Heterocyclic compounds of a ring with SULFUR and two NITROGEN atoms fused to a BENZENE ring. Members inhibit SODIUM-POTASSIUM-CHLORIDE SYMPORTERS and are used as DIURETICS.

Subtype-specific effects of lithium on glutamate receptor function. (1/267)

We report that substitution of sodium with lithium (Li+) in the extracellular solution causes subtype-specific changes in the inward and outward currents of glutamate receptors (GluRs), without a shift in reversal potential. Li+ produces an increase of inward and outward currents of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors and decreases in the currents of kainate (KA) and N-methyl-D-aspartate receptors. The greatest effect of Li+ was observed with GluR3. A concentration-response curve for GluR3 reveals that the potentiation caused by Li+ is greatest at saturating agonist concentrations. GluR1, which shows no potentiation by Li+ at 100 microM KA, shows a small but significant potentiation at saturating KA and glutamate concentrations. The effects of Li+ on outward current, where Li+ is not the primary charge carrier, and the lack of reversal potential shift argue for a mechanism of potentiation not associated with Li+ permeation. This potentiation of current is specific for Li+ because rubidium, although causing an increase of inward current, shifted the reversal potential and did not increase outward current. The effects of Li+ are different for KA, a weak desensitizing agonist, and glutamate, a strong desensitizing agonist, suggesting that Li+ might interact with a mechanism of desensitization. By using cyclothiazide (CTZ) to reduce desensitization of GluR3, we find that for low concentrations of KA and glutamate potentiation of the response by a combination of CTZ and Li+ is no greater than by CTZ or Li+ alone. However, at high concentrations of agonist, the potentiation of the response by a combination of CTZ and Li+ is significantly greater than by CTZ or Li+ alone. This potentiation was additive for glutamate but not for KA. At high agonist concentration in the presence of CTZ, the intrinsically lower desensitization produced with KA-evoked responses may preclude Li+ from potentiating the current to the same degree as it can potentiate glutamate-evoked responses. The additive effects of CTZ and Li+ were unique to the flop variant of GluR3.  (+info)

Trends in antihypertensive drug advertising, 1985-1996. (2/267)

BACKGROUND: Over the past decade, calcium channel blockers (CCBs) and ACE inhibitors have been used increasingly in the treatment of hypertension. In contrast, beta-blocker and diuretic use has decreased. It has been suggested that pharmaceutical marketing has influenced these prescribing patterns. No objective analysis of advertising for antihypertensive therapies exists, however. METHODS AND RESULTS: We reviewed the January, April, July, and October issues of the New England Journal of Medicine from 1985 to 1996 (210 issues). The intensity of drug promotion was measured as the proportion of advertising pages used to promote a given medication. Statistical analyses used the chi2 test for trend. Advertising for CCBs increased from 4.6% of advertising pages in 1985 to 26.9% in 1996, while advertising for beta-blockers (12.4% in 1985 to 0% in 1996) and diuretics (4.2% to 0%) decreased (all P<0.0001). A nonsignificant increase was observed in advertising for ACE inhibitors (3.5% to 4.3%, P=0.17). Although the total number of drug advertising pages per issue decreased from 60 pages in 1985 to 42 pages in 1996 (P<0.001), the number of pages devoted to calcium channel blocker advertisements nearly quadrupled. CONCLUSIONS: Increasing promotion of CCBs has mirrored trends in physician prescribing. An association between advertising and prescribing patterns could explain why CCBs have supplanted better-substantiated therapies for hypertension.  (+info)

A numerical model of the renal distal tubule. (3/267)

A numerical model of the rat distal tubule was developed to simulate water and solute transport in this nephron segment. This model incorporates the following: 1) Na-Cl cotransporter, K-Cl cotransporter, Na channel, K channel, and Cl channel in the luminal membrane; 2) Na-K-ATPase, K channel, and Cl channel in the basolateral membrane; and 3) conductances for Na, K, and Cl in the paracellular pathway. Transport rates were calculated using kinetic equations. Axial heterogeneity was represented by partitioning the model into two subsegments with different sets of model parameters. Model equations derived from the principles of mass conservation and electrical neutrality were solved numerically. Values of the model parameters were adjusted to minimize a penalty function that was devised to quantify the difference between model predictions and experimental results. The developed model could simulate the water and solute transport of the distal tubule in the normal state, as well as in conditions including thiazide or amiloride application and various levels of sodium load and tubular flow rate.  (+info)

A kinetic model of the thiazide-sensitive Na-Cl cotransporter. (4/267)

