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PubMed2003

Blood pressure- and pulse pressure-lowering effects, trough:peak ratio and smoothness index of telmisartan compared with lisinopril.

OBJECTIVE: To compare lisinopril with telmisartan, in regard to: 1) their effect on blood pressure (BP) and pulse pressure (PP), and 2) the duration and the homogeneity of their antihypertensive effect. PATIENTS AND METHODS: A randomized, open-label, crossover, comparative study of telmisartan 80 mg versus lisinopril 20 mg was conducted in 32 untreated hypertensive patients using clinic and 24-hour ambulatory BP measurements. Trough: peak ratio (TPR) and smoothness index (SI) were calculated for each drug. RESULTS: Using both measurement techniques no difference was detected between the 2 drugs in their effects either on BP (mean difference in 24-hour systolic BP 1.2 +/- 7.1 mm Hg, 95% confidence intervals -1.4, 3.8, and diastolic 0.7 +/- 5.1, -1.2, 2.5) or on PP (0.5 +/- 3.5, -0.7, 1.8). There was no difference between the TPR and the SI values of telmisartan (TPR 0.85/0.61 for systolic/diastolic BP and SI 1.46/1.2) and lisinopril (TPR 0.74/0.64 and SI 1.3/1.17). CONCLUSIONS: These data suggest that telmisartan is as effective as lisinopril in reducing BP and PP. Both drugs seem to provide smooth and sustained effects throughout the full 24-hour period.

Benzimidazoles↗

PubMed1982

Mechanisms of burn shock protection after severe scald injury by cold-water treatment.

Following a 3-second subxiphoid immersion of shaved, unresuscitated guinea pigs in 100 degrees C water, cardiac output (CO), mean systemic blood pressure (BP), total peripheral resistance (TPR), hematocrit (HCT), serum histamine (SH), and serum lactate (SL) were measured in untreated and cold-water treated animals up to 24 hours after injury. Animals receiving cold-water treatment (CWT) were immersed in 15 degrees C water for 15 minutes immediately after scald injury. CWT significantly (p less than 0.05) reduced SH and SL for up to 8 and 24 hours, respectively, after injury compared to untreated injured animals. HCT of CWT animals remained significantly lower than that of untreated animals for the first 8 hours after injury. However, CWT-animal HCT was not significantly different from control-animal HCT for this same period. CWT-animal BP was significantly greater than untreated-animal BP for the first 8 hours after injury. CWT- and untreated-animal TPR progressively rose after injury; however, at 24 hours after injury CWT-animal TPR was significantly reduced to 87% +/- 18.0 of preinjury values while untreated-animal TPR was maximally elevated to 170% +/- 10.0 of preinjury values. At 4 hours after injury CO of both untreated and SWT animals was significantly depressed at 56% +/- 3.0 and 50% +/- 10.0 of preinjury values, respectively. However, by 24 hours after injury untreated-animal CO remained depressed at 52% +/- 3.0 while CWT-animal CO was significantly improved at 92% +/- 19.0 of preinjury values. These studies document a beneficial hemodynamic response of severely burned animals after CWT and further verify the phenomenon of cold inhibition of burn wound tissue histamine release after severe scald injury. A correlation between decreased serum histamine and lactate levels and improved cardiovascular function following severe scald injury and CWT is also suggested.

Animals↗

PubMed2000

Left ventricular volumes and hemodynamic responses to postexercise ischemia in healthy humans.

