SEARCH · PubMed Health

Results for “TPR”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 937 records · Page 52Linked to original sources

PubMed1995

The tetratricopeptide repeats of Ssn6 interact with the homeo domain of alpha 2.

The tetratricopeptide repeat (TPR) is a 34-amino-acid degenerate sequence motif that is found in a large variety of proteins, both prokaryotic and eukaryotic. TPRs are usually found in tandem arrays of up to 16 copies. In this paper we identify a direct interaction between the TPRs of Ssn6, a general transcriptional repressor, and alpha 2, a cell-type regulator in Saccharomyces cerevisiae. Five of the Ssn6 TPRs were tested individually, and all were found to interact specifically with alpha 2. These results suggest a model for TPR-protein interactions and for the role that a tandem array of TPRs may have in mediating transcriptional repression.

Amino Acid Sequence↗

PubMed2001

Functional studies of Ycf3: its role in assembly of photosystem I and interactions with some of its subunits.

The Ycf3 protein is essential for the accumulation of the photosystem I (PSI) complex and acts at a post-translational level. The sequence of Ycf3 is conserved in cyanobacteria, algae, and plants and contains three tetratrico-peptide repeats (TPR). TPRs have been shown to function as sites for protein-protein interactions. The mutations Y95A/Y96A and Y142A/W143A in the second and third TPR repeats lead to a modest decrease of PSI, but they prevent photoautotrophic growth and cause enhanced light sensitivity even though the accumulated PSI complex is fully functional. This phenotype can be reversed under anaerobic conditions and appears to be the result of photooxidative damage. A temperature-sensitive ycf3 mutant, generated by random mutagenesis of a conserved region near the N-terminal end of Ycf3, was used in temperature-shift experiments to show that Ycf3 is required for PSI assembly but not for its stability. Immunoblot analysis of thylakoid membranes separated by two-dimensional gel electrophoresis and immunoprecipitations shows that Ycf3 interacts directly with the PSI subunits PsaA and PsaD, but not with subunits from other photosynthetic complexes. Thus, Ycf3 appears to act as a chaperone that interacts directly and specifically with at least two of the PSI subunits during assembly of the PSI complex.

Aerobiosis↗

PubMed2001

Breast-feeding and maternal cardiovascular function.

Two studies examined the effects of breast-feeding on maternal cardiovascular function. In the first experiment, groups of breast-feeding and bottle-feeding women were compared on preejection period (PEP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) recorded for 1-min periods before and during standard laboratory stressors. Compared with bottle-feeders, breast-feeders had higher CO throughout the session, and greater decreases in CO and increases in TPR during cold pressor. In the second experiment, HR and blood pressure (BP) were compared before and after one breast-feeding and one bottle-feeding session in a within-subjects design. Both feeding methods increased BP but decreased HR, and systolic BP was higher for the breast-feeding than the bottle-feeding condition. Both studies support the notion that breast-feeding alters maternal cardiovascular function, possibly through the actions of oxytocin.

Adaptation, Psychological↗

PubMed1989

Effects of atenolol vs diltiazem on the haemodynamic effects of an inhaled beta 2-adrenoceptor agonist.

To determine the effects of concurrent beta 1-adrenoceptor blocker or calcium channel antagonist administration on the haemodynamic sequelae of an inhaled beta 2-selective adrenoceptor agonist bronchodilator, we examined echocardiographically the effects of fenoterol (400 micrograms) by metered dose inhaler following oral pre-treatment with (a) placebo, (b) atenolol or (c) diltiazem. Following placebo, fenoterol produced significant decreases in diastolic blood pressure (14% +/- 6%), total peripheral vascular resistance (TPR) (31% +/- 9%) and end-systolic stress (ESS) (15% +/- 21%). Cardiac output rose significantly (42% +/- 23%) as did heart rate (25% +/- 13%). After atenolol, responses to fenoterol were significantly blunted. Post-fenoterol heart rate, systolic blood pressure, % fractional shortening, stroke volume, ejection fraction, cardiac output and pressure/volume ratio increased significantly less after atenolol pre-treatment as compared to placebo pretreatment. TPR decreased significantly less. After diltiazem pre-treatment, the response to inhaled fenoterol was not different from that following placebo pre-treatment. We conclude that atenolol blunts the haemodynamic changes induced by fenoterol inhalation whereas diltiazem has little effect.