The aim of this study was to construct a numerical model of the thiazide-sensitive Na-Cl cotransporter (TSC) that can predict kinetics of thiazide binding and substrate transport of TSC. We hypothesized that the mechanisms underlying these kinetic properties can be approximated by a state diagram in which the transporter has two binding sites, one for sodium and another for chloride and thiazide. On the basis of the state diagram, a system of linear equations that should be satisfied in the steady state was postulated. Numerical solution of these equations yielded model prediction of kinetics of thiazide binding and substrate transport. Rate constants, which determine transitional rates between states, were systematically adjusted to minimize a penalty function that was devised to quantitatively estimate the difference between model predictions and experimental results. With the resultant rate constants, the model could simulate the following experimental results: 1) dissociation constant of thiazide in the absence of sodium and chloride; 2) inhibitory effect of chloride on thiazide binding; 3) stimulatory effect of sodium on thiazide binding; 4) combined effects of sodium and chloride on thiazide binding; 5) dependence of sodium influx on extracellular sodium and chloride; and 6) inhibition of sodium influx by extracellular thiazide. We conclude that known kinetic properties of TSC can be predicted by a model which is based on a state diagram.  (+info)

Lack of AMPA receptor desensitization during basal synaptic transmission in the hippocampal slice. (5/267)

Excitatory postsynaptic currents in the CA1 region of rat hippocampal slices are mediated primarily by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in response to synaptically released glutamate. Outside-out patches from pyramidal cells in this region have shown that AMPA receptors are desensitized by short (1 ms) pulses of glutamate. We have taken a number of approaches to ask whether synaptic receptors desensitize in response to synaptically released glutamate in the slice. Recordings with paired pulses and minimal stimulation conditions that are presumably activating only a single release site do not show evidence for desensitization. Furthermore, cyclothiazide, a drug that blocks desensitization, does not alter paired-pulse ratios even under conditions of high probability of release, which should maximize desensitization. These results suggest that synaptic receptors do not desensitize in response to synaptically released glutamate during basal synaptic transmission.  (+info)

The concentration of synaptically released glutamate outside of the climbing fiber-Purkinje cell synaptic cleft. (6/267)

AMPA receptors and glutamate transporters expressed by cerebellar Bergmann glial cells are activated by neurotransmitter released from climbing fibers (). Based on anatomical evidence, this is most likely the result of glutamate diffusing out of the climbing fiber-Purkinje cell synaptic clefts (). We used the change in the EC50 of the Bergmann glia AMPA receptors produced by cyclothiazide (CTZ) to estimate the concentration of glutamate reached at the glial membrane. The decrease of the EC50 gives rise to a concentration-dependent potentiation of the AMPA receptor-mediated responses (). By comparing the increase in amplitude of the AMPA receptor response in the Bergmann glia (840 +/- 240%; n = 8) with the shift in the glutamate dose-response curve measured in excised patches (EC50, 1810 microM in control vs 304 microM in CTZ), we estimate that the extrasynaptic transmitter concentration reaches 160-190 microM. This contrasts with the concentration in the synaptic cleft, thought to rapidly rise above 1 mM, but is still high enough to activate glutamate receptors. These results indicate that the sphere of influence of synaptically released glutamate can extend beyond the synaptic cleft.  (+info)

The management of hypertensive disease in black patients. (7/267)

The ethnic differences in the incidence, pathophysiology and management of hypertensive disease, are particularly pertinent to the Black or Afro-Caribbean populations, who have a high prevalence of hypertension and associated complications, such as strokes and renal impairment. Our understanding of the underlying pathophysiology of hypertensive disease and the optimal treatment of hypertension in Black patients continues to evolve, especially with the introduction of new drugs and the need for prognostic data in this ethnic population. We review the management of hypertensive disease in the black population, emphasizing race-related differences in the pathophysiology of hypertension and the importance of tailored management in this group of patients, including sensible application of non-pharmacological measures with effective antihypertensive agents. For example, diuretics and calcium antagonists are suitable first-line agents in black hypertensives, whilst beta-blockers and the ACE inhibitors tend to be less effective at lowering blood pressure, due to the low renin state in these patients.  (+info)

A novel presynaptic inhibitory mechanism underlies paired pulse depression at a fast central synapse. (8/267)

Several distinct mechanisms may cause synaptic depression, a common form of short-term synaptic plasticity. These include postsynaptic receptor desensitization, presynaptic depletion of releasable vesicles, or other presynaptic mechanisms depressing vesicle release. At the endbulb of Held, a fast central calyceal synapse in the auditory pathway, cyclothiazide (CTZ) abolished marked paired pulse depression (PPD) by acting presynaptically to enhance transmitter release, rather than by blocking postsynaptic receptor desensitization. PPD and its response to CTZ were not altered by prior depletion of the releasable vesicle pool but were blocked by lowering external calcium concentration, while raising external calcium enhanced PPD. We conclude that a major component of PPD at the endbulb is due to a novel, transient depression of release, which is dependent on the level of presynaptic calcium entry and is CTZ sensitive.  (+info)

Benzothiadiazines are a class of heterocyclic chemical compounds that contain a benzene fused to a thiadiazine ring. They have been used in the synthesis of various pharmaceutical drugs, particularly those used for their anti-inflammatory, antihypertensive, and diuretic properties.

