PubMed Health⌕ Search

Biomedical subjects

J Díez

Publications and source records attributed to J Díez.

At least 91 records · Page 5Linked to original sources
PubMed1995

Increased serum concentrations of procollagen peptides in essential hypertension. Relation to cardiac alterations.

BACKGROUND: The serum concentrations of two procollagen-derived peptides, procollagen type III amino terminal peptide (PIIIP) and procollagen type I carboxy terminal peptide (PIP), have been proposed as useful markers of the tissue synthesis of collagen type III and type I, respectively. Therefore, this study was designed to evaluate fibrogenic activity in patients with essential hypertension by measuring serum PIIIP and PIP. Furthermore, since hypertensive heart disease is characterized by myocardial accumulation of collagen type III and type I, a second aim of the study was to assess whether some relation exists between the serum concentrations of PIIIP and PIP and several parameters of left ventricular anatomy and function in hypertensive patients. METHODS AND RESULTS: The study was performed in 50 patients with never-treated essential hypertension and in 30 normotensive control subjects. Measurements were repeated in 43 hypertensive patients after 6 months of treatment with the angiotensin-converting enzyme inhibitor lisinopril. The serum concentrations of PIIIP and PIP were measured by specific radioimmunoassay. Two-dimensional, targeted M-mode and Doppler ultrasound recordings were obtained in every subject to determine several parameters of the left ventricle anatomy and function. Ambulatory ECG monitoring was performed in each patient, and the recorded ventricular arrhythmias were categorized according to Lown-Wolf classification. Baseline serum PIIIP and PIP were increased (P < .001) in hypertensive patients as compared with normotensive subjects. An inverse correlation was found between serum PIIIP and the ratio between maximal early transmitral flow velocity and maximal late transmitral flow velocity measured during diastole (r = .3786, P < .01) in the group of hypertensive patients. Serum PIP was correlated directly with the left ventricular mass index (r = .3277, P < .05) in the group of hypertensive patients. Serum PIP concentrations increased in parallel with the increase in the grade of ventricular arrhythmias in the group of hypertensive patients. Treated patients attained normalization in blood pressure, amelioration of diastolic filling, regression of left ventricular mass index, and a diminution in the number of daily ventricular extrasystoles. In addition, serum PIIIP and PIP concentrations decreased significantly (P < .001) to normal values in patients treated with lisinopril. CONCLUSIONS: These findings suggest that tissue synthesis of collagen type III and type I is abnormally increased in essential hypertension and can be normalized by treatment with lisinopril. On the other hand, our results suggest that serum PIIIP and PIP are related to several anatomic and functional alterations of the hypertensive left ventricle. Serum procollagen peptide measurements may therefore provide indirect diagnostic information on the myocardial fibrosis associated with arterial hypertension.

Collagen↗
PubMed1995

Angiotensin converting enzyme inhibition prevents polyploidization of cardiomyocytes in spontaneously hypertensive rats with left ventricular hypertrophy.

Polyploidization of cardiomyocyte nuclei is a physiological phenomenon that increases in pathological conditions such as myocardial hypertrophy. The purpose of this study was to evaluate the potential benefit of the angiotensin converting enzyme (ACE) inhibitor quinapril in reversing the polyploidization of cardiomyocyte nuclei in spontaneously hypertensive rats (SHR) with established left ventricular hypertrophy (LVH). Sixteen week-old male SHR were treated with oral quinapril (average dose 10 mg/kg per day) for 20 weeks. Sixteen- and 36-week-old untreated SHR and 16- and 36-week-old normotensive Wistar-Kyoto (WKY) rats were used as controls. Nuclear polyploidization was determined by DNA flow cytometry of frozen tissues from the left ventricle, at least 20,000 nuclei being measured in each sample. The rates of tetraploidy in the 16- and 36-week-old SHR groups were 2.8 per cent (range 2.16-3 per cent) and 5.4 per cent (range 4.9-5.9 per cent), respectively. Treated SHR had a similar rate of DNA tetraploidy to the 16- and 36-week-old WKY rat groups: 1.8 per cent (range 1.5-2.3 per cent), 1.55 per cent (range 1.5-1.6 per cent), and 1.5 per cent (range 1.4-1.6 per cent), respectively. The differences in the percentage of tetraploid cardiomyocytes between the SHR untreated groups and the SHR treated group were statistically significant (P < 0.05). Regression of LVH and normalization of blood pressure were observed in treated rats. These results indicate that DNA tetraploidy in the myocardium of SHR increases with hypertrophy and decreases on quinapril treatment. It is suggested that ACE inhibition modifies nuclear processes involved in myocyte growth in arterial hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Association of increased erythrocyte Na+/H+ exchanger with renal Na+ retention in patients with essential hypertension.

