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PubMed2001

Modulation of recombinant human prostate-specific antigen: activation by Hofmeister salts and inhibition by azapeptides. Appendix: thermodynamic interpretation of the activation by concentrated salts.

Prostate specific antigen (PSA, also known as human kallikrein 3) is an important diagnostic indicator of prostatic disease. PSA exhibits low protease activity (>10(4)-fold less than chymotrypsin) under the usual in vitro assay conditions. In addition, PSA does not react readily with prototypical serine protease inactivators. We expressed human PSA (rh-PSA) in Escherichia coli and have demonstrated that rh-PSA has properties similar to those of native PSA isolated from human seminal fluid. Both PSA and rh-PSA are >10(3)-fold more active in the presence of 1.3 M Na(2)SO(4). This activation is anion-dependent, following the Hofmeister series when normality is considered: SO(4)(2)(-) approximately citrate > Ac(-) > Cl(-) > Br(-) > I(-). The nature of the cation has little effect on salt activation. The rate of inactivation of rh-PSA by DFP is 30-fold faster in the presence of 0.9 M Na(2)SO(4), and the rate of inactivation by Suc-Ala-Ala-Pro-Phe-CK is >20-fold faster under these conditions. Azapeptides containing Phe or Tyr at position P(1) also inactivate rh-PSA in the presence of high salt concentrations. These compounds represent the first described inhibitors designed to utilize the substrate binding subsites of PSA. CD spectroscopy demonstrates that the conformation of rh-PSA changes in the presence of high salt concentrations. Analytical ultracentifugation and dynamic light scattering indicate that PSA remains monomeric under high-salt conditions. Interestingly, human prostatic fluid contains as much as 150 micro mol citrate/g wet weight, which suggests that salt concentrations may regulate PSA activity in vivo.

Base Sequence↗
PubMed2002

Synthesis and structural studies of 1,1'-bis-amino-functionalized ferrocenes, ferrocene salts, and ferrocenium salts.

Having isolated and characterized a series of sodium cyclopentadienide salts, we have synthesized a number of 1,1'-bis-amino-functionalized ferrocenes, 1,1'-bis-amino-functionalized ferrocene salts, and 1,1'-bis-amino-functionalized ferrocenium salts. Among these are the first crystallographically characterized examples of cyclopentadienyl units containing (piperidin-N-ylethyl)- and (pyrid-2-ylmethyl)cyclopentadienyl side chains. In the cases of some of the ferrocenes, ferrocene salts, and ferrocenium salts, there are some interesting structural features in the solid state. These include C-H...N and C-H...pi cloud interactions as well as N-H...O and N-H...F hydrogen bonds.

Journal Article↗
PubMed2002

Absorption of calcium fumarate salts is equivalent to other calcium salts when measured in the rat model.

Calcium absorption from fumarate salts (calcium fumarate and calcium malate fumarate), which have recently been considered for use as sources for food and beverage enrichment, was compared to that from calcium citrate malate, calcium citrate, and calcium carbonate. Salts were instrinsically labeled with 45Ca and orally administered to Sprague-Dawley rats. Fractional absorption of calcium from each salt was determined using the femur uptake model. Fractional absorption from the five salts (0.30-0.27) was not significantly different (p > 0.05). Thus, when measured in the rat model, calcium from calcium fumarate and calcium malate fumarate is absorbed equally well as compared to other salts, which are common calcium sources in many foods, beverages, and supplements.

Absorption↗
PubMed1985

Renomedullary phospholipases in salt-sensitive and salt-resistant Dahl rats.

Renomedullary prostaglandin synthesis is lower in salt-sensitive (S) Dahl rats than in age-matched salt-resistant (R) rats on either 0.6% or 8.0% NaCl. The possible role of substrate availability to the cyclooxygenase in determining these differences was examined. S and R rats were started on diets with variable salt content (0.6%, 4.0% or 8.0% NaCl) at five weeks and were sacrified at either 11 or 16 weeks of age for comparisons of renomedullary phospholipase A1 and A2 activities (EC 3.1.1.4. and 3.1.1.32) and arachidonate incorporation into the lipids of renal medulla. Both phospholipase activities were higher in R rats at the two ages examined and for all levels of salt intake. These differences could not be accounted for by variable amounts of endogenous phospholipid substrate. High salt intake did not influence the in vitro A2 deacylating activities per mg protein. Arachidonate incorporation into renomedullary triglycerides remained constant with age in both strains while phospholipid labeling declined with age in S rats only so that, at 16 weeks of age, S rats had significantly lower incorporation into membrane phospholipids. This age-related decline in phospholipid labeling in S rats was prevented by 4.0% NaCl. These results suggest that low renomedullary phospholipase activities in S rats may restrict the release of substrate for prostaglandin synthesis and may also be related to reduced rates of fatty acid incorporation into membrane phospholipids.