Adult↗

PubMed1992

Agreement and reproducibility of the estimates of cardiovascular function by impedance cardiography and M-mode echocardiography in healthy subjects.

The reproducibility and agreement of the estimates of stroke volume (SV), cardiac output (CO) and total peripheral resistance (TPR) by transthoracic impedance cardiography (ZCG) and M-mode echocardiography (ECHO) were analyzed before and after the placebo-controlled administration of ascending doses of isosorbide dinitrate and nicorandil in 12 healthy subjects. There was no biostatistical agreement between the two methods in estimating cardiovascular function either before or after dosing (ZCG estimated substantially larger SV, CO and lower TPR). But, ZCG and ECHO estimated about similar overall treatment related changes (across treatments and periods) and reached substantially better agreement when the values were expressed as ratio of the baseline before dosing. Such improvement did not occur when the data were expressed as arithmetic difference from baseline. In spite of the improvement of agreement by expressing the data as ratio of baseline, the coefficients of reproducibility between the two methods (circa 25% of baseline) remained too large to judge the methods interchangeable.

Adult↗

PubMed2006

Tetratricopeptide repeats in the type III secretion chaperone, LcrH: their role in substrate binding and secretion.

Non-flagellar type III secretion systems (T3SSs) transport proteins across the bacterial cell and into eukaryotic cells. Targeting of proteins into host cells requires a dedicated translocation apparatus. Efficient secretion of the translocator proteins that make up this apparatus depends on molecular chaperones. Chaperones of the translocators (also called class-II chaperones) are characterized by the possession of three tandem tetratricopeptide repeats (TPRs). We wished to dissect the relations between chaperone structure and function and to validate a structural model using site-directed mutagenesis. Drawing on a number of experimental approaches and focusing on LcrH, a class-II chaperone from the Yersinia Ysc-Yop T3SS, we examined the contributions of different residues, residue classes and regions of the protein to chaperone stability, chaperone-substrate binding, substrate stability and secretion and regulation of Yop protein synthesis. We confirmed the expected role of the conserved canonical residues from the TPRs to chaperone stability and function. Eleven mutations specifically abrogated YopB binding or secretion while three mutations led to a specific loss of YopD secretion. These are the first mutations described for any class-II chaperone that allow interactions with one translocator to be dissociated from interactions with the other. Strikingly, all mutations affecting the interaction with YopB mapped to residues with side chains projecting from the inner, concave surface of the modelled TPR structure, defining a YopB interaction site. Conversely, all mutations preventing YopD secretion affect residues that lie on the outer, convex surface of the triple-TPR cluster in our model, suggesting that this region of the molecule represents a distinct interaction site for YopD. Intriguingly, one of the LcrH double mutants, Y40A/F44A, was able to maintain stable substrates inside bacteria, but unable to secrete them, suggesting that these two residues might influence delivery of substrates to the secretion apparatus.

Amino Acid Sequence↗

PubMed1978

The influence of thoracic epidural analgesia on the circulation at rest and during physical exercise in man.

The effects of thoracic epidural analgesia (TEA) on the circulation at rest, during, and after physical exercise were investigated in 10 volunteers. At rest, TEA did not affect oxygen consumption (VO2) or cardiac output (Q), but heart rate (HR) was, increased by 7 beats/min, and stroke volume decreased correspondingly by 13 ml. Systolic arterial blood pressure was slightly reduced, but no other changes in systemic or pulmonary circulatory parameters were produced. TEA did not change VO2 during exercise, a 2.11/min reduction of Q being accompanied by a 4.2% increase of oxygen utilization coefficient. HR showed a relative reduction of about 10%. At moderate work loads during TEA, systemic arterial blood pressures were significantly lower than during control exercise. The resulting rate pressure product (RPP) was markedly reduced, while total peripheral resistance (TPR) remained unchanged. During recovery after the termination of exercise during TEA, VO2, Q, HR, RPP and TPR fell more rapidly towards values obtained at rest. From a clinical point of view the results support the safeness of TEA and also support its use in surgical patients with heart disease.