The goal of this study was to investigate the activity of the Na+/H+ exchanger in erythrocytes of patients with essential hypertension and its relation with urinary Na+ excretion. The study was performed in cells from 27 untreated hypertensive patients and 30 normotensive controls with similar age and sex distribution. All subjects were studied after 4 days on a controlled Na+ diet (145 mmol/day). The activity of the Na+/H+ exchanger was determined by acidifying cell pH and measuring the initial rate of the net Na(+)-dependent H+ efflux. The activity of the Na+/H+ exchanger was higher in hypertensive patients than in controls (301 +/- 45 v 162 +/- 23 mmol/L cells/h, mean +/- SEM; P < .01). With the upper limit of the normotensive population as a cut-off point (385 mmol/L cells/h), a subgroup of 12 hypertensive patients had an abnormally high activity of Na+/H+ exchanger. Compared with controls and with patients with normal exchanger activity, patients with increased exchanger activity were characterized by lower net (P < .01) and fractional (P < .05) Na+ excretion. The accumulative Na+ balance was higher (P < .01) in hypertensive patients with increased activity of the exchanger (39.90 +/- 3.47 mmol) than in the remaining hypertensive patients (0.59 +/- 6.96 mmol) or in the normotensive population (-5.71 +/- 6.12 mmol). After analyzing the relationship of renin activity with Na+ excretion it was observed that renin activity was inappropriately low in 9 (75%) patients with increased exchanger, in 6 (40%) patients with normal exchanger, and in 6 (20%) normotensives, these differences being significant (P<.01).

Adult↗
PubMed1995

Quinapril decreases myocardial accumulation of extracellular matrix components in spontaneously hypertensive rats.

In genetic and acquired hypertension, a structural remodeling of the nonmyocyte compartment of myocardium, including the accumulation of fibrillar collagen and other components of the extracellular matrix (ECM) within the interstitium, represents a determinant of pathologic hypertrophy that leads to ventricular dysfunction. Therefore, to evaluate the potential benefit of the angiotensin converting enzyme (ACE) inhibitor quinapril in reversing the interstitial remodeling in spontaneously hypertensive rats (SHR) with established left ventricular hypertrophy (LVH), we treated 16-week-old male SHR with oral quinapril (average dose, 10 mg/kg body weight/day) for 20 weeks. Interstitial fibrosis was determined morphometrically using an automatic image analyzer. The amount of collagen was evaluated by measuring myocardial hydroxyproline concentration. Myocardial deposition of collagen molecules (types I, III, and IV) and other ECM components (fibronectin, laminin) was analyzed by immunohistochemical techniques using specific monoclonal antibodies. The activity of ACE was measured in left ventricular tissue by a fluorometric assay. In quinapril-treated SHR compared with 36-week-old untreated SHR and age- and sex-matched Wistar-Kyoto (WKY) controls, we found 1) a lesser degree of LVH and a lesser level of blood pressure, 2) a lesser degree of interstitial fibrosis, represented by less interstitial collagen volume fraction (5.73 +/- 0.45% v 3.42 +/- 0.28%, P < .05; WKY, 3.44 +/- 0.66%), 3) a lower hydroxyproline concentration (1.09 +/- 0.05 mumol/L/g dry weight/100 g body weight to 0.81 +/- 0.05 mumol/L/g dry weight/100 g body weight, P < .05; WKY, 0.96 +/- 0.06 mumol/L/g dry weight/100 g body weight), 4) a lesser presence of collagen fibers, and 5) a lesser presence of collagen IV, fibronectin, and laminin.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Calcium channel blockers and renal dysfunction in arterial hypertension.

