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PubMed1995

Cardiac and vascular structural changes in normotensive subjects with parental hypertension.

OBJECTIVE: To evaluate whether a predisposition to hypertension is associated with early cardiac and vascular alterations. SUBJECTS: Twenty-five normotensive subjects with both parents hypertensive (group 1) and 28 age- and sex-matched control subjects with both parents normotensive (group 2). METHODS: In the two groups the measurements included: clinic blood pressure; left ventricular end-diastolic diameter, septal wall thickness and posterior wall thickness (by echocardiography); minimal forearm and calf vascular resistances (i.e. resistance assessed immediately after prolonged ischaemia, which depends on arteriolar wall thickness); and baseline and postischaemic radial artery compliance-pressure curves over the systolodiastolic pressure range (by echotracking device and finger blood pressure). RESULTS: Group 1 had a slightly higher clinic blood pressure, and septal and posterior wall thickness, than group 2. Minimal forearm vascular resistance was clearly greater in group 1 than in group 2, whereas minimal calf vascular resistance was not significantly different in the two groups. Radial artery compliance was also similar in the two groups. CONCLUSIONS: Parental predisposition to hypertension is accompanied by cardiac and arteriolar structural changes qualitatively similar to those found in hypertensive patients, although arteriolar structural changes do not involve all vascular beds. Arterial compliance is not altered in this condition. Vascular changes may be determined by mechanisms other than blood pressure elevation.

Adult↗
PubMed1980

[Structural changes in the brain in transient cerebral circulatory disorders detected in vivo by using computerized axial tomography and radioisotope cerebral scintigraphy].

Computer-aided axial tomography and radioisotopic (with 99mTc) scintigraphy of the brain were used for examining 54 patients with transient cerebral circulation disturbances, the clinical manifestations of which subsides within a period of less than 24 hours. In 28% of the patients, structural changes in the brain were revealed. The computer-aided tomography appeared to be more informative for their discovery, than the radioisotopic scintigraphy. On the basis of the data obtained the patients were divided into the following three groups: a) functional, i. e. having no lifetime structural changes in the brain detected at the moment of the examination (72% of all the patients), b) ischemic-infarctic one with a minor cerebral infarctions (13.5% of the patients), and c) hemorrhagic, with small-sized hemorrhagic foci in the brain (11.5% of the patients). The existence of the latter group should be regarded as a warning of dangers entailed by routine prevention and treatment of transient cerebral circulation disturbances with antiaggregants and anticoagulants. A new classification and terminology of the clinical symptoms caused by transient cerebral circulation disturbances are offered.

Cerebral Hemorrhage↗
PubMed1989

Pertussis toxin induces structural changes in G alpha proteins independently of ADP-ribosylation.

Pertussis toxin catalyzes ADP-ribosylation of a family of GTP-binding proteins (G alpha proteins) involved in signal transduction. It is thought that this activity is responsible for the attenuating effects of the toxin on the actions of a number of hormones and neurotransmitters. By utilizing specific antisera for detecting on electrophoretic transfer blots (Western blots) alpha proteins that are subject to ADP-ribosylation, it was found that treatment of these proteins with pertussis toxin resulted in shifts in their electrophoretic mobility and marked enhancement of their immunoreactivity compared to untreated proteins. No changes in mobility or immunoreactivity with specific antisera were observed with beta subunits of G proteins. Both effects on alpha proteins required the same ingredients, including detergents, ATP, and sulfhydryl reducing agents, that other studies have shown are required for activation of the ADP-ribosylating activity of pertussis toxin. However, NAD+, the substrate for ADP-ribosylating activity, was not required. Moreover, inhibition of the ADP-ribosylating activity by 50 mM nicotinamide failed to block the NAD-independent effects of the toxin. These findings indicate that the toxin induces structural changes in alpha proteins independently of its ADP-ribosylating activity and raise the possibility that these structural changes are primary to ADP-ribosylation and causative of many of the biological effects of pertussis toxin.

Adenine Nucleotides↗
PubMedDate not supplied

Structural changes in the tympanic membrane after repeated tympanostomy tube insertion.