Adult↗

PubMed1984

Influence of alpha- and beta-adrenergic blockade on systemic and pulmonary hemodynamics during intravenous administration of local anesthetics.

The effects of alpha- and beta-adrenergic blockade on the systemic and pulmonary circulation during i.v. bolus injection of sub-seizure doses of lidocaine and bupivacaine were studied in dogs anesthetized with nitrous oxide. Pretreatment with hexamethonium or propranolol produced a marked decrease in cardiac output (CO), although pretreatment with phenoxybenzamine inhibited the decrease in CO during i.v. administration of lidocaine. Pretreatment with hexamethonium or phenoxybenzamine attenuated the increase in total peripheral resistance (TPR) following lidocaine 10 mg/kg i.v. In contrast, the propranolol-treated dogs developed a marked increase in TPR. The increases in mean pulmonary arterial pressure and pulmonary vascular resistance (PVR) following lidocaine 10 mg/kg i.v. were blocked by pretreatment with hexamethonium. Furthermore, PVR increased markedly with pretreatment with propranolol, although pretreatment with phenoxybenzamine prevented the large increase in PVR. These findings indicate that lidocaine has both a direct depressant effect and an indirect beta adrenergic stimulant effect on the heart. Systemic or pulmonary vasoconstriction following intravenous administration of lidocaine 10 mg/kg is associated primarily with an indirect stimulant effect mediated by alpha-adrenergic mechanisms. Bupivacaine, as well as lidocaine, has an indirect stimulant effect mediated by the autonomic nervous system.

Animals↗

PubMed1987

Dose-related effects of isoflurane on superior mesenteric vasoconstriction induced by endotoxemia in the rat.

To investigate the interplay between endotoxin-induced circulatory shock and the cardiovascular effects of different doses of isoflurane, mean aortic pressure (MAP), central venous pressure (CVP), mean pulmonary arterial pressure (MPAP), heart rate (HR), cardiac output and superior mesenteric artery flow (SMAF), were monitored in rats anesthetized with either 1.4% or 2.0% isoflurane in oxygen. Cardiac index (Cl), total peripheral vascular resistance (TPR) and superior mesenteric vascular resistance (SMVR) were derived. During continuous administration of isoflurane, endotoxin (LD90, 40 mg X kg-1 iv) was given after a 30-min baseline period, and data were collected for an additional 2-h period. Sham-challenged (saline) animals served as controls. The response to endotoxin in the systemic circulation showed a decrease in Cl and MAP, while HR and TPR increased. MPAP and CVP were essentially unchanged. There were no significant differences in the systemic circulation variables between endotoxin groups, apart from a more pronounced HR increase during 1.4% isoflurane. Regionally, however, SMAF was lower and SMVR was higher in the 2.0% versus the 1.4% isoflurane group following endotoxin. To conclude, the degree of mesenteric vasoconstriction during endotoxemia was dependent on the dose of isoflurane. This dose-related effect seems to be mediated through interaction with intrinsic vascular control, a higher dose allowing a more pronounced local blood flow reduction.

Animals↗

PubMed1989

The effect of general anaesthesia on the haemodynamic events during laparoscopy with CO2-insufflation.

Sixteen women were studied during elective diagnostic laparoscopy with CO2-insufflation to an intraabdominal pressure (IAP) of 2 kPa and Trendelenburg tilt to 30 degrees. They were allocated to either a halothane (Group I) or a balanced (Group II) anaesthesia with relaxation and controlled ventilation. Heart rate (HR), arterial pressure, stroke volume, CO2-elimination, end-tidal CO2 vol.% and total respiratory compliance (TRC) were the parameters measured, and mean arterial pressure (MAP), total peripheral resistance (TPR), stroke index (SI) and cardiac index (CI) were calculated. At maximum haemodynamic strain, SI and CI were on average reduced by 42% in both groups, without significant changes in HR and MAP. TPR increased by 50% in Group I and 100% in Group II. The reduction in SI was related to the changes in TRC. A small increment in CO2-elimination after CO2-insufflation was most pronounced in Group II. SI and CI did not reach the pre-insufflation values after return to the horizontal position and CO2-exsufflation. The haemodynamic differences between the two groups were small compared to the effects of the laparoscopy procedures.