Beside effective systemic blood pressure control, calcium channel blockers exert several effects on glomerular haemodynamics (namely, preglomerular vasodilatation at the early stage of the hypertensive process) and on cellular mechanisms of glomerular sclerosis (namely, inhibition of mesangial mechanisms of growth) that may provide a renal protective effect in patients with essential hypertension and, in turn, may prevent or attenuate the development of nephrosclerosis (Table 3). However, up to now, there have been relatively few attempts to corroborate this assumption in clinical practice. Furthermore, more clinical studies have been conducted with the dihydropiridine class of calcium channel blockers. Thus, prospective, long-term ongoing studies will help to delineate the long-range consequences of the renal actions of the different class of calcium channel blockers in essential hypertension.

Calcium Channel Blockers↗
PubMed1995

Are mast cells involved in hypertensive heart disease?

OBJECTIVE: To evaluate the potential relationship of mast cells with myocardial fibrosis in the cardiac ventricles of spontaneously hypertensive rats (SHR). DESIGN: Experiments were performed on hearts from 36-week-old SHR with established left ventricular hypertrophy (n = 12) and from 36-week-old normotensive Wistar-Kyoto (WKY) rats (n = 12). Furthermore, to evaluate whether antihypertensive treatment with the angiotensin converting enzyme inhibitor quinapril interferes with the potential relationship between mast cells and fibrosis in SHR, we treated 16-week-old SHR (n = 12) with oral quinapril (10 mg/kg body weight per day) for 20 weeks. METHODS: Mast cells were counted in 25 high-power fields. Toluidine blue-stained sections and avidin staining were used to detect mast cells. The extent of myocardial fibrosis was analysed in samples stained with Masson's trichrome. The amount of collagen was evaluated morphometrically, using an automatic image analyser, and biochemically, using myocardial hydroxyproline concentration. RESULTS: In the left ventricle of untreated SHR compared with age- and sex-matched normotensive WKY rats we found more extensive interstitial and perivascular fibrosis, an increased collagen volume fraction, an increased hydroxyproline concentration and an increased number of mast cells. Similar but less intense abnormalities were observed in the right ventricles of untreated SHR compared with the left ventricles of the same rats. In the left ventricles of quinapril-treated SHR compared with those of untreated SHR we found a marked decrease in fibrosis, a lower collagen volume fraction, a lower hydroxyproline concentration and fewer mast cells. Treatment with quinapril was also accompanied by normalization in the myocardial structure of the right ventricles of SHR. A positive correlation was found between the density of mast cells and the collagen volume fraction in the left ventricles of all of the rats. CONCLUSIONS: The present findings suggest that mast cells can play a part in the development of the myocardial fibrosis that occurs in the cardiac ventricles with hypertensive cardiac hypertrophy. In addition, the present results suggest that the ability of quinapril to interfere with mast cells might be involved in its cardioreparative properties.

Animals↗
PubMed1995

Insulin-like growth factor binding proteins in arterial hypertension: relationship to left ventricular hypertrophy.

OBJECTIVE: It was reported previously that circulating insulin-like growth factor I levels are abnormally elevated in patients with essential hypertension and left ventricular hypertrophy. Tissue availability of the factor depends on the distribution of the circulating bound factor between its high- and low-molecular mass binding proteins, only the latter being able to cross the endothelium. The aim of this study was to investigate whether the presence of the different serum binding proteins is altered in patients with essential hypertension and left ventricular hypertrophy. DESIGN: The study was performed in 30 never-treated patients with essential hypertension and 30 age- and sex-matched normotensive subjects. Patients were separated into two groups according to the presence or the absence of echocardiographically determined left ventricular hypertrophy. METHODS: Plasma insulin-like growth factor I levels were determined by specific radioimmunoassay. The different molecular forms of its serum binding proteins were analysed by Western blotting using [125I]-labelled insulin-like growth factor I. A densitometric scanning of the blots was performed to analyse the quantitative relationships between the different forms of binding proteins. RESULTS: Insulin-like growth factor I levels were significantly higher in the hypertensive patients with than in the hypertensive patients without left ventricular hypertrophy or in the normotensive subjects. Compared with the normotensive subjects, both hypertensive patients subgroups exhibited increased high-molecular mass binding protein type 3 and decreased low-molecular mass binding proteins types 1 and 2. However, changes in the binding proteins were more marked in the hypertensive patients without than in the hypertensive patients with left ventricular hypertrophy. Accordingly, the ratio of low- to high-molecular mass binding proteins (an index of insulin-like growth factor I bioavailability) was higher in the hypertensive patients with than in the hypertensive patients without left ventricular hypertrophy. CONCLUSIONS: These results show that the distribution of the molecular forms of serum insulin-like growth factor binding proteins is altered in patients with essential hypertension, independently of insulin-like growth factor I levels. This suggests that regulation of the binding proteins is abnormal in essential hypertension. Whether the tissue availability of circulating insulin-like growth factor I is higher in hypertensive patients with than in hypertensive patients without left ventricular hypertrophy merits further investigation.

