic contribution to heart rate in the absence of sympathetic activity was negligible in control rats and small during ANF. We conclude that the major influences of ANF on heart rate control are a decrease of intrinsic heart rate and enhanced parasympathetic inhibition of postganglionic presynaptic sympathetic activity.

Animals↗
PubMed1986

Cardiovascular effects of atrial natriuretic extract in the whole animal.

Atrial tissue extract (AE) and ventricular tissue extract cause identical decreases in total peripheral resistance when they are injected i.v. into anesthetized rats. However, only AE causes significant hypotension because of cardiac inhibition. This involves both bradycardia and failure of stroke volume to increase appropriately. The observations cannot be explained by direct action of AE on myocytes, but are more likely to be the result of interactions with cardiovascular reflex mechanisms. Excitation of chemosensitive cardiac receptors with vagal afferents appears to be an important afferent mechanism. The efferent limb for the negative chronotropic response resides partly in the vagus nerves and partly in cardiac sympathetic nerves. The negative inotropic response of AE was not altered by vagotomy, spinal section, atropine, or propranolol. These results suggest that atrial peptides may cause the release of a negatively inotropic substance from a site that is not yet identified.

Afferent Pathways↗
PubMed1978

Cardiac output and renal excretion rates during acute blood volume expansion in rats.

Selected central vascular parameters and renal excretion rates were monitored in anesthetized rats after acute, isohemic blood volume expansion by 33 percent. The infusate was an equilibrated mixture of animals' own blood and isotonic, isoncotic (6 percent) bovine albumin. Expansion increased mean arterial pressure by 35 percent, mean central venous pressure (CVP) by 850 percent, cardiac output (CO) by 56 percent, hematocrit (Hct) by 25 percent, plasma protein concentration (Ppr) by 25 percent, renal excretion rates of volume by 4,400 percent, of sodium by 2,800 percent, and of potassium by 360 percent of the respective preinfusion value. Hct and Ppr measurements suggested that 15 min after the end of the infusion, only 33 percent of infused volume remained within the circulation and that there was little further change in this during the remainder of the experiment. At the end of the elevated renal response, CVP and CO alone had returned to control values. Renal excretion rates were highly correlated with CO, but they were delayed by 2-5 min with respect to it. The results suggest that the renal response to acute volume expansion does not primarily control blood volume. Cardiac output may be the controlled variable in the response.

Animals↗
PubMed1978

Cardiac output, GFR, and renal excretion rates during maintained volume load in rats.

The correlation among cardiac output (CO), glomerular filtration rate (GFR), fractional tubular sodium rejection (TFRNa), and renal excretion rates of water and salt was investigated during ischemic blood volume expansion in rats. Initially circulating blood volume was equilibrated isovolemically with a reservoir volume of 6% albumin solution equal to one-third the estimated blood volume. Later the equilibrated reservoir contents were infused intravenously. CO was measured by thermodilution, GFR by inulin clearance. Significant linear correlations existed between GFR and the rates of urine flow (r = 0.90), sodium excretion (r = 0.75) and potassium excretion (r = 0.76) that prevailed 5--10 min after a given GFR change. The increased GFR was highly correlated with CO (r = 0.94), probably correlated with mean central venous pressure (r = 0.45), but not correlated with mean abdominal aortic blood pressure. The correlation between CO and time-delayed (5--10 min) TRFNa was also highly significant (r = 0.98). The saluresis appears to have been caused initially by increased tubular load and subsequently by decreased absolute tubular reabsorption.

Animals↗
PubMed1978

Apparent escape rate of RIHSA and 51Cr-labeled erythrocytes from the blood of volume-expanded rats.

The disappearance rate constant of radioiodinated human serum albumin (RIHSA) and 51Cr-tagged erythrocytes was measured in rats before and after intravenous, isoncotic blood volume expansion (6% bovine albumin; 75 or 33% of blood volume). Before volume expansion the average slope of the semilogarithmically plotted plasma RIHSA activity was -2.068 X 10(-3) +/- 0.146 X 10(-3) (SE) min-1. The slope was not significantly changed when tested by subsequent tracer injections which were made immediately after and 1 h after volume expansion. Preinfusion plasma volume (PV) was constant, but total erythrocyte volume (RCV) increased at a significant rate from 0.0253 +/- 0.0030 to 0.0300 +/- 0.0038 ml/g body wt over the 2-h period. PV was elevated and RCV was unchanged by the infusion, but both decreased significantly thereafter. The observed erythrocyte loss could not be accounted for by sampling or bleeding. Arterial hematocrit remained constant while RCV and PV were decreasing, and it was identical to whole-body hematocrit throughout. It was concluded that 1) isoncotic albumin expansion did not change the rate constant of transcapillary albumin loss; 2) nonsteady state PV could be calculated from a single preinfusion RIHSA dose; and 3) sequestration of blood may be a part of the rat's response to volume expansion.

