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Biomedical subjects

J Zicha

Publications and source records attributed to J Zicha.

At least 73 records · Page 4Linked to original sources
PubMed1994

Erythrocyte membrane microviscosity and blood pressure in rats with salt-induced and spontaneous hypertension.

OBJECTIVE: To study membrane viscosity in various rat strains with genetic forms of experimental hypertension. DESIGN: The relationship between blood pressure and membrane dynamics was investigated in erythrocytes from three different rat strains with experimental hypertension, namely two models of salt-induced hypertension (Sabra and Dahl rats) and Lyon hypertensive rats with spontaneous hypertension. METHODS: Membrane microviscosity was evaluated by diphenylhexatriene and trimethylamino-diphenylhexatriene fluorescence steady-state anisotropy. RESULTS: There were no significant differences among particular experimental groups in trimethylamino-diphenylhexatriene anisotropy that reflect microviscosity changes at the water-lipid interface of the external membrane leaflet. In contrast, the diphenylhexatriene anisotropy, which is related to the core membrane microviscosity, was significantly reduced in the Dahl salt-sensitive rats (irrespective of salt intake level) and in the Sabra hypertension-prone rats with developed salt hypertension. Erythrocyte membranes of Lyon hypertensive rats also had lower values of diphenylhexatriene anisotropy than the respective normotensive controls but this difference was not statistically significant. CONCLUSIONS: Systolic (and often also diastolic) blood pressure correlated negatively with the diphenylhexatriene anisotropy in each of the three strains studied, whereas the trimethylamino-diphenylhexatriene anisotropy of the erythrocyte membranes had no significant relationship to the blood pressure. Further experiments should clarify whether the observed relationship of the diphenylhexatriene anisotropy to blood pressure reflects true pathogenetic mechanisms or is a consequence of haemodynamic changes.

Animals↗
PubMed1993

Regulation of the dynamic properties of platelet plasma membrane by intracellular sodium ions.

Our previous experiments in human and rat platelets demonstrated that the absence of extracellular Na+ increased the fluorescence anisotropy of TMA-DPH (trimethylamino-diphenylhexatriene, probe preferentially incorporated into the outer leaflet of the plasma membrane). Here we investigated further the in vitro effects of Na+ ions on membrane dynamic properties. Na(+)-dependent changes were reversible and they required about 10-20 min to be induced. They were specifically located in the TMA-DPH environment because they were not observed with diphenylhexatriene (probe non-selectively incorporated into all hydrophobic domains of the cell). To evaluate the possible influence of the intracellular Na+, the effects of sodium replenishment, monensin, ouabain and thrombin on TMA-DPH anisotropy were measured. A rise in intracellular Na+ above the physiological level was associated with unchanged or slightly decreased TMA-DPH anisotropy whereas its decrease was accompanied by a pronounced rise in TMA-DPH anisotropy. Our data indicate that the changes in intracellular Na+ concentration, rather than those in extracellular Na+ concentration, are responsible for the alterations in platelet membrane fluidity probed by TMA-DPH.

Animals↗
PubMed1993

Renal renin activity is associated with alterations of the renin gene in recombinant inbred rat strains.

1. A structural alteration within the first intron of the renin gene in spontaneously hypertensive rats was demonstrated to co-segregate with blood pressure in some sets of F2 hybrids or recombinant inbred strains. There is no evidence as to whether restriction fragment length polymorphism of the renin gene is associated with any of the changes in the renin tissue level. For this reason we have determined renal renin activity in spontaneously hypertensive, Wistar-Kyoto and Brown Norway rats as well as in 22 recombinant inbred strains derived from F2 hybrids of spontaneously hypertensive and Brown Norway rats. 2. At the age of 4 months significantly lower renal renin activity was observed in spontaneously hypertensive rats than in both normotensive rat strains, Wistar-Kyoto and Brown Norway. The presence of the spontaneously hypertensive rat allele in recombinant inbred strains was associated with a substantially lower renal renin activity as compared with recombinant inbred strains bearing the Brown Norway rat allele. There was no relationship between renal renin activity and the polymorphism in either the angiotensinogen gene or the angiotensin-converting enzyme gene. 3. There was a borderline correlation between blood pressure and renal renin activity in recombinant inbred strains. Nevertheless, additional comparisons within recombinant inbred strains bearing the spontaneously hypertensive rat allele of the renin gene failed to reveal any significant relationship between blood pressure level and renal renin activity. 4. Our data suggest that the restriction fragment length polymorphism marking the renin gene of the spontaneously hypertensive rat is accompanied by an alteration in the renin-angiotensin system at the renal level.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensinogen↗
PubMed1993

Red cell ion transport abnormalities in experimental hypertension.