PURPOSE: The purpose of this study was to determine the cardiac mechanisms involved in cardiovascular adjustments during postexercise circulatory occlusion (OCCL). METHOD: Heart rate (HR), mean arterial pressure (MAP), left ventricular end-diastolic (EDV) and end-systolic volumes (ESV), stroke volume (SV), cardiac output (CO), and total peripheral vascular resistance (total peripheral resistance (TPR)) were assessed in nine healthy volunteers during rest and static exercise at 30% of maximum voluntary contraction followed by either OCCL for 3 min or non-OCCL in a randomized crossover protocol. RESULTS: During handgrip, HR (+20%; P < 0.001), CO (+11%; P = 0.003), MAP (+18%; P = 0.001), and TPR (+6%; P = 0.004) increased, SV (-8%; P = 0.001) and EDV (-5%; P < 0.001) decreased, while ESV did not change (P > 0.05). These responses were similar between conditions (P > 0.05). During OCCL, HR, SV, and CO returned to baseline, whereas MAP (+19%; P < 0.001) and TPR (+9%; P = 0.004) remained elevated. EDV (+12%; P < 0.001) and ESV (+23%; P < 0.001) increased in parallel above resting values. CONCLUSION: Activation of muscle metaboreceptors during OCCL increased MAP by elevating TPR. Despite the higher afterload and increased ESV, CO and SV were kept similar to resting values because EDV also increased, implying the involvement of the Frank-Starling mechanism.

Adult↗

PubMed1988

Trimethoprim resistance determinants encoding a dihydrofolate reductase in clinical isolates of Staphylococcus aureus and coagulase-negative staphylococci.

The molecular and biochemical basis of resistance to high concentrations (MIC greater than or equal to 1000 mg/L) of trimethoprim (Tpr(H] was examined in Australian isolates of Staphylococcus aureus and coagulase-negative staphylococci. The Tpr(H) determinant (dfr A) was located within a 2.75-Kb Bg/II fragment on the S. aureus aminoglycoside-resistance plasmids pSK1 and pSK16 as judged by comparative restriction mapping with two naturally-occurring variants, pSK9 and pSK14, which did not encode trimethoprim resistance. This was confirmed in DNA-DNA hybridisation experiments in which a 0.9-Kb sequence of pSK1 DNA was used as a specific probe for the Tpr(H) gene. Plasmid DNA from three strains of coagulase-negative staphylococci, and the chromosomal material of one other isolate, were found to share homology with the probe DNA. Dihydrofolate reductases produced by these strains were virtually identical to the type S1 enzyme encoded by the S. aureus plasmid pSK1. Interspecies transfer may have been responsible for the conservation of Tpr(H) gene sequences among staphylococci.

Chromosome Mapping↗

PubMed2006

Domain:domain interactions within Hop, the Hsp70/Hsp90 organizing protein, are required for protein stability and structure.

The major heat shock protein (Hsp) chaperones Hsp70 and Hsp90 both bind the co-chaperone Hop (Hsp70/Hsp90 organizing protein), which coordinates Hsp actions in folding protein substrates. Hop contains three tetratricopeptide repeat (TPR) domains that have binding sites for the conserved EEVD C termini of Hsp70 and Hsp90. Crystallographic studies have shown that EEVD interacts with positively charged amino acids in Hop TPR-binding pockets (called carboxylate clamps), and point mutations of these carboxylate clamp positions can disrupt Hsp binding. In this report, we use circular dichroism to assess the effects of point mutations and Hsp70/Hsp90 peptide binding on Hop conformation. Our results show that Hop global conformation is destabilized by single point mutations in carboxylate clamp positions at pH 5, while the structure of individual TPR domains is unaffected. Binding of peptides corresponding to the C termini of Hsp70 and Hsp90 alters the global conformation of wild-type Hop, whereas peptide binding does not alter conformation of individual TPR domains. These results provide biophysical evidence that Hop-binding pockets are directly involved with domain:domain interactions, both influencing Hop global conformation and Hsp binding, and contributing to proper coordination of Hsp70 and Hsp90 interactions with protein substrates.

Binding Sites↗

PubMed2002

Hemodynamic response patterns: responder type differences in reactivity and recovery.

