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PubMed2000

Effects of dehydration on plasma osmolality, thirst-related behavior, and plasma and brain angiotensin concentrations in Couch's spadefoot toad, Scaphiopus couchii.

Under dehydrating conditions, many terrestrial vertebrates species exhibit increases in plasma osmolality and their drinking behavior. Under some circumstances, this behavioral change is accompanied by changes in plasma and central angiotensin concentrations, and it has been proposed that these changes in angiotensin levels induce the thirst-related behaviors. In response to dehydration, the spadefoot toad, Scaphiopus couchii, exhibits thirst-related behavior in the form of cutaneous drinking. This behavior has been termed water absorption response (WR) behavior. Spadefoot toads live in harsh desert environments and are subject annually to dehydrating conditions that may induce thirst-related behavior. We tested the hypothesis that an increase in WR behavior is associated with both an increase in plasma osmolality and an increase in plasma and brain angiotensin concentrations. First, we determined the degree of dehydration that was necessary to initiate WR behavior. Animals dehydrated to 85% of their standard bladder-empty weight via deprivation of water exhibited WR behavior more frequently than control toads left in home containers with water available. Next, using the same dehydration methods, we determined the plasma osmolality and sodium concentrations of dehydrated toads. Toads dehydrated to 85% standard weight also had a significant increase in plasma osmolality, but exhibited no overall change in plasma sodium concentrations, indicating that while an overall increase in plasma osmolality appears to be associated with WR behavior in S. couchii, changes in sodium concentrations alone are not sufficient to induce the behavior. Finally, plasma and brain angiotensin concentrations were measured in control toads and toads dehydrated to 85% standard weight. Plasma and brain angiotensin concentrations did not increase in dehydrated toads, indicating that dehydration-induced WR behavior that is associated with changes in plasma osmolality may not be induced by changes in endogenous angiotensin concentrations in S. couchii.

Angiotensin II↗
PubMed2002

Study of bradykinin metabolism in human and rat plasma by liquid chromatography with inductively coupled plasma mass spectrometry and orthogonal acceleration time-of-flight mass spectrometry.

Bradykinin is a small peptide that acts mainly as a hormone by activating specific receptors that confer protection against the development of hypertension. The efficacy of bradykinin is influenced by the activities of various kininases present in plasma and blood. In this study, both human and rat plasma were incubated with a labelled form of bradykinin (at 4 and 12.5 microM), that will be referred to as bromobradykinin. The metabolic fate of bromobradykinin was monitored by liquid chromatography coupled to an orthogonal acceleration time-of-flight mass spectrometer (oaTOF). Quantification measurements of the bromine-containing metabolites were performed on-line, via flow splitting, by inductively coupled plasma mass spectrometry (ICPMS). The data obtained highlighted that the mechanism(s) of bradykinin metabolism in human and rat plasma are different, with the metabolism of bradykinin in rat plasma being much more aggressive than that observed in human plasma. In addition to the known bradykinin metabolites, e.g. [1,5], [1,7] from ACE, [1,8] from carboxypeptidase and [2,9] from aminopeptidase activity, we have identified the presence of new bradykinin metabolites in both human and rat plasma. These have been identified as fragment [5], the amino acid phenylalanine, which was present in both the human and rat plasma and the fragments [2,8] and [4,8] in rat plasma. To our knowledge it is the first time that these fragments have been recorded in human and rat plasma. The occurrence of these new fragments provides evidence for the presence of potentially new enzymes and mechanisms of bradykinin metabolism. The method described here provides a powerful technique for monitoring the activity of the many kininases involved in bradykinin metabolism such as ACE (angiotensin I converting enzyme), carboxypeptidase N and aminopeptidase P. In addition, this procedure could be used as a screening assay for selecting and monitoring the actions of inhibitors of the enzymes implicated in bradykinin metabolism directly in plasma or serum.

Animals↗
PubMed2003

Hyperphagia modifies FA profiles of plasma phospholipids, plasma FFA, and adipose tissue TAG.