One of the most well-known benzothiadiazines is benothiazine itself, which has been used as a precursor in the synthesis of various dyes and pigments. However, it is not used in medical applications.

The benzothiadiazines that are used medically are typically derivatives of the parent compound, such as clotrimazole and ftorafur. Clotrimazole is an antifungal medication used to treat various fungal infections, while ftorafur is an antineoplastic agent used in the treatment of certain types of cancer.

It's important to note that benzothiadiazines are not a commonly used class of drugs in medicine, and their use is typically limited to specific indications where they have been shown to be effective.

Benzothiadiazines, Chloroarenes, Experimental drugs, Nootropics). ...
Benzothiadiazines, Trifluoromethyl compounds, Carbonic anhydrase inhibitors, All stub articles, Cardiovascular system drug ...
Benzothiadiazines, Isopropyl compounds, Sultams). ...
Benzothiadiazines, Experimental drugs, All stub articles, Nervous system drug stubs). ...
Benzothiadiazines, Chloroarenes, Diuretics, Thioethers, All stub articles, Cardiovascular system drug stubs). ...
Benzothiadiazines, Fluoroarenes, Indoles, Tetrahydropyridines, Sulfones, All stub articles, Nervous system drug stubs). ...
... benzothiadiazines MeSH D02.886.590.700.135.138 - bendroflumethiazide MeSH D02.886.590.700.135.261 - chlorothiazide MeSH D02.886 ... benzothiadiazines MeSH D02.886.655.500.138 - bendroflumethiazide MeSH D02.886.655.500.261 - chlorothiazide MeSH D02.886.655.500 ...
Benzothiadiazines, Chloroarenes, All stub articles, Cardiovascular system drug stubs). ...
Benzothiadiazines, Sulfonamides, Organochlorides, Carbonic anhydrase inhibitors, All stub articles, Cardiovascular system drug ...
Benzothiadiazines, All stub articles, Heterocyclic compound stubs). ...
Benzothiadiazines, Organochlorides, Carbonic anhydrase inhibitors, Thiazides, All stub articles, Cardiovascular system drug ...
Benzothiadiazines, Chloroarenes, Thioethers, Carbonic anhydrase inhibitors, All stub articles, Antihypertensive agent stubs). ...
Benzothiadiazines, Chloroarenes, Organofluorides, Trifluoromethyl compounds, All stub articles, Cardiovascular system drug ...
Benzothiadiazines, Sultams, Chloroarenes, World Health Organization essential medicines, Wikipedia medicine articles ready to ...
Benzothiadiazines, Sultams, Merck & Co. brands, Carbonic anhydrase inhibitors, World Anti-Doping Agency prohibited substances, ...
Benzothiadiazines, Trifluoromethyl compounds, Pfizer brands, Carbonic anhydrase inhibitors, World Anti-Doping Agency prohibited ...
Benzothiadiazines, Chloroarenes, GABAA receptor negative allosteric modulators, Carbonic anhydrase inhibitors, Convulsants, ...
Benzothiadiazines / pharmacology* * Dioxoles / pharmacology* * Dose-Response Relationship, Drug * Excitatory Amino Acid ...
Benzothiadiazines, Chloroarenes, Experimental drugs, Nootropics). ...
Benzothiadiazines. Direct Parent. 1,2,4-benzothiadiazine-1,1-dioxides. Alternative Parents. Secondary alkylarylamines / ...
CH$COMPOUND_CLASS: Pesticides; Herbicides; Triazines; Thiazides; Benzothiadiazines. CH$FORMULA: C10H12N2O3S. CH$EXACT_MASS: ...
Benzothiadiazines (5) * Bendroflumethiazide (5) * Chlorothiazide (0) * Cyclopenthiazide (0) * Diazoxide (0) * ...
It belongs to the class of thiazide diuretics (or benzothiadiazines). Thiazide diuretics promote the flushing of sodium and ...
This graph shows the total number of publications written about "Quinolizines" by people in Harvard Catalyst Profiles by year, and whether "Quinolizines" was a major or minor topic of these publication ...
Synthesis and Biological Characterization of Unsymmetrical Dialkyl-Hydroxynaphthalenoyl-benzothiadiazines. Wagner R, Larson DP ...
This term commonly refers to the benzothiadiazines that inhibit sodium-potassium-chloride symporters and are used as diuretics. ...
Benzothiadiazines D3.438.174 D3.633.100.174 Benzothiazoles D3.438.185 D3.633.100.185 Benzothiepins D3.438.197 D3.633.100.197 ...