The original attractive hypothesis on the important role of elevated cell Na+ concentration in the pathogenesis of hypertension stimulated a search for generalized membrane defects and ion transport abnormalities in various easily accessible cells including erythrocytes. An attempt is made here to compare this hypothesis with the data on red cell ion transport alterations that were observed in experimental hypertension over the last 15 years. Several methodological (presence of extracellular Na+ in incubation media, kinetic approach to the evaluation of transport systems) and physiological problems (potassium depletion, age-dependent changes) are discussed in more detail because they can substantially modify the results obtained. Available data suggest a possible contribution of augmented Na+ leak to the development of both genetic and salt-dependent experimental hypertension. The role of alterations in the activity of the Na(+)-K+ pump or the Na(+)-K+ cotransport system still remains unclear.

Animals↗
PubMed1993

The Prague Hypertensive Rat: a new model of genetic hypertension.

Several animal models of genetic hypertension have been developed but not all of them possess a closely related control strain. Therefore, a new model based on Wistar rats is described in which both hypertensive and normotensive lines were bred from a single parental pair. Several basic data on the two lines (called the Prague Hypertensive Rat, PHR, and the Prague Normotensive Rat, PNR) are given. PNR had a longer survival compared with PHR. At the age of 7 weeks, systolic blood pressure was 161 +/- 14 mmHg in PHR males and 109 +/- 9 mmHg in PNR males. Its further increase with age was very slow in PNR but very steep in PHR. Typical left ventricular cardiac hypertrophy developed in PHR in which cardiac output was not significantly different from that of PNR but total peripheral resistance was higher. Kidney weight was also greater in PHR than in PNR. There was no difference in basic renal functions except of proteinuria which was higher in PHR than in PNR. No differences were observed in extracellular and interstitial fluid volumes whereas plasma and blood volumes were slightly but significantly greater in PHR than in PNR suggesting a shift of extracellular fluid towards the intravascular compartment. This hypertensive model the parameters of which resemble to those of human essential hypertension should be especially suitable for cross-transplantation studies.

Animals↗
PubMed1993

Red cell ouabain-resistant Na+ and K+ transport in Wistar, Brown Norway and spontaneously hypertensive rats.

Our previous studies concerning the role of furosemide-resistant cation leaks in genetic hypertension demonstrated that blood pressure of recombinant inbred strains (derived from F2 hybrids of spontaneously hypertensive and normotensive Brown Norway rats) cosegregated with inward Na+ leak (determined in saline medium) but not with Na+ efflux (measured in Mg(2+)-sucrose medium) or with Rb+ uptake (found in either medium). In the present study the alterations of particular components of ouabain-resistant (OR) Na+ and K+ (Rb+) transport in erythrocytes of spontaneously hypertensive rats (SHR) were analyzed using saline and Na(+)-free (Mg(2+)-sucrose or choline) incubation media. OR Na+ net uptake was elevated in SHR as compared to both normotensive strains--Brown Norway and Wistar rats. This was mainly due to an increased bumetanide-resistant (BR) Na+ inward leak. On the other hand, Wistar rats did not differ significantly from SHR in either OR Na+ efflux or OR Rb+ uptakes. Major augmentations of BR Na+ efflux and BR Rb+ uptake in SHR erythrocytes were seen not only in Mg(2+)-sucrose medium but also in choline medium. In both Na(+)-free media there was a considerable saturable Na+i-dependent component of BR Na+ and Rb+ fluxes which was more pronounced in SHR than in BN erythrocytes. A great caution is required for the interpretation of the data on "increased passive membrane permeability" obtained in SHR erythrocytes incubated in Na(+)-free media because of the presence of this saturable component which seems to be related to incompletely inhibited Na(+)-K+ pump.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Age-dependent changes of baroreflex efficiency in Dahl rats: effects of high salt intake.

The age-dependent changes in baroreflex control of heart rate were studied in inbred Dahl rats. At the age of 8 weeks the baroreflex slope was significantly greater in salt-resistant (R/Jr) than in salt-sensitive (S/Jr) rats fed a low-salt diet. The reverse was true in 16-week-old animals. High salt intake (8% NaCl diet for 4 weeks) suppressed baroreflex efficiency in both age groups of S/Jr animals whereas no effects occurred in R/Jr rats. Baroreflex slope was, however, significantly lower in young S/Jr rats with a severe form of salt hypertension than in adult salt-loaded S/Jr rats in which only a moderate blood pressure elevation was observed.

Aging↗
PubMed1993

[Bisoprolol in the treatment of hypertension].