Hyperphagia was achieved by continuous intracerebroventricular infusion of a melanocortin receptor antagonist (HS024; Neosystem, Strasbourg, France) in rats. The effects of hyperphagia on FA composition and concentration of plasma phospholipids (PL), plasma FFA, and adipose tissue TAG were studied in rats for 8 d [short-term hyperphagia (STH); n = 8], or 28 d [long-term hyperphagia (LTH); n = 9]. The control rats were treated with artificial cerebrospinal fluid for 8 d (n = 8) or 28 d (n = 10). The rats were fed the same regular diet. In STH rats the plasma PL and fasting plasma FFA contained higher concentrations of saturated FA (SFA) and monounsaturated FA (MUFA), and plasma FFA contained lower n-6 PUFA than in the control rats. In LTH rats the plasma PL contained higher concentrations of SFA, MUFA, and n-3 PUFA and higher proportions of 16:1n-7 and 18:1n-9 at the expense of 18:2n-6 than in the control rats. In LTH rats the abundant dietary intake of 18:2n-6 did not enrich 18:2n-6 of the plasma PL or adipose tissue TAG. In LTH rats the fasting plasma FFA contained more than twofold higher concentrations of SFA and MUFA, and higher proportions of 16:1n-7 and 18:1n-9 at the expense of 18:2n-6 than in the control rats. This animal obesity model shows that LTH affects the FA composition and concentration of plasma PL, plasma FFA, and adipose tissue TAG, a result consistent with changes associated with increased risk of various diseases in humans. These results also demonstrate that LTH alters the FA composition of plasma PL and adipose tissue TAG in a way that does not reflect the FA composition of dietary fat.

Adipose Tissue↗
PubMed1984

Characterization of fibronectin from fetal human plasma in comparison with adult plasma fibronectin.

Fibronectin was purified from fetal human plasma and characterized in comparison with fibronectin from adult human plasma. Fetal plasma fibronectin had an amino-acid composition, immunological properties, and cell-attachment-promoting activity similar to those of adult plasma fibronectin. However, fetal plasma fibronectin was shown to have a distinct carbohydrate composition which is characterized by the presence of fucose. To ascertain the differences in the carbohydrate moiety, 14C-labeled glycopeptides were prepared and sequentially analyzed with columns of immobilized concanavalin A and lentil lectin. Glycopeptides from fetal plasma fibronectin contained a population of glycopeptides which bound to both lectin gels. Almost all of the glycopeptides in this population lost their ability to bind to lentil lectin upon fucosidase digestion, indicating that fetal plasma fibronectin possesses a substantial amount of fucosylated biantennary glycans. In contrast, glycopeptides from adult plasma fibronectin practically lacked such glycopeptides. Another difference observed was that fetal plasma fibronectin had a larger amount of concanavalin A-unbound glycopeptides than did adult plasma fibronectin. These results indicate the presence of age-related variation in glycosylation of human plasma fibronectin.

Adult↗
PubMed2003

Developmental and diel changes in plasma thyroxine and plasma and ocular melatonin in the larval and juvenile bullfrog, Rana catesbeiana.

Diel variation in plasma thyroxine (T(4)), and plasma and ocular melatonin was studied in Rana catesbeiana tadpoles and postmetamorphic froglets on 12:12 and 6:18 light/dark (LD) regimens. A progressive rise in plasma T(4) initiates metamorphosis while melatonin can modulate metamorphic progress. Changes in the phase of the rhythms of these two hormones during development might influence the hormonal regulation of metamorphosis. The hormones studied exhibited LD cycle-specific diel fluctuations except in froglet plasma T(4) and all hormones at prometamorphosis on 6L:18D. On 12L:12D, plasma T(4) and ocular melatonin peaked during the scotophase at prometamorphosis and early climax, whereas the plasma melatonin acrophase shifted from the light to the dark at climax. A nocturnal peak of plasma melatonin closely correlated with the onset and offset of dark appeared in the froglet, while the peak of ocular melatonin shifted to the light. Compared to 12L:12D, the peaks of the diel fluctuations on 6L:18D occurred later than on 12L:12D in synchrony with an earlier onset, and increase in length, of the scotophase. The phase of the hormone rhythms changed during metamorphosis in such a way that the peaks of melatonin had a different relationship to the T(4) peaks as development proceeded. On both LD cycles, the 24-h mean of plasma T(4) rose at climax and fell in the froglet whereas plasma melatonin decreased at climax and then rose to a high level in the froglet. After only minor changes during metamorphosis, froglet ocular melatonin levels decreased on 12L:12D and increased on 6L:18D. The findings indicate that the hormonal flux during metamorphosis has circadian aspects, which might explain variations in the response to exogenous hormone treatment at different times of the day and LD cycle-specific timing of development. A fall in plasma melatonin at climax appears to be as much a part of the hormonal changes of metamorphosis as a rise in plasma T(4).