Adult↗
PubMed1994

Treatment with lisinopril normalizes serum concentrations of procollagen type III amino-terminal peptide in patients with essential hypertension.

Procollagen type III amino-terminal peptide (PIIIP) is cleaved off procollagen type III during the biosynthesis of type III collagen. Thus, to assess the synthesis of collagen type III in essential hypertension, we determined the serum concentrations of PIIIP in 24 patients with never-treated essential hypertension and in 30 normotensive controls. In addition, serum concentrations of PIIIP were measured in 15 patients after receiving lisinopril during 6 months. Serum PIIIP was higher in hypertensives than controls (11.20 +/- 0.76 v 8.47 +/- 0.77 ng/mL, mean +/- SEM, P < .01). A direct correlation was found between serum PIIIP and plasma renin activity (r = 0.54, P < .01) in the group of hypertensives. In addition, serum PIIIP was correlated inversely with maximal early transmitral flow velocity measured during diastole by Doppler echocardiography (r = -0.74, P < .001) in the group of hypertensive patients. The serum PIIIP levels decreased significantly in patients treated with lisinopril (11.76 +/- 0.84 v 8.47 +/- 0.66 ng/mL, P < .01). A significant increase of plasma renin activity and a significant decrease of plasma aldosterone was observed in these patients after treatment with lisinopril. These results suggest that increased collagen type III synthesis is present in patients with essential hypertension. Abnormal synthesis of collagen type III in essential hypertension may be related to the activity of circulating renin-angiotensin-aldosterone system. Whether an excessive synthesis of myocardial collagen type III is responsible for increased serum PIIIP present in essential hypertension deserves further investigation.

Adult↗
PubMed1994

Insulin-like growth factor-1 and cardiac mass in essential hypertension: comparative effects of captopril, lisinopril and quinapril.

BACKGROUND: Preliminary studies have shown that patients with essential hypertension and left ventricular hypertrophy have an excess of circulating insulin-like growth factor-1 (IGF-1). In addition, an association has been found between the decrease in IGF-1 after antihypertensive treatment and regression of left ventricular hypertrophy. OBJECTIVES: To determine whether the effect of angiotensin converting enzyme (ACE) inhibitors on left ventricular hypertrophy in patients with essential hypertension is related to ACE inhibitor effects on IGF-1 levels. PATIENTS AND METHODS: The relationship between echocardiographically determined left ventricular hypertrophy and plasma IGF-1 levels was investigated in 87 patients with essential hypertension before and after 6 months of randomly allocated treatment with captopril (n = 30), lisinopril (n = 37) or quinapril (n = 20). The control group consisted of 30 age- and sex-matched normotensive subjects without left ventricular hypertrophy. RESULTS: Baseline IGF-1 levels were higher in hypertensive patients than in normotensive controls (280 +/- 21 versus 240 +/- 15 ng/ml, means +/- SEM, P < 0.02). IGF-1 levels were higher in hypertensive patients with left ventricular hypertrophy (n = 25, 316 +/- 41 ng/ml) than in those without left ventricular hypertrophy (n = 62, 242 +/- 16 ng/ml, P < 0.05). There was a direct correlation between baseline IGF-1 and left ventricular mass in the hypertensive patients (r = 0.365, P < 0.001). All three ACE inhibitors caused similar reductions in IGF-1 levels, the left ventricular mass index and blood pressure after the treatment period. The effect of ACE inhibition on mean blood pressure was similar in patients with (-13%) and without (-12%) a regression of left ventricular hypertrophy. The mean change in IGF-1 levels with treatment was more pronounced in those patients in whom left ventricular hypertrophy regressed (-25 versus -12%). CONCLUSIONS: These results indicate that circulating IGF-1 levels are increased in essential hypertension. Furthermore, there is an association between high IGF-1 levels and left ventricular hypertrophy in hypertensive patients. Our findings suggest that the ability of ACE inhibitors to induce regression of hypertensive cardiac hypertrophy may be related to their ability to normalize IGF-1 and also supports the view that ACE inhibition affects left ventricular mass through pathways other than blood pressure reduction.