Age Factors↗
PubMed1985

Exchangeable sodium in DOC-salt and post-DOC-salt hypertension in rats.

Eighteen male Sprague-Dawley rats were fed a sodium-free diet and given NaCl (154 mmol/l) labelled with 22Na (37 Bq/l [1 microCi/l]) to drink. Following equilibration, each had a unilateral nephrectomy; 10 days later the animals started a series of 10 injections of deoxycorticosterone (12.5 mg twice-weekly for 5 weeks). Thereafter the animals were split into two groups, one to continue with DOC injections and diet as previously (DOC-salt), the other to stop DOC injections and continue a sodium-free diet and labelled saline of lower concentration (89 mmol/l) (post-DOC). During the period of DOC injections to both groups, blood pressure and exchangeable sodium rose significantly and were significantly correlated. In the post-DOC group, hypertension persisted and was not significantly different from that in the DOC-salt group. However, in the post-DOC-salt group, exchangeable sodium fell to levels similar to those found in uninephrectomized control animals of similar age which had never been given DOC or a high salt intake and had never been hypertensive. Thus an expanded sodium space does not contribute to maintenance of hypertension in the post-DOC-salt model.

Animals↗
PubMed2000

Marked reduction of mortality in salt-loaded Dahl salt-sensitive rats by the new, selective endothelin ETA receptor antagonist, J-105859.

OBJECTIVE: To examine the chronic effects of a newly synthesized, potent and selective endothelin (ET) ETA receptor antagonist, J-1 05859, on mortality in salt-loaded Dahl salt-sensitive (DS) rats and to confirm the potential of this compound as an ETA antagonist METHODS: Vehicle and J-105859 were administered to salt-loaded DS rats for 12 weeks. Throughout the experimental period, blood pressure was measured continuously using a telemetry system and the survival rate was determined. The surviving animals were subsequently sacrificed and autopsy was performed. Binding and functional assays were also carried out to characterize J-1 05859. RESULTS: The Ki values of J-1 05859 for cloned human ETA and ETB were 0.025 and 48 nmol/l, respectively. J-105859 inhibited ET-1-induced contractions in rabbit iliac artery (pA2 = 10.08) and BQ-3020 (ETB agonist)-induced contractions in pulmonary artery (pA2 = 7.63). The pressor response to intravenous (i.v.) ET-1 (0.5 nmol/kg) was significantly inhibited by J-1 05859 at a dose of 0.03 mg/kg i.v. Chronic treatment with J-1 05859 [0.1 and 1 mg/kg per day orally (p.o.)] from the prehypertensive stage decreased the mortality of salt-loaded DS rats and markedly inhibited the development of brain lesions. The survival rates in the control and J-1 05859 (0.1 and 1 mg/kg per day) groups were 34, 80 and 100%, respectively. Development of hypertension was markedly inhibited at a dose of 1 mg/kg per day. CONCLUSION: J-105859 is a selective, potent, orally active ETA-selective antagonist ETA antagonists may reduce morbidity as well as mortality in salt-sensitive hypertension.

Alkanes↗
PubMed1988

Cardiac hypertrophy and salt status in chronic myocardial infarction in the rat: effects of enalapril versus salt restriction.