Adolescent↗

PubMed1990

Comparison of six different regimens for the control of atrophic rhinitis in swine.

Effectiveness of six different programs of atrophic rhinitis (AR) control was evaluated under field conditions. Efficacy of treatments was recognized on the basis of--comparative evaluation of the average daily gain (ADG), morphometric examination of turbinate bones and computer conchal morphometry (TPR). Usefulness of the evaluated regimes differed significantly. TPR appeared to be the most objective method for AR evaluation. Correlation between severity of turbinate atrophy and ADG was only partial.

Animals↗

PubMed1989

Baroreceptor resetting and other determinants of baroreflex properties in hypertension.

1. Rapid resetting of the arterial baroreceptor threshold in the normal circulation extends the pressure range over which baroreflexes operate at high gain. During sustained falls and rises in resting blood pressure (BP), changes in reflex threshold may be greater or less than those of the receptors, through interactions with other sources of afferent drive (e.g. cardiac baroreceptors). In chronic hypertension the magnitude of the reflex resetting again corresponds to that of the arterial baroreceptors, probably because of the resetting of the threshold of the cardiac receptors. 2. 'Baroreflexes' in intact animals are compound reflexes with input from both arterial and non-arterial baroreceptors (e.g. cardiac/pulmonary baroreceptors). The steady-state responses can be characterized by BP-autonomic output function curves, which are often sigmoidal, with a well-defined effector response range and gain. Both sets of input contribute to the high gain component close to resting, with the arterial baroreceptors the major source of reflex drive; the non-arterial baroreceptors also contribute over this part of the reflex and their role increases considerably at high and low BP. 3. In chronic mild/moderate hypertension the changes in baroreflex properties are similar to those of moderate acute rises in BP or in cardiac load; heart rate range of the vagal component of the cardiac baroreflex is depressed, gain is slightly enhanced and the Valsalva-total peripheral resistance (TPR) reflex is unaltered. In severe hypertension: (i) vagal heart rate range and gain are further depressed; and (ii) there is depression of the Valsalva-TPR reflex, much as observed in constrictor reflexes during acute hypertension in normal animals. Circulatory disturbances produce engagement of non-arterial baroreceptors more readily in hypertensives than in normotensives; depression of baroreflexes in hypertension is due partly to enhanced drive from these receptors and partly due to reduction in the gain of the arterial baroreceptors. 4. The reflex vagal depression and that of neural constrictor reflexes can be considered as important homeostatic mechanisms that limit the effects of circulatory perturbations on cardiac filling pressures and on excessive rises in vascular resistance.

Animals↗

PubMed1992

Subpressor calcium infusion increases isovolumic left ventricular relaxation time and atrial natriuretic peptide in humans.

1. Subpressor calcium infusion for 1 h, which raised calcium levels to the upper limit of normal in normal subjects, increased plasma and urinary levels of atrial natriuretic peptide (ANP). 2. Heart rate fell, presumably due to carotid baroreflex stimulation (supported by the fall in noradrenaline) and the resultant fall in cardiac output prevented the expected rise in blood pressure due to the rise in total peripheral resistance (TPR). Thus the increase in ANP was not explained by an increase in blood pressure or noradrenaline. 3. There was no evidence for increased atrial stretch (no increase in atrial area or early velocity of left ventricular filling) as a mechanism for increased ANP. 4. Isovolumic left ventricular relaxation time increased, early velocity of ventricular filling decreased and TPR increased, consistent with increased tone in left ventricular and arteriolar muscle. 5. This suggests a direct effect of calcium on the atrial myocyte, stimulating ANP either through contractile or secretory mechanisms.