We examined whether responder type groups reflecting patterns of hemodynamic reactivity might also differ in recovery responses. Cardiac output (CO), total peripheral resistance (TPR), systolic and diastolic blood pressure, heart rate, and Heather index were assessed at rest and during speech and cold pressor tasks in young adults. Participants (n = 152) were classified as myocardial, vascular, or mixed-mild responders based on CO and TPR responses to speech presentation. Vascular responders exhibited slower CO and TPR speech recovery than the myocardial and/or mixed-mild groups. Responder type differences in reactivity showed limited task-generalizability. The sustained vascular response pattern of the vascular group is consistent with that seen in hypertension. In light of associations of heightened TPR with markers of disease risk, this suggests potentially negative health implications for vascular responders.

Adolescent↗

PubMed1983

Increased cardiac output and lowered peripheral resistance during metoprolol treatment.

Echocardiography was performed at every six months in hypertensives well controlled on metoprolol, 100 mg twice a day. After six months' treatment blood pressure was reduced from 177/110 mm Hg to 147/88 (p less than 0.02). LV wall thickness (septum + posterior wall) was unchanged 2.10 cm (2.14), and a significant drop in cardiac output (CO) to 5.0 l/min (6.1, p less than 0.02) was recorded (pretreatment values in brackets). After 24 months' treatment LV wall thickness was reduced to 1.94 cm (p less than 0.02), total peripheral resistance (TPR) to 17.3 mm Hg/l/min (23.4, p less than 0.02) and CO increased to 6.7 l/min (6.1, n.s.). After six months' treatment, there was thus a drop in BP with a significant drop in CO and unchanged TPR. After 24 months' treatment, however, CO was back to the pretreatment level and the drop in BP was entirely caused by a drop in TPR which was probably secondary to a reduction in the wall thickness of the arterial resistance vessels as judged by the relationship between the reduction in wall thickness in the LV and the reduction in TPR during the treatment.

Adult↗

PubMed1993

Post-exercise reduction in blood pressure in hypertensive subjects: effects of angiotensin converting enzyme inhibition.

1. Much attention has been given to the effects of various classes of antihypertensive drugs on blood pressure and haemodynamics. The effects of a single bout of exercise on post-exercise blood pressure have also been studied by several investigators. However, the combined effects of prior exercise and antihypertensive medication has drawn less attention. 2. We examined the separate and combined effects of a single bout of exercise and of angiotensin converting enzyme (ACE) inhibition with a new ACE inhibitor (fosinopril, 20 mg day(-1)) on post-exercise blood pressure and systemic and regional haemodynamics. Ten patients with mild-to-moderate hypertension were studied with a double-blind, randomized crossover, placebo- and rest period-controlled study design. 3. At rest, mean arterial pressure (MAP, -10 +/- 2 mm Hg), total peripheral resistance (TPR, -11 +/- 5%) and forearm vascular resistance (FVR, -17 +/- 8%) were significantly (P < 0.05) reduced during ACE inhibition as compared with the placebo phase. 4. During the placebo phase, MAP (-3 +/- 1 mm Hg), TPR (-10 +/- 4%) and FVR (-9 +/- 4%) were lower after exercise as compared with the control rest period. 5. During ACE inhibition, MAP (-3 +/- 1 mm Hg) and TPR (-8 +/- 4%) were lower, but FVR (+32 +/- 15%) was increased after exercise as compared with the control rest period. 6. Thus, blood pressure and TPR decreased similarly after exercise during the placebo phase and during ACE inhibition. However, differences in post-exercise forearm haemodynamics during the placebo phase and during ACE inhibition indicate that underlying regional haemodynamics are modified.

Adult↗

PubMed1991

Influence of dopamine and dobutamine on the cardiovascular depression during a standard halothane anaesthesia in dorsally recumbent, ventilated ponies.