The effects of salt restriction and the ACE inhibitor enalapril were compared in a model of chronic myocardial infarction in the rat. Total exchangeable sodium was measured by an isotopic dilution technique to quantitate the effects of the low salt diet and ACE inhibitor on body sodium and extracellular fluid. Rats with infarction developed a marked increase in cardiac weight (4.29 +/- 0.18 mg/g body weight) compared with control rats (3.64 +/- 0.08 mg/g, p less than 0.01). There was hypertrophy of both left and right ventricles. Salt restricted rats with infarction developed identical cardiomegaly (4.30 +/- 0.11 mg/g), although total exchangeable body sodium fell by 10% (p less than 0.001). In contrast, rats with infarction receiving enalapril developed significantly less cardiomegaly (3.97 +/- 0.10 mg/g) while body sodium remained unchanged. Rats with infarction had a significant increase in lung weight which was not changed by salt restriction but which was abolished by enalapril. These results suggest that salt restriction does not prevent the progression of cardiomegaly in chronic left heart failure. In contrast our results confirm the ability of ACE inhibitors to prevent progressive cardiomegaly and left heart failure without affecting long-term changes in sodium balance.

Animals↗
PubMed2003

Influence of two doses of irbesartan on non-dipper circadian blood pressure rhythm in salt-sensitive black hypertensives under high salt diet.

The authors examined whether the blockage of angiotensin II receptors by irbesartan (IRB) can reverse the "non-dipper" circadian rhythm of blood pressure (BP) to a "dipper" pattern in black salt-sensitive hypertensive patients submitted to a high-sodium loading. Twelve black salt-sensitive hypertensive patients (seven men; age, 35-58 years) on a high-sodium diet (300 mmol Na+ per day) were followed for 8 weeks. A placebo was given during the first 2 weeks, followed by 2 weeks on IRB 150 mg/d, 2 weeks on placebo, and 2 weeks on IRB 300 mg/d. On the last day of placebo, IRB 150 mg/d, and IRB 300 mg/d treatments, 24-hour BP and urinary 24-hour excretion of Na+ and potassium were measured. On placebo, ambulatory mean arterial pressure (MAP) was 112 mm Hg+/-2 (24 h), 112 mm Hg+/-2 (daytime), and 111 mm Hg+/-2 (nighttime), showing a clear circadian non-dipper profile. Versus placebo, IRB 150 mg/d reduced MAP by 4.2 mm Hg+/-1.1 (24 h), 2.6 mm Hg+/-0.8 (daytime) and 6.0 mm Hg+/-1.3 (nighttime; P<0.05 vs. placebo) and IRB 300 mg/d reduced MAP by 7.8 mm Hg+/-1.4 (24 h), 3.9 mm Hg+/-1.1 (daytime), and 11.8 mm Hg+/-2.1 mm Hg (all P<0.02 vs. placebo); nighttime/daytime MAP decrease was 0.7+/-0.8% on placebo, 3.5+/-2.1% on IRB 150 mg/d, and 7.0+/-1.2% on IRB 300 mg/d (P<0.02 for trend). Compared with placebo, IRB significantly increased serum potassium and plasma renin activity and reduced fractional excretion of potassium and plasma aldosterone levels in a dose-dependent manner. Body weight and urinary sodium excretion did not change throughout the study. It was concluded that the angiotensin receptor blocker IRB can reverse the BP non-dipper profile in salt-sensitive hypertensive patients on a high-salt diet, restoring nocturnal BP decline by a predominantly dose-dependent reduction of nighttime BP. Although the increment of potassium balance and reduction of aldosterone may account for this effect, it occurs independently of increased natriuresis. It is speculated that blunting of nighttime BP decrease in black salt-sensitive hypertensive patients may be related to a deficient suppression of the renin-angiotensin system during the night.

Adult↗
PubMed2001

The salt stress-inducible protein kinase gene, Esi47, from the salt-tolerant wheatgrass Lophopyrum elongatum is involved in plant hormone signaling.