Adult↗
PubMed1994

Immunohistochemical detection of chloride/bicarbonate anion exchangers in human liver.

Sodium-independent Cl-/HCO3- exchange activity has been observed in isolated rat hepatocytes and intrahepatic bile duct epithelial cells, where it is involved in intracellular pH regulation and, possibly, biliary bicarbonate secretion. Monoclonal antibodies to the membrane domain of human chloride/bicarbonate anion exchanger proteins, AE1 and AE2, were prepared so that we might determine by immunohistochemical methods the presence and location of these antiporters in the human liver. To obtain the antibody against AE1, we immunized mice with injections of washed human erythrocytes. The selected monoclonal antibody was found to be specific for the 17-kD proteolytic membrane fragment of AE1 protein. The antibody to AE2 was produced with a 14-mer synthetic peptide, whose sequence corresponds specifically to amino acid residues 871 to 884 in the deduced primary structure of human kidney AE2 protein. When the monoclonal antibody to AE2 peptide was employed for the immunohistochemical study of liver specimens (by both immunofluorescence and immunoperoxidase), a clearly defined staining was present at the canalicular membrane of hepatocytes, as well as the luminal side of the membrane of bile duct epithelial cells from small and medium-sized bile ducts. No staining was observed in the liver parenchyma with the monoclonal antibody to AE1, which instead strongly decorated the erythrocytes in liver blood vessels. We conclude that AE2 immunoreactivity is present in human liver, where it localizes very specifically to the membrane regions, which appear most probably involved in the transport of bicarbonate to bile (i.e., the canalicular membrane of hepatocytes and the apical side of epithelial cells of small and medium bile ducts).

Amino Acid Sequence↗
PubMed1993

Abnormal expression of anion exchanger genes in primary biliary cirrhosis.

BACKGROUND: Chloride-bicarbonate anion exchangers (AE) are thought to be essential to the generation of ion fluxes into biliary, salivary, pancreatic, and other secretions. In primary biliary cirrhosis (PBC), chronic cholestasis is frequently associated with pluriglandular exocrine failure. The present study examined the expression of AE genes in PBC at the messenger RNA (mRNA) level. METHODS: Two AE messages, i.e., AE1 and AE2 mRNAs, were analyzed by a polymerase chain reaction-based procedure in liver specimens and peripheral mononuclear cells of patients with PBC and control subjects (with normal livers or with miscellaneous liver diseases). RESULTS: AE1 mRNA was detected in only a few liver biopsy specimens of patients with PBC and control subjects, whereas AE2 mRNA was found in all liver specimens tested. In lymphoid cells, however, both transcripts were consistently detected. AE2 mRNA levels in liver as well as in lymphoid cells were significantly lower in PBC patients than in controls. In contrast to AE2 mRNA, AE1 mRNA levels were increased in lymphoid cells from patients with PBC. Interestingly, the levels of liver AE2 mRNA in a few PBC patients treated with ursodeoxycholic acid were within the range of the controls. CONCLUSIONS: The expression of AE genes is altered in patients with PBC. It is suggested that this disturbance may have a role in the cholestasis, exocrine failure, and immunodysfunction of PBC.

Adult↗
PubMed1993

New observations on antigenic diversification of RNA viruses. Antigenic variation is not dependent on immune selection.

Recent results have revealed novel features in the process of antigenic diversification of FMDV. (i) Antigenic variation is not necessarily the result of immune selection. (ii) Single, critical amino acid replacements may either have a minor effect on antigenic specificity or cause a drastic antigenic change affecting many epitopes on an antigenic site. (iii) The effect of such a critical replacement may be suppressed by additional substitutions at neighbouring sites. (iv) Antigenic diversification does not necessarily involve net accumulation of amino acid substitutions over time. We review evidence that some of these features apply also to other riboviruses and retroviruses. A model is proposed to relate antigenic variation without immune selection to the quasispecies structure of RNA virus populations.