The influence of different rates of dopamine and dobutamine on the cardiovascular depression during a standard halothane anesthesia was studied in dorsally recumbent ventilated ponies. Haemodynamic and respiratory responses were investigated by means of cardiac output (CO) determination (thermodilution technique), mean systemic (MAP) and pulmonary artery pressure (MPAP) (direct intravascular method) and arterial blood analysis (blood gases and packed cell volume). An important cardiopulmonary depression characterized by decreases (55% of the standing values) in CO, cardiac index (CI), MAP, MPAP and other cardiovascular related parameters occurred in the dorsally recumbent anaesthetized ponies after a stabilization period of 30 minutes. Dopamine at 2 different infusion rates (2.5 and 5.0 micrograms/kg/min) induced few changes of the cardiopulmonary parameters (non-significant increases in MAP, CI, left ventricular work [LVW], stroke volume [SV]; non-significant decrease in total peripheral resistance [TPR]). Several minor time related influences were also observed (increases in MPAP and total pulmonary resistance [TpR]). Arterial blood gases did not change during the different dopamine infusions. Low doses of dobutamine (1.25 micrograms/kg/min) were efficient to counteract the cardiovascular depression. Significant increases in CO, CI, MAP, MPAP and SV were observed. TPR and TpR tended to decrease but non-significantly. Heart rate and blood gases remained constant. The higher doses of dobutamine (2.5 and 5.0 micrograms/kg/min) accentuated these changes but a significant increase in heart rate with even periods of severe tachycardia and an increase of the packed cell volume were also observed. Apparently, low doses of dobutamine were indicated for the management of the cardiovascular depression during anaesthesia in the dorsally recumbent ventilated horse.

Anesthesia↗

PubMed1977

Responses of the cardiovascular system of the rat to alpha-and beta-adrenoceptor agonists.

1 The effects of intravenously infused phenylephrine and isoprenaline upon the cardiovascular system of the rat anaesthetized with pentobarbitone, have been investigated.2 Phenylephrine produces a dose-dependent rise in mean arterial blood pressure (MABP) that is due mainly to an increase in total peripheral vascular resistance (TPR), though at all doses tested cardiac output was invariably raised.3 The increase in cardiac output was due in each instance to an increase in stroke volume, heart rate being unchanged. This increase in cardiac output is probably brought about by effects of phenylephrine on the capacitance vessels rather than by an effect on the heart.4 Evidence is presented to show that the effects of phenylephrine are mediated largely by alpha-adrenoceptors, but that beta-adrenoceptors which affect TPR are also stimulated by the amine.5 Isoprenaline produces a dose-dependent fall in MABP that is due entirely to a fall in TPR since the cardiac output increases.6 Unlike phenylephrine, the increase in cardiac output obtained with isoprenaline was achieved by an increase in heart rate while stroke volume remained close to control values. It is contended that the augmented venous return required for the elevated cardiac output results in this case mainly from the isoprenaline-induced fall in TPR which enhances transfer of blood from arteries to the veins.7 Evidence is presented to show that the effects of isoprenaline are mediated mainly by beta-adrenoceptors.8 Under the present experimental conditions the adrenoceptor-mediated cardiovascular changes are little modified reflexly by the arterial baroreceptors.

Adrenergic alpha-Agonists↗

PubMed1989

The pharmacological evaluation of LY 170680, a novel leukotriene D4 and E4 antagonist in the guinea-pig.