In an animal model (rat) a polyethylene tympanostomy tube was repeatedly inserted (four periods lasting 2 weeks) into the upper rear quadrant of the right tympanic membrane (TM). The intervals between the different tubulation periods (TPs) lasted 3 weeks. The corresponding quadrant of the left TM was subjected to repeated myringotomies (four times). The structural changes in the TMs were evaluated otomicroscopically and by histological techniques 3 weeks and 3 months after the final TP. Repeated tympanostomy tube insertion caused a dramatically thickened pars tensa. The thickened areas were characterized by a scar tissue exhibiting sclerotic plaques and a dense connective tissue with bone-like formations. Occasionally, islands of keratinizing stratified squamous epithelium were noted within the thickened pars tensa as well as interrupting the epithelial lining facing the tympanic cavity. Similar structural changes occurred after myringotomy without tube insertion, but they were not so pronounced as after repeated tympanostomy tube insertion. The changes were not restricted to the manipulated quadrants, but also affected the untouched anterior quadrants. Throughout the observation period the anterior quadrants improved, while the rear quadrants remained severely affected.

Animals↗
PubMed1995

Continuous nitric oxide inhalation reduces pulmonary arterial structural changes, right ventricular hypertrophy, and growth retardation in the hypoxic newborn rat.

Breathing low oxygen levels for several weeks produces progressive pulmonary artery hypertension and smooth muscle hypertrophy and hyperplasia in many species. Because nitric oxide (NO) is an important regulator of pulmonary vascular tone, we examined whether the continuous inhalation of low levels of NO gas would attenuate pulmonary arterial structural changes in hypoxic rat pups. Nine-day-old rat pups and their mothers continuously breathed at FIO2 0.21 or 0.10 with or without adding 20 ppm (by volume) NO for 2 weeks. Lung tissue was obtained for vascular morphometric analysis, and the hearts were dissected to measure right ventricular weight and levels of mRNA encoding rat atrial natriuretic factor (rANF). In addition, femur and skull length were radiographically determined. Breathing at FIO2 0.10 for 14 days increased pulmonary arterial wall thickness and the proportion of muscular arteries in the lung periphery. Right ventricular weight and right ventricular rANF gene expression increased, whereas body weight and skeletal growth were reduced (all P < .05). Continuous inhalation of 20 ppm NO at FIO2 0.10 for 2 weeks decreased hypoxic pulmonary vascular structural changes and somatic growth retardation and prevented the increase of right ventricular weight and right ventricular rANF mRNA levels. These observations suggest that chronically breathing NO attenuates pulmonary vascular smooth muscle hypertrophy and/or hyperplasia and extension into distal arterial walls, right ventricular hypertrophy, and growth retardation of newborns breathing at a low oxygen level.

Administration, Inhalation↗
PubMed1995

Transient versus persistent functional and structural changes associated with facilitation of Aplysia sensorimotor synapses are second messenger dependent.

Increases in activity of both protein kinase A (PKA) and protein kinase C (PKC) contribute to short-term facilitation of Aplysia sensorimotor synapses evoked by serotonin (5-HT). We report here that increasing levels of cAMP in sensory neurons evokes increases in both synaptic efficacy and in the number of sensory neuron varicosities contacting the major axons of motor cell L7 at intermediate times (3 hr) that persist for 24 hr. Treatment with phorbol esters results in a large transient increase in synaptic efficacy that is accompanied by a large transient increase in the number of sensory neuron varicosities with the newest varicosities most susceptible to elimination. The reversal of the synaptic facilitation and the structural changes does not appear to be the result of long-term inhibitory actions of persistent PKC activation by phorbol esters, since changes in synaptic efficacy can be evoked by additional applications of either phorbol esters or 5-HT. The short-lived changes in structure evoked by phorbol esters occur in preexisting sensory neurites and not by new growth, since increases in PKC activity with phorbol esters lead to reductions in neurite extension and to retractions by sensory neuron growth cones. The action of phorbol esters on growth cone extension is reversible with washout. The results suggest that increases in PKA and PKC activities by 5-HT contribute to short (minutes) and intermediate (hours) forms of facilitation of sensorimotor synapses while increases in PKA activity also mediate long-term (days) maintenance of synaptic facilitation.

Animals↗
PubMed1990

Regression of cardiovascular structural changes--a preventive strategy.

Left ventricular hypertrophy is an independent "risk factor" for all kinds of cardiovascular disease. Structural vascular changes are of importance for the maintenance and progression of high blood pressure. To try to achieve regression of these structural changes seems a logical option as part of a preventive strategy in hypertension. The effect of antihypertensive therapy on structural cardiovascular changes in animal models and man is reviewed. A prolonged normalization of blood pressure without reflexogenic activation of trophic factors, if possible started early in the development of hypertension seems to be the optimal therapy to attain regression. There are some data indicating that regression of cardiac hypertrophy can improve cardiac function and reduce arrhythmias and furthermore that regression of structural vascular changes can positively affect the progression of hypertension. Although these preliminary result look promising there are still no data on how regression induced by antihypertensive therapy affects the mortality and morbidity associated with left ventricular hypertrophy.