Animals↗
PubMed1980

Plasma catecholamines and plasma renin activity at birth and during the first days of life.

1. Plasma noradrenaline and adrenaline concentrations and plasma renin activity were measured in 21 mothers at delivery and in their babies at birth (umbilical cord blood) and on days 1 and 5 of extrauterine life. 2. At birth plasma renin activity was significantly higher in the newborn than in mothers. Plasma renin activity increased further, but not significantly, on day 1 of life and significantly decreased on day 5. On day 5, 10 min head-up tilting caused no change in plasma renin activity. 3. Plasma noradrenaline in the newborn was higher than in mothers at birth and significantly decreased thereafter. Plasma adrenaline levels at birth were similar in the newborn and their mothers and significantly lower in the newborn in subsequent days. Tilting caused no increase in either plasma adrenaline or noradrenaline levels. 4. No correlation was found between plasma noradrenaline and adrenaline levels and plasma renin activity, or between noradrenaline, adrenaline or plasma renin activity and blood pressure.

Blood Pressure↗
PubMed1994

Plasma proteins and lymphocyte phenotypes in long-term plasma donors.

BACKGROUND: The possible effects of long-term plasma donation remain unknown, but it is important to investigate them so that donor safety is ensured. The purpose of this study was to determine if long-term plasma donation alters plasma proteins or lymphocyte phenotypes. STUDY DESIGN AND METHODS: Two groups of long-term plasma donors, source plasma donors (n = 20) and Rh immune globulin plasma donors (n = 26), were compared with whole blood donors (n = 29) and nondonor controls (n = 30). Blood samples were obtained prior to donation. Serum protein, albumin, globulin, and immunoglobulin levels were determined. In an assay using whole blood, lymphocyte phenotypes were characterized with a panel of single- and dual-labeled monoclonal antibodies and subsequent analysis by flow cytometry. RESULTS: As compared to the nondonor controls and/or whole blood donors, the mean values for serum protein, globulin, and IgG levels were lower in both plasma donor groups, with a significant negative correlation between donation frequency and serum protein values for the source plasma donors. Albumin levels were within normal ranges for both groups of plasma donors. No significant differences existed among the donor groups in total white cell counts, the percentage or absolute number of lymphocytes, T (CD3) cells, or helper T (CD4) cells. However, there were increased percentages of B (CD19) cells and decreased percentages of suppressor T (CD8+/CD11b+) cells and natural killer cells in both groups of plasma donors as compared to nondonor controls. CONCLUSION: Many plasma donors have low levels of serum protein, globulin, and IgG. In addition, they have increased percentages of B cells and decreased percentages of suppressor T and natural killer cells. The clinical significance of these findings warrants further investigation.

Adult↗
PubMed1979

Initiation of plasma prorenin activation by Hageman factor-dependent conversion of plasma prekallikrein to kallikrein.

Plasma prorenin is an inactive form of renin (EC 3.4.99.19) that can be converted to active renin in acid-treated plasma by an endogenous serine protease that is active at alkaline pH (alkaline phase activation). To identify this enzyme we first tested the ability of Hageman factor fragments, plasma kallikrein (EC 3.4.21.8), and plasmin (EC 3.4.21.7) to activate prorenin in acid-treated plasma. All three enzymes initiated prorenin activation; 50% activation was achieved with Hageman factor fragments at 1 microgram/ml, plasma kallikrein at 2-4 microgram/ml, or plasmin at 5-10 microgram/ml. We then showed that the alkaline phase of acid activation occurred normally in plasminogen-free plasma but was almost completely absent in plasmas deficient in either Hageman factor or prekallikrein; alkaline phase activation was restored to these latter plasmas when equal parts were mixed together. Therefore, both Hageman factor and prekallikrein were required for alkaline phase activation to occur. We then found that, although plasma kallikrein could activate prorenin in plasma deficient in either Hageman factor or prekallikrein, Hageman factor fragments were unable to activate prorenin in prekallikrein-deficient plasma. These studies demonstrate that alkaline phase prorenin activation is initiated by Hageman factor-dependent conversion of prekallikrein to kallikrein which, in turn, leads to activation of prorenin. In this fashion, we have revealed a possible link between the coagulation-kinin pathway and the renin-angiotensin system.