1. This paper describes the evaluation of LY170680 (5-less than 3-[2(R) (carboxyethylthio)-(S)-hydroxypentadeca 3(E)5(Z)-dienyl]phenyl greater than 1H tetrazole, as an antagonist of the cysteinyl leukotrienes C4, D4, E4, in a variety of in vitro and in vivo models. 2. In vitro, LY170680 was a potent, selective, and competitive antagonist of LTD4, and LTE4. It produced a concentration-dependent rightward displacement of the concentration-response curves elicited by either LTD4 or LTE4 on both the guinea-pig ileal and tracheal preparation. The pA2 values for LY170680 were estimated to be 8.1 +/- 0.2 (n = 8) and 8.1 +/- 0.1 (n = 6) on trachea, and 8.7 +/- 0.1 (n = 12) and 9.0 +/- 0.3 (n = 6) on ileum for both LTD4 and LTE4 respectively. The slopes of the Schild plots in these studies were all close to unity. 3. LY170680 was shown to be a modest antagonist of the LTC4-induced responses on guinea-pig ileum (pA2 7.0 +/- 0.2 n = 5), but had no discernable effects against contractions induced by histamine, prostaglandin E2 (PGE2), PGF2 alpha or acetylcholine. The compound also reduced the LTC4-induced responses on trachea, but in a non competitive manner. 4. Intravenous LY170680 reduced in a dose-dependent manner (ED50 3.8 mg kg-1, 60 min pretreatment) the fall in compliance in the anaesthetized guinea-pig, and the rise in total pulmonary resistance (TPR) (ED50 2.0 mg kg-1, 30 min pretreatment) in the artificially ventilated guinea-pig, produced by intraveous LTD4. 5. LY170680 (5mgkg-1, i.v.) was also effective in reducing the increase in TPR to intravenous antigen in sensitized animals pretreated with mepyramine, indomethacin and propranolol. 6. The compound was only moderately effective (ED5o 40mgkg-1 p.o.) in preventing the rise in TPR induced by intravenous LTD4, when given orally. 7. Inhaled LY170680 was particularly effective in preventing the increase in TPR produced by an exposure to aerosolised LTD4. An estimated 1-2 pg of LY170680 delivered to the airways by nebuliser 1 hour beforehand, produced a 6 fold lateral displacement to the right of the dose-response curve to LTD4. 8. Studies in conscious animals indicated that inhaled LY170680 produced a dose-dependent reduction in the increased volume of gas, trapped in the lung following exposure to aerosolised LTD4. Duration studies also indicated that an estimated inhaled dose of 10 g LY170680 significantly reduced the LTD4-induced' increase in trapped lung gas volume for at least 4 h. Inhaled LY170680 also reduced LTC4-induced increase in gas trapping in a manner similar to LTD4. However, histamine-induced gas trapping was unaffected.

Administration, Inhalation↗

PubMed1994

Haemodynamic changes induced by short- and long-term sodium chloride or sodium bicarbonate intake in deoxycorticosterone-treated rats.

The contribution of chloride to the haemodynamic changes of salt-dependent deoxycorticosterone (DOC) hypertension was studied in young Wistar rats subjected to dietary loading with sodium chloride (NaCl) or sodium bicarbonate (NaHCO3). Mean arterial pressure (MAP), cardiac output, systemic resistance (TPR) and arterial rigidity (estimated from pulse pressure/stroke volume ratio, PP/SV) were determined in conscious chronically cannulated rats. DOC-induced increase of MAP and TPR appeared earlier in NaCl-loaded than in NaHCO3-loaded rats. After 4-6 weeks of hypertensive treatment MAP, TPR and PP/SV ratio were higher in DOC-treated rats fed NaCl diet than in those fed NaHCO3 diet. In contrast, after a long-term hypertensive regimen (lasting for 7-9 weeks) there was no significant difference in either MAP or TPR between rats loaded with NaCl or NaHCO3. On the other hand, DOC hypertension induced by a long-term feeding of NaHCO3 diet was not associated with an increase of arterial rigidity which was characteristic for DOC-NaCl hypertensive rats. Thus, a sufficiently long selective dietary sodium loading is capable to increase the systemic resistance but not to alter the arterial rigidity. This was also confirmed by a comparison of blood pressure-matched DOC hypertensive rats fed NaCl or NaHCO3 diets. These animals did not differ in the degree of systemic resistance elevation but the arterial rigidity was increased only in NaCl-loaded rats.

Animals↗

PubMed1988

Central haemodynamics during morphine abstinence in anaesthetized rats.