Animals↗
PubMed1981

[Structural changes in the microcirculatory bed and perivascular connective tissue in the myocardium during experimental hypercholesterolemia].

Light and electron microscopy were used in rabbits to study the effect of hypercholesterolemia (HC) on the microcirculatory bed (MCB), perivascular connective tissue and specialized cells of the myocardium. Within the first hours (1, 3, 6, 15, 24, 48 h) after cholesterol single administration to the animals, there were structural changes in the MCB, aggregation and superficial changes in red blood cells (echinocytes), stases, the presence of unusual ultrastructures in elastic membranes (EM) of the arterioles, in the amorphous substance of perivascular connective tissue, specifically near the venules, and focal dystrophy in cardiomyocytes. The ultrastructures detected in the EM of the arterioles and perivascular tissue seem likely to be the complexes of atherogenous lipoproteins and glycosaminoglycans. The transfer of the animals on the atherogenous diet entailed the reconstruction of small arteries of the myocardium and formation in them of so-called "Conti's pillows" as well as lipid deposition. A complex of structural changes revealed in the myocardium in the early stages of HC indicates the increased permeability of the microvessels, alterations in the blood rheological properties and circulatory disorders. A relationship was found between the intensity of the changes cited and blood cholesterol level. Injury to the MCB of an organ is likely to play an initial part in the mechanisms of atherogenesis.

Animals↗
PubMed1990

A structural change in the Neurospora plasma membrane [H+]ATPase induced by N-ethylmaleimide.

The reaction of N-ethylmaleimide (NEM) with Cys-532 of the Neurospora plasma membrane [H+]ATPase results in inhibition of ATP hydrolysis which is protected by MgADP (Pardo, J. P., and Slayman, C. W. (1989) J. Biol. Chem. 264, 9373-9379). To examine the conformational state of the ATPase upon NEM modification, we have used limited trypsinolysis and domain-specific antibodies. The NEM-reacted ATPase shows increased sensitivity to trypsin, particularly in the central hydrophilic region of the polypeptide thought to contain the ATP binding and phosphorylation sites. In addition, competitive enzyme-linked immunosorbent assays indicate that the C-terminal domain of the ATPase becomes more accessible to antibody binding while the N-terminal region becomes more protected. The NEM-induced structural change is accompanied by loss of the ability to form a phosphoenzyme intermediate. The change in tertiary conformation occurs specifically upon NEM reaction with Cys-532 since neither NEM modification of Cys-545 nor fluorescein 5'-isothiocyanate modification of Lys-474 alters the tryptic digestion pattern of the ATPase. Furthermore, modification of Cys-532 with the less bulky sulfhydryl reagent methyl methanethiosulfonate does not result in a detectable structural change or loss of enzymatic activity. Thus, the introduction of a relatively bulky maleimide group at Cys-532 has specific and far-reaching effects upon the structure and function of the ATPase.

Adenosine Triphosphate↗
PubMed1989

Structural changes in bacteriorhodopsin during proton translocation revealed by neutron diffraction.

A neutron diffraction study of spectroscopic states for the light-energized proton pump bacteriorhodopsin (BR) is presented. The photocycle states BR-568 and M were generated at temperatures above 4 degrees C and were measured after trapping at--180 degrees C. In the BR-568 to M-state transition, which is known to be a key step in transmembrane proton pumping, reversible structural changes of the protein were detected. These structural alterations occur in the neighborhood of the cyclohexene ring and at the Schiff's base end of the chromophore retinal. They are interpreted as a 1-2 degree tilt of three or four of the transmembrane alpha-helices or as positional changes of four or five amino acids. The structural changes observed are inherent in the transport mechanism of bacteriorhodopsin.

Bacteriorhodopsins↗
PubMed1991

Long-term structural changes in pH-sensitive hydrogels.