Protein kinases play a central role in signal transduction in all organisms and to study signal transduction in response to salt stress we have identified and characterized a gene encoding a protein kinase that is induced by salt stress and abscisic acid (ABA) in the salt-tolerant wild wheatgrass Lophopyrum elongatum (Host) A. Love. The product of the early salt stress-induced gene, Esi47, was found to belong to the "novel Arabidopsis protein kinase" group of plant serine/threonine protein kinases. Transient gene expression assays in barley aleurone tissue showed Esi47 to suppress the gibberellin induction of the barley low-pI alpha-amylase gene promoter, thus providing evidence for the role of this protein kinase gene in plant hormone signaling. Esi47 contains a small upstream open reading frame in the 5'-untranslated region of its transcript that is implicated in mediating the repression of the basal level of the gene expression and in regulating the ABA inducibility of the gene, as shown in the transient gene expression assay in maize callus. Three Arabidopsis homologs of Esi47 were identified, and different members of this clade of genes showed differential patterns of regulation by salt stress and ABA in Arabidopsis roots and leaves. At least one of the Arabidopsis homologs contains a small open reading frame in its 5'-untranslated region, indicating that the unusual regulatory mechanism identified in Esi47 may be widely conserved.

5' Untranslated Regions↗
PubMed1972

Salt responses of enzymes from species differing in salt tolerance.

Enzymes which are affected by the addition of inorganic salts during in vitro assay were extracted from salt-sensitive Phaseolus vulgaris, salt-tolerant Atriplex spongiosa, and Salicornia australis and tested for sensitivity to NaCl. In each case malate dehydrogenase, aspartate transaminase, glucose 6-phosphate dehydrogenase, and isocitrate dehydrogenase showed NaCl responses similar to those found for commercially available crystalline enzymes from other organisms. Enzymes extracted from plants grown in saline cultures showed no important changes in specific activity or salt sensitivity. Interaction of pH optima and NaCl concentrations suggests that enzymes may differ in the way they respond to salt treatment.

Journal Article↗
PubMed2002

The Arabidopsis salt overly sensitive 4 mutants uncover a critical role for vitamin B6 in plant salt tolerance.

Salt stress is a major environmental factor influencing plant growth and development. To identify salt tolerance determinants, a genetic screen for salt overly sensitive (sos) mutants was performed in Arabidopsis. We present here the characterization of sos4 mutants and the positional cloning of the SOS4 gene. sos4 mutant plants are hypersensitive to Na(+), K(+), and Li(+) ions. Under NaCl stress, sos4 plants accumulate more Na(+) and retain less K(+) compared with wild-type plants. SOS4 encodes a pyridoxal kinase that is involved in the biosynthesis of pyridoxal-5-phosphate, an active form of vitamin B6. The expression of SOS4 cDNAs complements an Escherichia coli mutant defective in pyridoxal kinase. Supplementation of pyridoxine but not pyridoxal in the growth medium can partially rescue the sos4 defect in salt tolerance. SOS4 is expressed ubiquitously in all plant tissues. As a result of alternative splicing, two transcripts are derived from the SOS4 gene, the relative abundance of which is modulated by development and environmental stresses. Besides being essential cofactors for numerous enzymes, as shown by pharmacological studies in animal cells, pyridoxal-5-phosphate and its derivatives are also ligands for P2X receptor ion channels. Our results demonstrate that pyridoxal kinase is a novel salt tolerance determinant important for the regulation of Na(+) and K(+) homeostasis in plants. We propose that pyridoxal-5-phosphate regulates Na(+) and K(+) homeostasis by modulating the activities of ion transporters.

Adaptation, Physiological↗
PubMed1983

Recent changes in salt use and stroke mortality in England and Wales. Any help for the salt-hypertension debate?

This analysis attempts to fill the gap in the epidemiological evidence about the relation between dietary salt and hypertension. Changes in the purchase of salt in England and Wales are compared with changes in mortality from cerebrovascular disease (1958-78). Stroke mortality, a major sequel of hypertension, has declined in this period. Consumer purchases of salt have decreased also, as suggested by the National Food Survey. While these trends are consistent with the salt-hypertension hypothesis, the picture is confused by an increase in meals eaten outside the home, by the consumption of more processed food, and by a higher prevalence of refrigerators. Other events, such as medical treatment of hypertension or changes in the case fatality rate, could have contributed to the decline in stroke mortality. This secular trend analysis, using available data, does not clarify the salt-hypertension debate.

Aged↗
PubMed2003

Enhancement of intrarenal angiotensinogen in Dahl salt-sensitive rats on high salt diet.