Central haemodynamics were studied in one group of morphine-dependent rats, and in a non-dependent control group, before and after administration of repeated bolus doses of naloxone. Dependence was induced by s.c. morphine pellet implantations. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO) and mean transit time (MTT) were measured in the conscious state, after induction of chloralose anaesthesia and after the administration of naloxone (0.005, 0.05, 0.5 and 5 mg kg-1 i.v.). Total peripheral resistance (TPR), stroke volume (SV) and central blood volume (CBV) were subsequently calculated. The haemodynamic variables did not differ significantly in the conscious state, except for a lower SV, when compared with the non-dependent control group. However, in response to anaesthesia the dependent rats exhibited a greater fall in MAP, mainly due to a TPR decrease. Naloxone elicited a marked increase in MAP in the morphine-dependent group, which was mainly caused by an increase in TPR. Naloxone induced no significant change compared with the control group in CO and CBV, while SV increased concomitantly with a lowered HR after naloxone in the morphine-dependent group. These results suggest that the withdrawal hypertension during morphine abstinence was mainly explained by an increase in TPR, reflecting an augmented tone of the resistance vessels. The minor changes in CBV indicate that the tone of the venous capacitance vessels was largely unaffected by naloxone-induced morphine abstinence.

Animals↗

PubMed2006

Forearm plethysmography in the assessment of vascular tone and resistance vasculature design: new methodological insights.

AIM: High peripheral resistance and structural alteration in resistance arteries are central phenomena in essential hypertension and have been widely examined by forearm venous occlusion plethysmography; at rest for studying vascular tone, and during reactive hyperaemia for studying vascular structure. This work concerns the influence of venous pressure on hyperaemic vascular resistance (Rmin), the reproducibility of hyperaemic and resting vascular resistances (Rrest) and the relation between forearm and total peripheral vascular resistance (TPR). METHODS: In four healthy subjects, intravenous and intra-arterial blood pressures were measured simultaneously with plethysmographic recordings of hyperaemic and resting forearm blood flows. Reproducibility was examined in 15 young and 14 middle-aged healthy subjects and in 21 untreated hypertensive patients. RESULTS: Rmin remained low in the first recorded cardiac cycle, but rose in the second, even though corrected for the venous pressure rise, suggesting vascular tone recovery along with venous congestion. Between-day reproducibility of Rmin was high in middle-aged normotensive (8.7%) and hypertensive subjects (10.6%), but Rmin fell significantly between successive days in the young subjects. Rrest correlated with TPR, but required up to 40 min to reach steady state and showed high day-to-day variation in young (21.8%) and hypertensive subjects (16.2%). CONCLUSIONS: During hyperaemia, vascular resistance should be measured in the first cardiac cycle following venous occlusion to minimize influences of venous pressure rise and possible tone recovery. Rrest seems to reflect TPR. About 20 subjects may be needed to detect 15% changes between days in Rrest, fewer when concerning Rmin and TPR.

Adult↗

PubMed1993

Influence of intravenous infusion of ethanol on regional blood flow in conscious rats.

The effects of intravenous infusions of ethanol and saline (0.9% NaCl) on mean arterial pressure (MAP), heart rate (HR), total peripheral resistance (TPR), cardiac contractility (dP/dtmax) and systemic haemodynamics were studied in conscious, unrestrained rats by the radioactive microsphere technique. Saline (0.03 and 0.06 mL min-1 kg-1 for 12 min each dose) in the time-control group did not affect MAP, HR, TPR, dP/dtmax or vascular conductances in any organs or beds. While the low dose ethanol (2.4 mg min-1 kg-1) did not alter MAP, HR, TPR, systemic haemodynamics or dP/dtmax, the high dose (4.8 mg min-1 kg-1) slightly reduced MAP and TPR but did not affect HR, cardiac output or dP/dtmax. Both doses of ethanol vasodilated the intestine and spleen, but vasoconstricted the skin. The high dose caused additional vasodilatation in the heart and testes and the low dose also constricted the skeletal muscle bed. Our results show that ethanol, at non-hypotensive or slightly hypotensive doses, has marked vasodilator effects in the heart, intestine, spleen and testes.