Angiotensin I↗
PubMed1997

Correspondence of salivary and plasma concentrations of atrazine in rats under variable salivary flow rate and plasma concentration.

The stability of the saliva/plasma (S/P) concentration ratio of atrazine was determined under varying conditions of salivary flow rate and plasma concentration of atrazine in Sprague-Dawley rats. In the salivary flow study, whole saliva samples were collected at different salivary flow rates while the plasma concentration of atrazine was maintained at a steady-state level of approximately 150 micrograms/L. In the plasma level study, whole saliva samples were collected at two steady-state plasma concentrations of atrazine (50 and 250 micrograms/L), while salivary flow rate was maintained at a relatively constant level. In both studies, atrazine concentrations in whole saliva and arterial plasma demonstrated a consistent relationship, but salivary concentrations were always lower than those of arterial plasma. Linear regression analysis demonstrated that the S/P concentration ratio of atrazine was not significantly different for salivary flow rates ranging from 23 to 92 microL/min/kg body weight, and did not vary for atrazine plasma concentrations between 30 and 433 micrograms/L. The S/P concentration ratio of atrazine was relatively constant throughout each experimental period (0.68 +/- 0.1 and 0.70 +/- 0.11 for salivary flow and plasma level studies, respectively) and did not differ significantly between rats. When data from both studies were pooled, salivary concentrations were highly correlated with plasma concentrations (r2 = .94). It is concluded that under these experimental conditions, the stability of the S/P concentration ratio of atrazine is not affected by variations in salivary flow rate or atrazine plasma concentrations. The results from this study support the conclusion that atrazine salivary concentrations can be used to predict plasma levels of atrazine in rats.

Analysis of Variance↗
PubMed1987

Total plasma concentrations, red blood cell concentrations, and radioreceptor assay values compared with unbound plasma concentrations of thioridazine and thioridazine metabolites in psychiatric patients.

Neuroleptic drug concentrations at the receptor sites are likely to be reflected more closely by the unbound than by the total plasma concentrations. The aim of this study was to establish whether or not the unbound plasma concentrations of thioridazine and its main nonconjugated metabolites show a stronger correlation to the red blood cell (RBC) concentration than to the total plasma concentration of the drug. The total and unbound plasma concentrations and the RBC concentrations of thioridazine and its metabolites were therefore determined in thioridazine-treated patients. "Calculated unbound concentration values" were derived from the determined total concentrations of the drug, the concentrations of drug-binding proteins, and previously determined kappa values. Since the RBC concentrations showed the best correlation to the unbound plasma values, they may be a more accurate tool than the total plasma concentrations for monitoring thioridazine treatment. The determined unbound plasma concentrations were better correlated to the calculated unbound concentrations than to the total plasma concentrations. The total plasma concentrations, but neither the unbound plasma nor the RBC concentrations, were significantly correlated to the concentrations of the drug-binding protein alpha 1-acid glycoprotein. Radioreceptor assay values were strongly correlated to the weighted sum of the total and unbound plasma concentrations of thioridazine and its metabolites.

Adolescent↗
PubMed1994

Patients with severe von Willebrand disease are insensitive to the releasing effect of DDAVP: evidence that the DDAVP-induced increase in plasma factor VIII is not secondary to the increase in plasma von Willebrand factor.