Animals↗
PubMed1977

Changes in interstitial pressure during acute interstitial volume depletion in normally hydrated rats.

Interstitial fluid pressure was measured in normally hydrated rats during acute interstitial volume depletion by intravenous hyperoncotic bovine serum albumin infusion. Body fluid volumes, systemic arterial and venous pressure and selected blood and urine variables were also measured. The infusion increased plasma volume twice as much as do iso-oncotic infusions which cause comparable increases in mean central venous pressure. The kidneys responded with a diuresis and natriuresis closely resembling those which follow iso-oncotic infusion in normally hydrated rats. At the end of the elevated renal response plasma volume and plasma protein concentration were not restored to pre-infusion values; total interstitial fluid volume was decreased to one half its control value. Interstitial fluid pressure decreased linearly with volume so that effective interstitial compliance was constant at 0.0717 ml/mm Hg per gram dry tissue weight (1.79 ml/mm Hg per 100 g BW). This was not significantly different from the value 0.0704 previously found in normally hydrated rats but very significantly higher than that in dehydrated rats with comparable interstitial depletion. It is concluded that interstitial compliance is normal over a wide range of interstitial fluid volume in normally hydrated rats but that it can be altered in states of chronic body water depletion.

Animals↗
PubMed1976

Changes in interstitial pressure during and after blood volume expansion in rats.

Interstitial fluid pressure was measured via a chronically implanted capsule before, during and after acute isotonic, iso-oncotic blood volume expansion in normal or in 48-h dehydrated rats. At the same time, the patterns of body fluid distribution, of selected renal responses and of mean arterial and mean central venous pressure responses were studied. Dry tissue weight (DTW) was subsequently determined by freeze drying of the shaved carcass. Dehydration decreased plasma volume and interstitial fluid volume significantly below normal values. The initial intracapsular pressure in dehydrated animals (-3.7 +/- 0.6 mm Hg) was not significantly different from that in normal rats (-2.5 +/- 0.5), but dehydrated rats showed initially a very significantly lower effective interstitial compliance (0.0005 ml/mm Hg per gram DTW) than did the normal group (0.0704). In the course of the renal response to the volume load, effective interstitial compliance increased to 0.0350 in dehydrated rats but showed no change in normal rats. Neither group completely corrected its elevated blood volume; both returned their central venous pressures to pre-infusion levels; both decreased their interstitial fluid volumes below pre-infusion levels and both decreased their intracapsular fluid pressures 1 mm Hg below the level prevailing in non-infused animals at that time. It is concluded that a reduction in interstitial hydrostatic pressure can be a functionally important influence in the apparent control of central venous pressure following acute blood volume expansion.

Animals↗
PubMed1975

On the role of the interstitial volume in the response of the rat to blood volume expansion.

Patterns of body fluid distribution and selected cardiovascular and renal responses were studied following vascular expansion in normal rats and in rats with altered interstitial fluid volume produced by dehydration, prehydration or hyperoncotic albumin infusion. In all four groups the patterns of the renal excretory response and the accompanying change in central venous pressure (CVP) were closely parallel and the disturbance in CVP was finally corrected in the presence of a considerable residual vascular expansion. During the diuresis and saluresis following iso-oncotic vascular expansion in prehydrated and dehydrated rats, both groups removed fluid chiefly from the interstitium; this fluid removal was attributable mainly to urinary excretion in prehydrated rats but mainly to redistribution into the cellsin dehydrated rats. In the latter series, preferential renal excretion of sodium over water was observed. Hyperoncotic vascular expansion led to a peak renal excretory response only 70% of that following iso-oncotic expansion. The excreted volume was accounted for by a similar depletion of interstitial fluid after the iso-oncotic load. These findings are consistent with the hypothesis that the renal response to volume expansion regulates some parameter which is more closely related to the mean central venous pressure than to the vascular volume. This regulation was associated with incomplete correction of the vascular expansion and absolute decrease in interstitial fluid volume compared to the initial size of that compartment. This provides support for a functionally important influence of the interstitial volume on venous compliance.

Animals↗