This study was performed to examine whether there is an inappropriate regulation of intrarenal angiotensinogen in Dahl-salt sensitive rats (DS) fed a high salt diet (HS). Dahl salt-resistant rats (DR) and DS were maintained on HS (8% NaCl) or low salt diet (LS, 0.3% NaCl) for 4 weeks. Systolic blood pressure (SBP), measured by tail-cuff plethysmography, was unaltered in DR (DR+HS, 127+/-3 mm Hg, n=5; DR+LS, 126+/-3, n=5); however, SBP was significantly increased in DS+HS (208+/-7, n=9) compared with DS+LS (134+/-2, n=5). HS suppressed plasma renin activity in both strains (0.7+/-0.2 ng of angiotensin I/mL per hour in DS+HS, 3.1+/-0.5 in DS+LS, 0.8+/-0.2 in DR+HS, 5.1+/-0.7 in DR+LS). Plasma angiotensinogen levels, measured by Western blot analysis, were also suppressed by HS in both strains (36 919+/-2170 integrated densitometric unit in DS+HS, 53 028+/-2752 in DS+LS, 44 722+/-1721 in DR+HS, 55782+/-3785 in DR+LS). However, kidney angiotensinogen levels were significantly increased in DS+HS (75 850+/-4171, integrated densitometric unit) compared with DS+LS (47 232+/-3470), DR+HS (44 748+/-8236), and DR+LS (42 504+/-4052). Urinary excretion of angiotensinogen, measured by radioimmunoassay of angiotensin I after incubation with excess renin, had a similar profile. Urinary excretion of angiotensinogen was significantly increased in DS+HS (2958+/-531 pmol/d) compared with DS+LS (56+/-4), DR+HS (31+/-12), and DR+LS (21+/-7). These data indicate that intrarenal angiotensinogen is enhanced in DS+HS, which is reflected by the increased urinary excretion of angiotensinogen. The results suggest that DS on HS have an inappropriate augmentation of intrarenal angiotensinogen, which may contribute to impaired sodium excretion during a high salt diet and the development of hypertension in this strain.

Angiotensinogen↗
PubMed2003

Dietary salt regulates renal SGK1 abundance: relevance to salt sensitivity in the Dahl rat.

Serum and glucocorticoid-induced kinase 1 (SGK1) activates the epithelial sodium channel (eNaC) in tubules. We examined renal SGK1 abundance in salt-adaptation and in salt-sensitive hypertension. Sprague-Dawley and Dahl salt-sensitive rats were placed on either 8% or 0.3% NaCl diets for 10 days. Plasma aldosterone levels were approximately 2.5-fold greater on 0.3% versus 8% NaCl diets in both rat strains. Both serum and glucocorticoid-induced kinase 1 transcript and protein abundance were less (P<0.01) in Sprague-Dawley rats and greater (P<0.01) in Dahl salt-sensitive rats on 8% versus 0.3% NaCl diets. The cDNA sequences of serum and glucocorticoid-induced kinase 1 in both strains of rat were the same. The present results provide evidence that the abundance of serum and glucocorticoid-induced kinase 1 in rat kidney may play a role in salt adaptation and the pathogenesis of hypertension and suggests that aldosterone is not the primary inducer of SGK1 in the Sprague-Dawley rat.

Administration, Oral↗
PubMed1996

Plasma and renal prorenin/renin, renin mRNA, and blood pressure in Dahl salt-sensitive and salt-resistant rats.

We measured plasma prorenin and renin levels, renal renin mRNA, renal anti-renin and anti-prorenin-prosequence immunoreactivity, and blood pressure in maturing Brookhaven Dahl salt-sensitive (Dahl S) and salt-resistant (Dahl R) rats during 14 days of low (0%), medium (0.4%), or high 4%) NaCl diets. Blood pressure was higher in Dahl S rats and did not increase with high NaCl. Seven-week-old Dahl R rats had twofold and sixfold higher levels of plasma prorenin and renal prosequence immunoreactivity, respectively, which by 9 weeks were the same as in Dahl S rats. The anti-renin antiserum, BR1-5, was found to detect prorenin better than renin; Dahl S rats had suppressed renal anti-renin immunoreactivity relative to Dahl-R rats. Dahl R rats were unresponsive to high NaCl, whereas in Dahl S rats, plasma renin and renal prosequence immunoreactivity fell by 90% (P < .01), renal anti-renin immunoreactivity and renal renin MRNA fell by 35% (P < .05 for both), and plasma prorenin fell by 30% (P = NS). NaCl depletion increased prorenin/renin parameters similarly in both strains. There were direct relationships among all of the prorenin/renin parameters. Between low and high salt diets in Dahl S rats, plasma renin increased 20-fold, plasma total renin (renin plus prorenin) and renal renin mRNA both increased threefold, and plasma prorenin increased twofold. The results indicate that under steady-state conditions, plasma and renal renin/prorenin parameters change concordantly and that plasma total renin (renin plus prorenin) reflects changes in renal renin mRNA. The lower blood pressure of Dahl R rats is associated with later maturation-related declines in plasma and renal prorenin. Suppression of plasma renin may delay the salt-induced blood pressure rise in Dahl S rats. Finally, the renin system and blood pressure of Dahl R rats have remarkable disregard for a high salt diet.