Bisoprolol is an effective antihypertensive drug which reduces significantly the systolic, and diastolic blood pressure, the pulse rate in a recumbent, sitting and standing position. Recommended dosage is 10-15 mg once a day. Bisoprolol is suitable for use in hypertensive patients with associated diseases, in particular angina pectoris and impaired rhythm.

Bisoprolol↗
PubMed1993

Red cell ouabain-resistant Na+ and K+ transport in Wistar, brown Norway and spontaneously hypertensive rats.

Our previous studies concerning the role of furosemide-resistant cation leaks in genetic hypertension demonstrated that blood pressure of recombinant inbred strains (derived from F2 hybrids of spontaneously hypertensive and normotensive Brown Norway rats) cosegregated with inward Na+ leak (determined in saline medium) but not with Na+ efflux (measured in Mg(2+)-sucrose medium) or with Rb+ uptake (found in either medium). In the present study the alterations of particular components of ouabain-resistant (OR) Na+ and K+ (Rb+) transport in erythrocytes of spontaneously hypertensive rats (SHR) were analyzed using saline and Na(+)-free (Mg(2+)-sucrose or choline) incubation media. OR Na+ net uptake was elevated in SHR as compared to both normotensive strains--Brown Norway and Wistar rats. This was mainly due to an increased bumetanide-resistant (BR) Na+ inward leak. On the other hand, Wistar rats did not differ significantly from SHR in either OR Na+ efflux or OR Rb+ uptakes. Major augmentations of BR Na+ efflux and BR Rb+ uptake in SHR erythrocytes were seen not only in Mg(2+)-sucrose medium but also in choline medium. In both Na(+)-free media there was a considerable saturable Na+i-dependent component of BR Na+ and Rb+ fluxes which was more pronounced in SHR than in BN erythrocytes. A great caution is required for the interpretation of the data on "increased passive membrane permeability" obtained in SHR erythrocytes incubated in Na(+)-free media because of the presence of this saturable component which seems to be related to incompletely inhibited Na(+)-K+ pump.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Age-dependent changes of baroreflex efficiency in Dahl rats: effects of high salt intake.

The age-dependent changes in baroreflex control of heart rate were studied in inbred Dahl rats. At the age of 8 weeks the baroreflex slope was significantly greater in salt-resistant (R/Jr) than in salt-sensitive (S/Jr) rats fed a low-salt diet. The reverse was true in 16-week-old animals. High salt intake (8% NaCl diet for 4 weeks) suppressed baroreflex efficiency in both age groups of S/Jr animals whereas no effects occurred in R/Jr rats. Baroreflex slope was, however, significantly lower in young S/Jr rats with a severe form of salt hypertension than in adult salt-loaded S/Jr rats in which only a moderate blood pressure elevation was observed.

Aging↗
PubMed1993

Recombinant inbred strains in hypertension research.

It was recognized that recombinant inbred strains are a very powerful system for the study of the genetics of hypertension, linkage analysis and gene mapping. Such set of recombinant inbred strains has been developed in the cooperation of Prof V. Kren and Dr. M. Pravenec in Prague. These recombinant inbred strains were used to search for the genes of spontaneous hypertension and to test the phenotypic differences. It was found that 1) the major histocompatibility complex of the rats showed a significant association with blood pressure, 2) the restriction fragment length polymorphism in kallikrein gene family as well as renin gene cosegregated with blood pressure, 3) Na+ leak in red blood cells cosegregated with blood pressure, 4) the relative heart and kidney weights are not closely related to mean arterial pressure and 5) the platelet aggregation and blood pressure are independent traits. The results indicate the usefulness of recombinant inbred strains in the analysis of the relationship between phenotype and genotype.

Animals↗
PubMed1993

The influence of prenatal exposure to different salt diets on body and organ weights in newborn Dahl rats.

Present study tried to evaluate the influence of different diets (low- and high-salt, bicarbonate) administered during prenatal period on body and organ weights of newborn Dahl salt-sensitive (DS) and salt-resistant (DR) rats. Blood pressure of DR dams was not influenced by dietary loading but it was significantly increased by high-salt diet in DS rats. Blood pressure of all DS dams was higher when compared to the respective DR rats. There were significant negative correlations between mean arterial pressure of DS (but not DR) dams and body weight of newborns in all dietary groups. Litter sizes were comparable in all groups studied. High-salt diet increased body weight and relative heart weight of newborns of both genotypes. On the other hand, the influence of bicarbonate diet on body weight was more pronounced in DS pups whereas the effect on relative heart weight was seen only in DR newborns. The relative heart and kidney weights were significantly higher and relative liver weight significantly lower in newborns of DR dams when compared to those of DS dams irrespective of mother's diet. There was a tendency in all organs of DS newborns to contain less water in comparison with respective DR pups. It should be noted that in newborns of both genotypes bicarbonate diet lowered relative DNA content more than relative protein content. In conclusion, high-salt and bicarbonate diets exert dissimilar effects on prenatal body and organ development in Dahl rats.