The long-term swelling properties of lightly cross-linked copolymer hydrogels consisting of methyl methacrylate (MMA) and N,N-dimethylaminoethyl methacrylamide (DMAA) were studied as a function of pH at 25 degrees C and 37 degrees C. In acidic pH regions, the swelling equilibria were found to be stable over 200 d. In alkaline pH environments, however, the 'equilibrium' swelling increases slowly with time. Gas chromatography of the supernatant shows that substantial methanol is produced, along with trace amounts of N,N-dimethylethylene diamine. Thus, the primary mechanism underlying the structural changes appears to be hydrolysis of ester groups in the MMA side-chains, with a much smaller contribution due to amidolysis of the DMAA side-chains. The implications of these structural changes for the application of this hydrogel, as well as other related hydrogels as long-term implantable biomaterials, are discussed.

Gels↗
PubMed1988

Long-term antihypertensive treatment may induce normalization of left ventricular mass before complete regression of vascular structural changes: consequences for cardiac function at rest and during stress.

In 14 essential hypertensive patients, aged 26-59 years, blood pressure, left ventricular mass index (LVMI), systolic function (M-mode echo, two-dimensionally guided), post-ischaemic 'maximal' forearm blood flow (strain gauge venous occlusion plethysmography), plasma renin activity, plasma catecholamines and aldosterone were measured before and after 6 and 12 months of treatment (eight patients were given captopril, 100 mg/day, + hydrochlorothiazide 25 mg/day in five patients, and six patients were given nitrendipine, 20 mg/day, + atenolol 50 mg/day in four patients). Minimal vascular resistance (mean blood pressure/peak forearm blood flow) was taken as an index of arterial structural changes. After 6 months of treatment significant reductions in blood pressure (P less than 0.001), LVMI (P less than 0.001) and minimal vascular resistance were observed. After 12 months of treatment blood pressure, LVMI and minimal vascular resistance were further reduced. The LVMI was normalized in nine cases and the minimal vascular resistance in two cases only. Aldosterone and plasma catecholamines did not change, whereas plasma renin activity was increased during captopril only. Before and during treatment the left-ventricular shortening fraction in relation to end-systolic stress in each patient at rest, and at peak of handgrip and cold pressor tests, fell within the 95% confidence limits of correlation obtained in normals. Thus, in essential hypertensives long-term treatment can induce normalization of LVMI before complete regression of arterial structural changes in the forearm. Left ventricular systolic function is preserved after normalization of LVMI, both at rest and during stress.

Adult↗
PubMed1995

Structural changes in the water-oxidizing complex monitored via the pH dependence of the reduction rate of redox state S1 by hydrazine and hydroxylamine in isolated spinach thylakoids.

A detailed kinetic analysis is presented for the pH dependence of the reduction of the water-oxidizing complex (WOC) in redox state S1 by hydrophilic amines NH2R (R = NH2, OH) in suspensions of isolated thylakoids. Measurements of patterns of the oxygen yield induced by a train of single-turnover flashes and evaluation of the data within the framework of an extended Kok model [Messinger, J., Wacker, U., & Renger, G. (1991) Biochemistry 30, 7852-7862] led to the following results: (a) the rate constants kS1(NH2R) exhibit strikingly similar pH dependencies for NH2OH and NH2NH2 with "titration waves" at pH 5.3-5.6; 6.2-6.5, and above a critical pH value of about 7.4; (b) the differences in the reaction mechanism between NH2OH (1-electron reduction) and NH2NH2 (2-electron reduction) are almost pH-independent; (c) the ratio of the rate constants, kS1(NH2OH)/kS1(NH2NH2), decreases by a factor of about 9 within the range 5 < pH < 8.5. A detailed analysis reveals that these data cannot be consistently explained by the assumption that the unprotonated forms NH2OH and NH2NH2 are the active species while the protonated cations [NH3OH]+ and [N2H5]+ are nonreactive. A quantitative description is achieved by the additional postulate that pH-dependent structural changes take place in the WOC, thereby modulating the reactivity toward exogenous redox active amines of the type NH2R. On the basis of the results of this study and a recent report [Messinger, J., & Renger, G. (1994) Biochemistry 33, 10896-10905], it is inferred that the WOC undergoes three specific structural changes, with characteristic pH values of 5.3-5.5, 6.2-6.5, and above 7.4.

Hydrazines↗
PubMed1981

Structural changes after transmitter release at the frog neuromuscular junction.