Adult↗

PubMed2005

Renal tubular function in children with beta-thalassemia minor.

BACKGROUND: beta-thalassemia minor is a common heterozygous haemoglobinopathy that is characterized by both microcytosis and hypochromia. It requires no treatment. It has been postulated that low-grade haemolysis, tubular iron deposition and toxins derived from erythrocytes might cause renal tubular damage in adult patients with beta-thalassemia minor. Our aim was to investigate the renal tubular functions in children with beta-thalassemia minor and to determine its possible harmful effects. METHODS: The study was conducted on 32 children (14 female and 18 male) at the age of 5.8 +/- 3.1 years (range 2-14 years) with beta-thalassemia minor. The patients were classified as anaemic (haemoglobin (Hb) </= 11 g/dL) (Group 1, n = 14) and non-anaemic (Hb > 11 g/dL) (Group 2, n = 18). A control group was formed with 18 healthy children whose ages and sexes match those in other groups (Group 3, n = 18). Fractional excretion of sodium (FE(Na), %), fractional excretion of magnesium (FE(Mg), %), fractional excretion of uric acid (FE(UA), %) and tubular phosphorus reabsorption (TPR,%) were calculated with standard formulas. Urinary calcium excretion (mg/kg per 24 h), zinc (Zn) (microg/dL), glucosuria (mg/dL), beta-2 microglobulin (mg/dL) and N-acetyl-beta-D-glycosaminidase (NAG, U/mmol creatinine) levels were measured through biochemical methods. RESULTS: There was no statistically significant difference among the three groups in terms of the results of FE(Na) (%), FE(Mg) (%), FE(UA) (%), TPR (%), calciuria (mg/kg per 24 h), NAG, urine Zn, proteinuria, glucosuria or urine beta- 2 microglobulin levels (P > 0.05). CONCLUSION: On the contrary of children with beta-thalassemia major, renal tubular dysfunction has not been determined in children with beta-thalassemia minor in the present study.

Acetylglucosaminidase↗

PubMed1999

Contribution of the leg vasculature to hypotensive effects of an antiorthostatic posture change in humans.

1. Previous results from our laboratory have shown that vasodilatation in the legs prevents mean arterial pressure (MAP) from increasing during water immersion. Therefore, we tested the hypothesis that vasodilatation in the legs is necessary for the hypotensive effects to occur during a moderate antiorthostatic posture change. 2. Ten healthy males underwent a 5 min posture change from upright seated to horizontal supine (SUP) and back to seated again with (OCCL-SUP) and without simultaneous total arterial (154 +/- 1 mmHg) thigh occlusion, and a control seated period, also with and without arterial occlusion. Cardiac output (CO) was measured by a non-invasive foreign (N2O) gas rebreathing technique. 3. MAP (brachial auscultation) decreased during SUP from 94 +/- 3 to 84 +/- 2 mmHg (P < 0.0001) and total peripheral vascular resistance (TPR = MAP/CO, n = 8) decreased by 15 +/- 4 % (P < 0.001). During OCCL-SUP, MAP decreased from 98 +/- 2 to 90 +/- 2 mmHg (P < 0.005) and TPR decreased by 14 +/- 3 % (P < 0.01). 4. In conclusion, vasodilatation in the legs is not necessary for the decrease in MAP to occur during a moderate antiorthostatic manoeuvre. Therefore, vasodilatation in more central vascular beds (e.g. abdomen) can alone account for the hypotensive effects.

Adult↗

PubMedDate not supplied

Characterization and mechanisms of the cardiovascular and haemodynamic alterations induced by scorpion venom in rats.