It is generally held that factor VIII (FVIII) does not increase in the plasma of severe von Willebrand disease (vWD) patients treated with DDAVP because they lack von Willebrand factor (vWF), which is the plasma carrier for FVIII. To test this hypothesis, FVIII plasma levels were monitored in severe vWD patients treated with DDAVP after normalization of vWF plasma levels with infusions of cryoprecipitate. Each of four severe vWD patients underwent four different treatments at intervals of at least 15 d: (1) cryoprecipitate plus DDAVP; (2) cryoprecipitate plus saline; (3) cryoprecipitate plus recombinant FVIII (rFVIII); (4) saline plus rFVIII. Cryoprecipitate increased the plasma levels of FVIII and vWF. The infusions of saline or DDAVP after cryoprecipitate did not further increase FVIII and vWF plasma levels and had no effect on the plasma levels of tissue plasminogen activator (tPA), which are raised by DDAVP in normal subjects and in patients with vWD of other types. The infusion of rFVIII further increased by 182 +/- 32 U/dl (mean +/- SEM) the plasma levels attained after cryoprecipitate, which disappeared from the circulation with a half-life of 11.95 +/- 0.86 h. In contrast, the infusion of rFVIII after saline increased by only 107 +/- 18 U/dl the plasma levels of FVIII, which disappeared from the circulation with a half-life of 2.68 +/- 0.14 h, indicating that the vWF infused with cryoprecipitate is able to bind additional FVIII. These studies indicate that DDAVP does not increase the plasma levels of FVIII in patients with severe vWD even after normalization of plasma vWF. The possibility is discussed that severe vWD patients may be insensitive to the releasing effect of DDAVP.

Deamino Arginine Vasopressin↗
PubMed1997

High plasma levels of apo(a) fragments in Caucasians and African-Americans with end-stage renal disease: implications for plasma Lp(a) assay.

Apolipoprotein(a) [apo(a)] is a plasma glycoprotein that is highly polymorphic in size due to differences in the number of a tandemly arrayed cysteine-rich repeat called kringle (K)4 at its N-terminus. Most plasma apo(a) is covalently attached to apolipoprotein B-100 and circulates as part of lipoprotein(a) [Lp(a)]. A fraction of apo(a) circulates free of lipoproteins. Almost all of the free apo(a) consists of fragments containing variable numbers of K4 repeats derived from the N-terminal region. Previously we provided evidence suggesting that the apo(a) fragments present in human plasma are the source of the apo(a) fragments in human urine. If this were the case, it would be expected that plasma levels of fragments would be higher in subjects with end-stage renal disease (ESRD). In this paper we quantified the levels of apo(a) fragments and plasma Lp(a) in 26 Caucasian and 26 African-American subjects with ESRD and 52 healthy subjects matched for race, sex and the size of the apo(a) isoforms. The plasma levels of apo(a) fragments and Lp(a) were both higher in the ESRD subjects. In addition, the ratio of apo(a) fragments to total immunodetectable apo(a) was increased in ESRD. To determine how much the increase in the apo(a) fragments contributed to the increase in plasma Lp(a) in ESRD, the plasma Lp(a) levels were measured employing two different anti-apo(a) enzyme-linked immunoabsorption assays (ELISA). One assay detected both free and bound apo(a), whereas the other assay detected only bound apo(a). Although the plasma levels of apo(a) in the ESRD subjects tended to be higher using the assay that detected both fragments and full-length apo(a), the increase was modest. Thus, although a greater proportion of the apo(a) in ESRD plasma circulates as fragments, most of the elevation in plasma levels of Lp(a) associated with renal insufficiency is due to an increase in intact Lp(a).

Adolescent↗
PubMed2005

Plasma asymmetric dimethylarginine (ADMA) concentration is independently associated with carotid intima-media thickness and plasma soluble vascular cell adhesion molecule-1 (sVCAM-1) concentration in patients with mild-to-moderate renal failure.