The sequence of structural changes that occur during synaptic vesicle exocytosis was studied by quick-freezing muscles at different intervals after stimulating their nerves, in the presence of 4-aminopyridine to increase the number of transmitter quanta released by each stimulus. Vesicle openings began to appear at the active zones of the intramuscular nerves within 3-4 ms after a single stimulus. The concentration of these openings peaked at 5-6 ms, and then declined to zero 50-100 ms late. At the later times, vesicle openings tended to be larger. Left behind at the active zones, after the vesicle openings disappeared, were clusters of large intramembrane particles. The larger particles in these clusters were the same size as intramembrane particles in undischarged vesicles, and were slightly larger than the particles which form the rows delineating active zones. Because previous tracer work had shown that new vesicles do not pinch off from the plasma membrane at these early times, we concluded that the particle clusters originate from membranes of discharged vesicles which collapse into the plasmalemma after exocytosis. The rate of vesicle collapse appeared to be variable because different stages occurred simultaneously at most times after stimulation; this asynchrony was taken to indicate that the collapse of each exocytotic vesicle is slowed by previous nearby collapses. The ultimate fate of synaptic vesicle membrane after collapse appeared to be coalescence with the plasma membrane, as the clusters of particles gradually dispersed into surrounding areas during the first second after a stimulus. The membrane retrieval and recycling that reverse this exocytotic sequence have a slower onset, as has been described in previous reports.

Animals↗
PubMed1988

Cardiovascular structural changes induced by isolation-stress hypertension in the rat.

The cardiovascular structural remodelling associated with psychogenic hypertension was investigated in genetically normotensive rats subjected to isolation stress. Male Wistar rats were stressed by intermittent social isolation and compared to control rats living in groups. The stressed rats had higher systolic blood pressures than the control rats throughout the study. After 1 week of isolation, ornithine decarboxylase activity, a marker for hypertrophy, was increased in the right ventricle of the stressed rats. After 6 weeks of intermittent isolation, the myocardium of the stressed rats was hypertrophied, involving both right and left ventricles. The aorta was also hypertrophied, whereas the tail artery remained unaffected. Later, after 12 weeks of isolation, the left ventricular hypertrophy persisted whereas the right ventricle and aorta returned to normal. It seems, therefore, that social stress hypertension is accompanied by very early structural changes, which affect at least the heart and the aorta, and cannot be directly linked to the severity or duration of hypertension.

Animals↗
PubMed1989

[Structural changes of the heart in craniocerebral trauma].

A study is presented of structural changes in the myocardium due to head injuries. General histological, histochemical, histoenzymological methods and electron microscopy were used. The authors revealed a complex of dystrophic and adaptative changes in the contractile myocardium, interstitial connective tissue and blood circulatory bed. These changes depended directly on the character of the craniocerebral injury and time from the beginning of the trauma.

Brain Injuries↗
PubMed1986

[Structural changes in the sugar chains of gamma-glutamyltranspeptidase by malignant transformation].

Structures of the sugar moieties of gamma-glutamyl transpeptidases purified from the kidney and the liver of rat, mouse, and cattle were studied after being chemically released as oligosaccharides. The results indicated that both organ-specific and species-specific differences exist in the sugar chains of the enzyme. Comparative studies of sugar chains of the heavy and light subunits of the rat kidney enzyme revealed that high mannose-type sugar chains are found only in the heavy subunit. By the same analysis of the oligosaccharide fractions obtained from four isozymic forms of the rat kidney enzyme, it was found that all these enzymes contain 2 mole of neutral sugar chains but different numbers of acidic sugar chains in one molecule. Comparative studies of oligosaccharides obtained from the enzymes purified from rat AH-66 hepatoma and from normal rat liver revealed that more than 40% of the sugar chains of the hepatoma enzyme contain bisecting N-acetylglucosamine residues which are not found in those of the liver enzyme. By making use of the structural changes associated with malignant transformation, a new diagnostic method or hepatoma was developed. In principle, the method consists of affinity chromatography of the desialylated serum enzyme using an erythroagglutinating lectin agarose column.

Animals↗
PubMedDate not supplied

[The role of structural changes in T4 bacteriophage tail proteins].

Conformational changes in bacteriophage tail proteins after heating and ionic strength alteration leading to dissociation of tail sheath have been studied using protein fluorescence, differential scanning microcalorimetry and electron microscopy methods. Autonomous structural changes in tube-baseplate proteins have been revealed. They take place under the same conditions as those which release the bonds holding the sheath protein subunits to those of the tube in isolated sheathed tails. The conformational changes in the tube-baseplates are reversible similarly to the process of assembly and disassembly of the extended sheath. Morphological changes in the tube have been found at the temperature above the transition registered by protein fluorescence but not by calorimetry. This suggests that revealed spectral alterations reflect changes in quaternary structure of tail tube in particular.

Calorimetry, Differential Scanning↗