Animals↗
PubMed2002

Note: storage practices, salt intake and iodine content of salt consumed in rural households of Haryana State, North India.

A survey of 180 rural families from different zones of Haryana State was carried out to know the type and intake of salt used and the domestic storage practices followed by rural households using a questionnaire method. Salt samples from rural households were analyzed for their iodine content. Results indicated that most of the people in rural Haryana consume powdered salt and stored it in airtight containers. Daily intake per person ranged from 9.91 to 11.42 g. In the wet zone a higher percentage of families consume iodized salt. Analysis of iodine in salt samples showed that of samples from three zones, 39% contained no iodine; with 9% < 15 ppm; 14% 15-29 ppm and 37% > or = 30 ppm.

Climate↗
PubMed2004

Studies on tellurium-containing heterocycles. Part 20. Reactions of 2-benzoselenopyrylium salts and 2-benzotelluropyrylium salts with nucleophiles: formation of 1-functionalized 1H-isoselenochromenes and 1H-isotellurochromenes.

The reactions of the 2-benzoselenopyrylium (1A) and 2-benzotelluropyrylium cations (1B) with a variety of nucleophiles have been investigated. LiAlH(4), sodium alkoxide (NaOMe, NaOi-Pr and NaOt-Bu), diethylamine, n-butylamine and acetone reacted with 1 to give the 1H-isochromenes (2) and the corresponding 1-substituted products (4-9) under mild conditions in almost good to high yields. The 1-alkyl(phenyl)isoselenochromenes (10-13) and 1-benzylisochromenes (18A, 18B), which were produced by the reaction of the salts 1 with Grignard reagents, were converted to the corresponding 1,3-disubstituted 2-benzopyrylium salts (14-17, 19) by treatment with triphenylcarbenium tetrafluoroborate (Ph(3)C(+) BF(4)(-)), respectively. The 1-benzylselenopyrylium salts (19A) and 1-benzyltelluropyrylium salts (19B) exist in the solvent as an equilibrium mixture of the salts (19) and the corresponding (Z)-benzylidene compounds (20).

Acids, Heterocyclic↗
PubMed2005

Renoprotective effect of pravastatin in salt-loaded Dahl salt-sensitive rats.

The pathophysiological features of nephrosclerosis may be analogous to those of atherosclerosis, which is intimately related to lipid metabolism. Thus, we examined whether a lipid-lowering agent, pravastatin, would ameliorate renal damage in hypertensive model animals. Salt-loaded Dahl salt-sensitive (S) rats were given pravastatin (2 mg/ml in drinking water) for 5 weeks. Pravastatin decreased systolic blood pressure. Although pravastatin did not influence the serum total, high-density, or low-density lipoprotein cholesterol, serum triglycerides were decreased. Pravastatin decreased urinary protein excretion and ameliorated histopathological damage in salt-loaded Dahl S rats. Increased urinary excretion of 8-iso-prostagaldin F2alpha and 8-hydroxy-2'-deoxyguanosine and renal superoxide overproduction and decreased reduced glutathione in the renal parenchyma were ameliorated with pravastatin in Dahl S rats fed a high salt diet. Therefore, pravastatin inhibited the progression of renal injury in salt-loaded Dahl S rats, through its antioxidant as well as its depressor effects.

Animals↗