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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Red blood cell Na+ content as well as ouabain-resistant Na+ and Rb+ (K+) transport (susceptible or resistant to inhibition by loop diuretics) were determined in spontaneously hypertensive rats (SHR) and normotensive Brown Norway (BN) rats the erythrocytes of which were incubated in either saline or Mg(2+)-sucrose medium. Elevated ouabain-resistant Na+ net uptake contrasted with slightly decreased red blood cell Na+ content in SHR compared with BN rats. Acceleration of furosemide- and bumetanide-sensitive Na+ fluxes contributed to enhanced ouabain-resistant Na+ influx into SHR erythrocytes in saline medium, whereas higher furosemide- or bumetanide-resistant Na+ efflux caused greater ouabain-resistant Na+ efflux in Mg(2+)-sucrose medium. Furosemide- and bumetanide-resistant Rb+ leaks were augmented in SHR erythrocytes. The association of the disclosed ion transport alterations with blood pressure was examined in 20 recombinant inbred strains derived from F2 SHR x BN hybrids. Ouabain-resistant Na+ uptake as well as furosemide- and bumetanide-resistant Na+ inward leaks (but not red blood cell Na+ content or furosemide- and bumetanide-sensitive Na+ net uptake) cosegregated with systolic and pulse pressures but not diastolic pressure of the recombinant inbred strains. In contrast, neither ouabain-resistant Na+ efflux nor any component of ouabain-resistant Rb+ uptake correlated positively with blood pressure of the recombinant inbred strains. Increased ouabain-resistant Na+ influx was compensated for by accelerated ouabain-sensitive Na+ extrusion because red blood cell Na+ content was not elevated in the hypertensive strains. Thus, high cell Na+ turnover rates might be related to genetic hypertension if an altered Na+ inward leak would be less effectively compensated for in tissues involved in cardiovascular regulation.
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PMID:Association of red blood cell sodium leak with blood pressure in recombinant inbred strains. 139 93

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)
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PMID:Red cell ouabain-resistant Na+ and K+ transport in Wistar, Brown Norway and spontaneously hypertensive rats. 818 Jan 50

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)
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PMID:Red cell ouabain-resistant Na+ and K+ transport in Wistar, brown Norway and spontaneously hypertensive rats. 821 51

This review deals with the largest set of rat recombinant inbred (RI) strains and summarizes past and recent accomplishments with this platform for genetic mapping and analyses of divergent and complex traits. This strain, derived by crossing the spontaneously hypertensive rat, SHR/Ola, with a Brown Norway congenic, BN-Lx, carrying polydactyly-luxate syndrome, is referred to as HXB/BXH. The RI strain set has been used for linkage and association studies to identify quantitative trait loci for numerous cardiovascular phenotypes, including arterial pressure, stress-elicited heart rate, and pressor response, and metabolic traits, including insulin resistance, dyslipidemia and glucose handling, and left ventricular hypertrophy. The strain's utility has been enhanced with development of a new framework marker-based map and strain distribution patterns of polymorphic markers. Quantitative trait loci for behavioral traits mapped include loci for startle motor response and habituation, anxiety and locomotion traits associated with elevated plus maze, and conditioned taste aversion. The polydactyly-luxate syndrome Lx mutation has allowed the study of alleles important to limb development and malformation phenotypes as well as teratogens. The RI strains have guided development of numerous congenic strains to test locus assignments and to study the effect of genetic background. Although these strains were originally developed to aid in studies of rat genetic hypertension and morphogenetic abnormalities, this rodent platform has been shown to be equally powerful for a wide spectrum of traits and endophenotypes. These strains provide a ready and available vehicle for many physiological and pharmacological studies.
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PMID:Genetic Models in Applied Physiology. HXB/BXH rat recombinant inbred strain platform: a newly enhanced tool for cardiovascular, behavioral, and developmental genetics and genomics. 1273 93