BACKGROUND: Patients with renal insufficiency have an increased risk of cardiovascular disease that is not fully explained by the presence of known cardiovascular risk factors. In patients with end-stage renal disease, increased serum concentration of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), has been linked to excess cardiovascular morbidity. We investigated, in patients with mild-to-moderate renal failure, the relationship between plasma ADMA and three surrogate markers of atherosclerosis that have been shown to have prognostic value, namely carotid intima-media thickness (IMT), plasma soluble vascular cell adhesion molecule-1 (sVCAM-1), and plasma C-reactive protein (CRP). METHODS: We used baseline data of an ongoing randomized trial in which the effects of oxidative stress-lowering treatment on vascular function and structure are studied in patients with chronic nondiabetic renal failure without clinical evidence of atherosclerosis (GFR 15 to 70 mL/min/per 1.73 m(2) according to the Cockcroft-Gault equation; ATIC study). RESULTS: Data from 93 patients were used. Creatinine clearance was inversely related to plasma ADMA concentration (standardized beta after adjustment = -0.342, P = 0.023). Plasma ADMA was strongly related to carotid IMT in univariate (beta = 0.459, P < 0.0001) and multivariate analysis (beta= 0.444, P < 0.0001). Plasma ADMA was also significantly related with plasma soluble vascular cell adhesion molecule-1 (sVCAM-1) in univariate (beta = 0.260, P = 0.010) and multivariate (beta = 0.242, P = 0.022) analysis. Plasma ADMA was not significantly related to C-reactive protein (beta = -0.134, P = 0.204). CONCLUSION: In patients with mild-to-moderate renal failure, renal function is inversely associated with plasma ADMA, which, in turn, is positively associated with carotid IMT and plasma sVCAM-1 concentration. Increased plasma ADMA may be a link between renal function and cardiovascular disease in patients with mild-to-moderate renal failure.

Adult↗
PubMed1987

Antithrombin III (ATIII) activity in plasmas from normal and diseased horses, and in normal canine, bovine and human plasmas.

Plasma Antithrombin III (ATIII) activity was quantitated in 24 clinically normal Standardbred/Thoroughbred horses using a clotting time technique. ATIII activity ranged from 80 to 106% of the pooled reference standard plasma, with a mean of 94%. Horses presenting with impaction or spasmotic colic (n=17) had normal plasma ATIII activity, while 15 horses presenting with acute diarrhea/colitis had significantly lower plasma ATIII activity with a mean of only 74% of the reference plasma. Seven horses presenting with liver disease had significantly higher plasma ATIII activity with a range of 127 to 177% of the pooled reference plasma. Fifty-seven equine plasmas were retested using a rapid chromogenic substrate technique for quantitating plasma ATIII activity. A good correlation (r =+0.83) existed between clotting time and chromogenic determinations of ATIII. Pooled normal canine, human and bovine plasmas had only 65, 62 and 79%, respectively, of the ATIII activity of the equine reference plasma.

Journal Article↗
PubMed1962

Influence of guinea pig plasma factors on phagocytosis of Pasteurella pestis. II. Plasma from plague-infected guinea pigs.

Stanziale, W. G. (Fort Detrick, Frederick, Md.) and J. D. White. Influence of guinea pig plasma factors on phagocytosis of Pasteurella pestis. II. Plasma from plague-infected guinea pigs. J. Bacteriol. 83:182-186. 1962.-The phagocytosis enhancing property of normal guinea pig plasma was altered during experimental plague infection. The most notable changes occurred in the plasma from afebrile, moribund animals and from those convalescing from acute infection. The plasma of the moribund guinea pigs, which was obtained 7 to 8 days after exposure to Pasteurella pestis, inhibited phagocytosis to a considerable degree. Plasma from convalescent guinea pigs enhanced phagocytosis to a higher degree than the plasma of normal animals. In contrast, plasma from recovered guinea pigs in which cultural or serological evidence of infection was not demonstrated enhanced phagocytosis to a degree equivalent to that of normal plasma. Plasma taken from guinea pigs during the febrile phase of plague infection enhanced phagocytosis to a lower degree than did normal plasma.

Animals↗
PubMed1976

The effect of plasma calcium on plasma ADH levels in anephric patients.

Ten anephric patients were studied before and during hemodialysis. The extracorporeal circuit was primed with 5% albumin in 0.9% sodium chloride. Ultrafiltration volume removed by the hemodialyzer was replaced continuously. Modifications of a standard chronic renal failure dialysate were used to minimize changes in plasma urea while varying plasma sodium and calcium in opposite directions. Plasma ionized calcium concentrations in two patients confirmed other studies demonstrating a correlation between plasma total calcium and ionized calcium under these conditions. Plasma ADH determined by bioassay did not correlate with plasma osmolality, plasma sodium concentration, plasma potassium concentration, blood pressure, or pulse rate. The change in plasma ADH during dialysis was significantly correlated only with the change in plasma calcium (r = 0.47, p less than 0.05). The data support the hypothesis that plasma calcium plays a role in the regulation of ADH release in man, independent of the renin-aldosterone system.