The scope of this work was to investigate the nature, chronology and mechanisms of the cardiovascular disorders induced by scorpion envenomation. Anaesthetized rats were instrumented for measurement of cardiac output (CO), renal (RBF) and muscular (HBF) blood flows (pulsed Doppler flowmetry), blood pressure, heart rate and dP/dt. Buthus occitanus venom (BO) was administered intravenously in the absence/presence of different pre-treatments. BO dose-dependently (150-300 microg/kg) increased blood pressure, dP/dt, total peripheral (TPR), renal (RVR) and muscular (HVR) vascular resistances, and decreased CO, RBF and HBF. Recovery occurred after 150 but not after 300 microg/kg. BO, 600 microg/kg, produced qualitatively similar effects but arrhythmias developed and mortality increased. Pre-treatment with phentolamine prevented the rises in TPR, RVR, HVR and blood pressure and the decreases in CO, RBF and HBF induced by BO, 300 microg/kg. Pre-treatment with propranolol prevented the rise in dP/dt and the occurrence of arrhythmias and limited the rise in RVR and the drop in RBF induced by BO, 300 microg/kg. Phentolamine, propranolol and their combination also prevented BO, 600 microg/kg-induced mortality. Other pre-treatments (bosentan, losartan, diltiazem, mepyramine) were almost ineffective vs. BO effects. Finally, BO, 300 microg/kg, induced a 30-40-fold increase in plasma epinephrine and norepinephrine levels, but no change in plasma endothelin-1 levels. Thus in anaesthetized rats, the pattern of the cardiac and systemic and regional haemodynamic effects of BO is typically that of and results from catecholamine outpouring-induced alpha- and beta-adrenoceptor stimulation.

Animals↗

PubMed1992

Plasma endothelin-1 during central hypovolaemia in man.

Endothelin-1 (ET-1) is a potent vasoconstricting peptide with effect on resistance as well as capacitance vessels. We followed ET-1 in arterial plasma together with heart rate (HR), central venous pressure (CVP), mean arterial pressure (MAP), and thoracic electrical impedance (TI) in seven men during central hypovolaemia induced by 50 degrees head-up tilt. During tilting plasma ET-1 increased from 1.1 +/- 0.2 to 1.4 +/- 0.3 pmol l-1 (mean +/- SE) concomitant with an increase in total peripheral resistance (TPR) (from 15 +/- 2 to 25 +/- 3 mmHg min l-1) (P < 0.01), and HR (from 67 +/- 2 to 94 +/- 5 beats min-1) (P < 0.01) while MAP remained unchanged. CVP decreased (from 1.8 +/- 0.9 to -1.6 +/- 1.0 mmHg) (P < 0.01) during tilting and remained unchanged during sustained tilt despite further reduction of central blood volume as recorded by TI. Presyncopal symptoms occurred after 28 +/- 6 min associated with decreases in HR (to 70 +/- 6 beats min-1), MAP (from 90 +/- 3 to 52 +/- 4 mmHg) and TPR (to 11 +/- 2 mmHg min l-1) (P < 0.01). At this time plasma ET-1 reached its highest level of 1.6 +/- 0.3 pmol l-1 (P < 0.01). Data show that head-up tilt is associated with increased plasma concentrations of ET-1 which may play a role in maintaining vascular tone in situations with a reduced central blood volume.

Adult↗

PubMed1995

Increase by NG-nitro-L-arginine methyl ester (L-NAME) of resistance to venous return in rats.

1. The effects of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), on mean circulatory filling pressure (MCFP), total peripheral resistance (TPR), cardiac output (CO) and resistance to venous return (Rv) were studied in rats. 2. In conscious, unrestrained rats, L-NAME (0.5-16 mg kg-1) dose-dependently increased mean arterial pressure (MAP) but not MCFP, an inverse index of venous compliance, either in the absence or presence of the ganglionic blocker mecamylamine (10 mg kg-1). 3. In pentobarbitone-anaesthetized rats, L-NAME (2, 4, 8 mg kg-1) increased MAP and reduced CO in a dose-related manner but did not change MCFP, TPR (+84, +140 and +192%) as well as Rv (+62, +72, +110%) were dose-dependently increased by L-NAME. 4. Our results show that L-NAME reduces CO by increasing arterial as well as venous resistances. L-NAME does not affect MCFP.

Amino Acid Oxidoreductases↗