Animals↗

PubMed2000

A tetratricopeptide repeat half-site in the aryl hydrocarbon receptor is important for DNA binding and trans-activation potential.

Similar to certain unliganded steroid hormone receptor complexes, the unliganded aryl hydrocarbon receptor has been shown to consist of a multimeric core complex that includes the 90-kDa heat shock protein (hsp90) and the immunophilin-like hepatitis B X-associated protein 2 (XAP2). Immunophilins and XAP2 associated with these complexes bind to the carboxyl-terminal end of hsp90 through an interaction with their tetratricopeptide repeat (TPR) domains. The consensus TPR binding motif contains two domains, A and B. Recently, the carboxyl terminus of XAP2 has been shown to contain a highly conserved TPR domain that is required for the assembly of XAP2 with both hsp90 and AhR. A search of the murine AhR sequence identified domain B (A-F-A-P) of the consensus TPR sequence directly adjacent to the carboxyl-terminal side of the helix-loop-helix region of the murine and human AhR. We hypothesized that this conserved domain B region may be involved with mediating interactions between either AhR-hsp90, AhR-XAP2, and/or AhR-AhR nuclear translocator protein. Site-directed mutagenesis of the amino-terminal alanine residue of this region to an aspartic acid (A78D) completely inhibited 2,3,7, 8-tetrachloro-p-dioxin (TCDD) -dependent activation of a xenobiotic response element (XRE) driven gene expression construct in transfected COS-1 and BP8 cells. The A82F mutation caused a 40 to 50% decrease in TCDD-dependent activation. The inability of A78D and the reduction of A82F to trans-activate XRE-driven reporter activity did not result from impaired AhR-XAP2-hsp90 interactions, TCDD-dependent AhR translocation to the nucleus, or AhR-AhR nuclear translocator protein interactions. In vitro DNA binding analysis demonstrated that loss of trans-activation potential by the A78D mutation resulted from impaired XRE binding. This study underscores the potential importance of AhR mutations that occur naturally outside of known functional domains.

Amino Acid Sequence↗

PubMed1994

Possible role of insertion sequence IS257 in dissemination and expression of high- and low-level trimethoprim resistance in staphylococci.

The transposon-like structure Tn4003 and related elements were found to encode high- and low-level trimethoprim resistance (Tpr) in Staphylococcus aureus and coagulase-negative staphylococci. By using transcriptional fusions in Escherichia coli, the variation in resistance levels was found to correlate with the transcriptional activity of the region presumed to carry the promoter for the operon containing the Tpr dihydrofolate reductase gene, dfrA, encoded by these elements. The reduced transcriptional activities exhibited by elements encoding low-level Tpr appear to be a consequence of deletions adjacent to the copy of IS257 which normally encodes the -35 sequences of these promoters. The data obtained not only support the involvement of IS257 in the transcription of the proposed thyE-dfrA-orf-140 operon of Tn4003 but may also implicate this insertion sequence in the mechanisms resulting in the variation in Tpr levels observed in staphylococci.

Base Sequence↗

PubMed1997

Inducible expression of a Porphyromonas gingivalis W83 membrane-associated protease.

The Tpr protease of Porphyromonas gingivalis W83 is a membrane-associated enzyme capable of hydrolyzing a chromogenic bacterial collagenase substrate. An isogenic mutant lacking a functional tpr gene had a greatly reduced ability to hydrolyze the collagenase substrate. Activity was restored to the tpr mutant by introducing a shuttle plasmid containing the tpr gene. Expression of the gene is induced by nutrient limitation, as shown by enzymatic and Northern analyses.

Collagenases↗