Antigenic Variation↗
PubMed1993

Erythrocyte anion exchanger activity and intracellular pH in essential hypertension.

The present study was designed to examine the activity of the sodium-independent chloride-bicarbonate anion exchanger and the sodium-proton exchanger in erythrocytes of 30 normotensive and 35 hypertensive subjects and its relation to the previously reported decrease in erythrocyte pH. Erythrocyte cytosolic pH was measured by the pH-sensitive fluorescent probe 2'-7'-bis(2-carboxyethyl)- 5(6)-carboxyfluorescein. The activity of the anion exchanger was determined by acidifying cell pH and measuring the initial rate of the net sodium-independent, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid-sensitive, bicarbonate influx driven by an outward proton gradient. The activity of the sodium-proton exchanger was determined by acidifying cell pH and measuring the initial rate of the net sodium-dependent proton efflux driven by an outward proton gradient. The activity of the anion exchanger was higher in hypertensive than control individuals (18,863 +/- 1081 vs 15,629 +/- 897 mmol/L cells per hour, P < .05). The activity of the sodium-proton exchanger was higher in hypertensive than control individuals (301 +/- 45 vs 162 +/- 23 mmol/L cells per hour, P < .005). Basal erythrocyte pH was lower in hypertensive than control individuals (7.27 +/- 0.02 vs 7.33 +/- 0.01, mean +/- SEM, P < .05). With the 100% confidence (lower) limit of the normotensive population as a cutoff point, a subgroup of 11 hypertensive patients had an abnormally low erythrocyte pH (< 7.19).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effects of antihypertensive therapy on left ventricular hypertrophy of essential hypertension: a role for insulin-like growth factor I?

In a previous work we have found than an association exists between the presence of left ventricular hypertrophy (LVH) and increased circulating levels of insulin-like growth factor I (IGF-I) in essential hypertension. To address whether this association is of pathophysiological relevance the relationship between echocardiographically determined LVH and IGF-I levels was investigated in 49 patients with essential hypertension before and after one year of antihypertensive treatment with different regimens (nonpharmacological measures, bisoprolol, captopril). The control group consisted of 30 normotensive subjects without LVH. Before treatment IGF-I levels were higher (p < 0.05) in hypertensives with LVH, n = 17, (81.3 +/- 14.3 ng/ml) compared with hypertensives without LVH, n = 32, (57.4 +/- 3.9 ng/ml) and controls (61.3 +/- 3.9 ng/ml). A positive correlation was found between IGF-I levels and LVMI in the whole group of hypertensives (r = 0.32, p < 0.05). After one year of treatment hypertensives with initial LVH separated in two subgroups: those in which LVH regressed (n = 10) and those in which LVH persisted (n = 7). A similar diminution of BP was observed in the two subgroups of hypertensives. The IGF-I levels decreased significantly in patients in which LVH regressed (101.6 +/- 21.7 vs. 61.2 +/- 8.5 ng/ml; p < 0.05) and increased slightly in patients in which LVH persisted (51.2 +/- 8.9 vs. 68.5 +/- 7.9 ng/ml). Six patients in which LVH regressed showed a diminution of IGF-I after treatment. These six patients had received captopril as treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

The stilbene disulfonic acid DIDS stimulates the production of TNF-alpha in human lymphocytes.

Exposure of human peripheral blood mononuclear cells (PBMC) to the stilbene derivative DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid) (60 microM and above) significantly increased the release of tumor necrosis factor-alpha (TNF-alpha), as determined by TNF-alpha activity in the incubation media. When the TNF-alpha message was analyzed in PBMC by a reverse transcription/polymerase chain reaction (RT/PCR)-based procedure, it was found that incubation with DIDS (60 microM) was followed by a time-dependent accumulation of TNF-alpha mRNA. Measurements of intracellular pH showed that the presence of increasing concentrations of DIDS resulted in a progressive intracellular alkalinization of PBMC. It is suggested that the known DIDS effect of inhibiting transmembrane anion exchange, i.e., chloride/bicarbonate exchange, might play a role in the stimulation of TNF-alpha production by PBMC exposed to DIDS.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