Adult↗
PubMed1993

Increased production rates of LDL are common in individuals with low plasma levels of HDL cholesterol, independent of plasma triglyceride concentrations.

Reduced plasma levels of high density lipoprotein (HDL) cholesterol are associated with increased risk for coronary heart disease. Although plasma HDL levels are, in general, inversely related to plasma triglyceride (TG) concentrations, a small proportion of individuals with low HDL cholesterol concentrations have normal plasma TG levels. We wished to determine whether subjects with low plasma levels of HDL cholesterol could be characterized by common abnormalities of lipoprotein metabolism independent of plasma TGs. Therefore, we studied the metabolism of low density lipoprotein (LDL) apolipoprotein B (apo B) and HDL apolipoprotein A-I (apo A-I) in subjects with low plasma HDL cholesterol concentrations with or without hypertriglyceridemia. Nine subjects with low plasma HDL cholesterol levels and normal levels of plasma TGs and LDL cholesterol were studied. Autologous 131I-LDL and 125I-HDL were injected intravenously, and blood samples were collected for 2 weeks. LDL apo B and HDL apo A-I levels were measured by specific radioimmunoassays. Fractional catabolic rates (FCRs, pools per day) and production rates (PRs, milligrams/kilogram.day) for each apolipoprotein were determined. The results were compared with those obtained previously in nine subjects with low plasma HDL cholesterol levels and hypertriglyceridemia and in seven normal subjects. The normal subjects had an HDL apo A-I FCR (mean +/- SD) of 0.21 +/- 0.04. Despite large differences in plasma TG levels, the HDL apo A-I FCRs were similar in the low-HDL, normal-TG group (0.30 +/- 0.09) and the low-HDL, high-TG group (0.33 +/- 0.10), although only the latter value was significantly increased versus control subjects (p < 0.03). Increased apo A-I FCRs were associated with reduced HDL apo A-I levels in both groups of patients. Apo A-I PRs were similar in all groups. In contrast, LDL apo B PR was increased approximately 50% in the low-HDL, normal-TG group (19.3 +/- 6.6; p < 0.01) compared with normal subjects (12.5 +/- 2.6). There was a strong trend toward a greater LDL apo B PR in the low-HDL, high-TG group (17.6 +/- 4.5; p = 0.06 versus normal subjects) as well. LDL apo B FCRs were similar in all three groups. LDL apo B concentrations were also increased in the group with low HDL cholesterol and normal TG levels. Both groups with low HDL cholesterol levels had cholesterol-depleted LDL and HDL particles.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1973

Modulation of plasma aldosterone concentration by plasma potassium in anephric man in the absence of a change in potassium balance.

In studies on seven anephric patients, glucose and insulin administration before hemodialysis produced a significant reduction in plasma potassium concentration (mean reduction = 1.3, 1.7, and 1.4 meq/liter at 60, 120, and 180 min, respectively) which was accompanied by a significant and sustained reduction in plasma aldosterone concentration. There was a significant correlation between plasma aldosterone and plasma potassium concentration (r = +0.74, P < 0.001) and between changes in the concentration of plasma aldosterone occurring in individual patients and the corresponding changes in plasma potassium concentration (r = +0.52, P < 0.01). There was no significant change in plasma sodium concentration, and plasma corticoid concentration, which was monitored as an index of ACTH elaboration, was reduced at 60 min but increased subsequently as symptoms attributable to hypoglycemia were observed. These studies demonstrate that plasma aldosterone concentration can be modulated acutely by transitory changes in plasma potassium concentration without a change in potassium balance. The effect of glucose and insulin administration on intracellular potassium in the adrenal cortex is uncertain, and although increased net movement of potassium into cells is the presumptive mechanism of the reduction in plasma potassium concentration, whether the potassium content of the adrenal cortex may have increased or decreased or remained essentially unchanged, cannot be inferred from our data.

Aldosterone↗