Animals↗
PubMed1993

[Arterial hypertension in clinical practice].

Based on their epidemiological survey in the South Moravian region where 64,083 men and women, mean age 43.1 years, were examined, the authors submit the results of screening, prevalence, control and complications of hypertension. They draw attention to the high rate and almost 50% detection of new patients, in particular of productive age. The results indicate the high risk of arterial hypertension in the genesis of cerebrovascular and cardiovascular disease, on the inadequate control of the disease in field practice and the favourable effect on the prevalence of cerebrovascular disease when effective therapy is used, as apparent from a five-year perspective study. The authors emphasize the significant role of secondary prevention on the course, prognosis and complications of this disease of the circulation.

Adult↗
PubMed1992

Complete dissociation of DOCA-salt hypertension and red cell ion transport alterations.

Our previous study revealed major ion transport alterations that resulted in a pronounced elevation of red cell Na+ content in DOCA-salt treated homozygous vasopressin-deficient (DI) Brattleboro rats in which only a moderate increase of systolic blood pressure occurred. In contrast, no changes of red cell Na+ content were observed in heterozygous vasopressin-secreting (non-DI) Brattleboro rats with a severe DOCA-salt hypertension. Using a chronic supplementation of DI rats with an antidiuretic agonist dDAVP (1-desamino-8-D-arginine vasopressin) we did not demonstrate any significant changes of red cell ion transport in dDAVP-treated DI rats with a fully developed DOCA-salt hypertension. The absence of ion transport alterations seems to be mainly due to dDAVP-induced correction of altered K+ metabolism seen in DOCA-salt treated DI animals. It can be concluded that DOCA-salt hypertension can develop even without red cell ion transport alterations which are usually caused by cell K+ depletion.

Animals↗
PubMed1992

Red cell sodium in DOCA-salt hypertension: a Brattleboro study.

The alteration of red cell Na+ content (Na+i), its causes and the possible relationship to the development of DOCA-salt hypertension were studied in Brattleboro rats. A pronounced hypertension developed in heterozygous (non-DI) animals that synthesize vasopressin (VP) although no substantial Na+i elevation was observed in their erythrocytes. In contrast, Na+i rose progressively in red cells of homozygous VP-deficient (DI) rats in which only marginal increase of systolic blood pressure was found after six weeks of DOCA-salt regimen. DOCA-salt treatment of non-DI rats did not cause major alterations in ouabain-resistant (OR) net Na+ uptake or ouabain-sensitive (OS) net Na+ extrusion but moderately increased furosemide-sensitive (FS) Rb+ uptake. The same treatment of DI rats doubled Na+i by an increased OR net Na+ uptake (due to a major elevation in both Na(+)-K+ cotransport and Na+ leak). Consequently, OS net Na+ extrusion was augmented in red cells of these animals. This was accompanied by an about threefold elevated FS Rb+ uptake. It can be concluded that a) the alterations of OR and/or OS Na+ or K+ transport observed in erythrocytes of Brattleboro DI rats are not essential for the development of severe DOCA-salt hypertension, b) red cell ion transport abnormalities revealed in DOCA-salt treated DI rats might be rather ascribed to cell potassium depletion, and c) increased inward Na(+)-K+ cotransport and Na+ leak causes red cell Na+i elevation that stimulates Na(+)-K+ pump activity.

Animals↗
PubMed1992

The hypertriglyceridemic rat as a genetic model of hypertension and diabetes.

Hypertriglyceridemia was demonstrated in untreated hypertensive patients as well as in animals with genetic and experimental hypertension. The main purpose of the present study was to evaluate the possibility to use the hereditary hypertriglyceridemic (HTG) nonobese rats in hypertensive research. Direct measurement of blood pressure demonstrated significantly higher systolic, diastolic and mean arterial pressures in HTG rats in comparison with control Wistar rats. There was significant positive correlation between blood pressure and plasma triglyceride concentration (r = 0.585, n = 40, p less than 0.001). In addition, there were significantly increased plasma norepinephrine and epinephrine concentrations in HTG rats, suggesting that the stimulation of sympathetic nervous system could be one of the pathogenetic mechanisms involved in the increase of blood pressure of HTG rats.

Animals↗