Benzothiadiazines D3.438.174 D3.633.100.174 Benzothiazoles D3.438.185 D3.633.100.185 Benzothiepins D3.438.197 D3.633.100.197 ...
Benzothiadiazines D3.438.174 D3.633.100.174 Benzothiazoles D3.438.185 D3.633.100.185 Benzothiepins D3.438.197 D3.633.100.197 ...
Benzothiadiazines D3.438.174 D3.633.100.174 Benzothiazoles D3.438.185 D3.633.100.185 Benzothiepins D3.438.197 D3.633.100.197 ...
Benzothiadiazines D3.438.174 D3.633.100.174 Benzothiazoles D3.438.185 D3.633.100.185 Benzothiepins D3.438.197 D3.633.100.197 ...
Kolesnik, N.P., Rozhenko, A.B., Kinzhybalo, V., Lis, T., Shermolovich, Y.G. 1-Oxo-1-fluoro-1,2,4-benzothiadiazines - A new type ...
Adenosine Triphosphate, Animals, Benzothiadiazines, Binding Sites, Cell Line, Cell Membrane, Diazoxide, Electric Conductivity, ...
Benzothiadiazines [D03.633.100.174] * Benzothiazoles [D03.633.100.185] * Benzothiepins [D03.633.100.197] * Benzoxazines [ ...
Benzothiadiazines [D02.886.590.700.135] Benzothiadiazines * Bosentan [D02.886.590.700.143] Bosentan * Bumetanide [D02.886. ...
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This graph shows the total number of publications written about "Benzoxepins" by people in this website by year, and whether "Benzoxepins" was a major or minor topic of these publications ...
This graph shows the total number of publications written about "Quinolines" by people in this website by year, and whether "Quinolines" was a major or minor topic of these publications ...
Benzothiadiazines [D03.633.100.174] * Benzothiazoles [D03.633.100.185] * Benzothiepins [D03.633.100.197] * Benzoxazines [ ...
"Benzothiadiazines" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... This graph shows the total number of publications written about "Benzothiadiazines" by people in this website by year, and ... Below are the most recent publications written about "Benzothiadiazines" by people in Profiles. ... whether "Benzothiadiazines" was a major or minor topic of these publications. To see the data from this visualization as text, ...
Benzothiadiazines. Diuretics. Thiazides. Genre(s):. Archival Materials. Articles. Abstract:. In this article, Freis discussed ... Antihypertensive Action of Benzothiadiazines. Contributor(s):. Freis, Edward D.. New York State Journal of Medicine. ...
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Several drugs, such as benzimidazoles, thiophenes, and benzothiadiazines are currently in preclinical development.[65,86,87,88, ...
MeSH Terms: Animals; Benzothiadiazines/chemistry*; Benzothiadiazines/pharmacology; Cysteine/analysis; Cysteine/metabolism*; ...
These findings are compatible with the hypothesis that the use of thiazide diuretics increases the risk of symptomatic cholecystitis. However, we cannot rule out the possibility that our results are in part explained by unconsidered factors related to the indication for antihypertensive therapy or b …
Electrolyte homeostasis is maintained by several ion transport systems. Na-(K)-Cl cotransporters promote the electrically silent movement of chloride across the membrane in absorptive and secretory epithelia. Two kidney-specific Na-(K)-Cl cotransporter isoforms are known, so far, according to their …
Amphotericin B or potassium-depleting diuretics (benzothiadiazines and related drugs, ethacrynic acid and furosemide) - ...
Amphortericin B or potassium-depleting diuretics (benzothiadiazines and related drugs, ethacrynic acid and furosemide)-enhanced ...
Benzothiadiazines,N0000007554, Benzopyrans,N0000007553, Benzophenones,N0000007552, Phenylacetates,N0000007551, Benzomorphans, ...
Antihypertensive Action of Benzothiadiazines Digital Record Identifier: 101584929X29 Dates: Publication: 15 January 1968 ...
Antihypertensive Action of Benzothiadiazines Digital Record Identifier: 101584929X29 Dates: Publication: 15 January 1968 ...
Benzothiadiazines D3.438.174 D3.633.100.174 Benzothiazoles D3.438.185 D3.633.100.185 Benzothiepins D3.438.197 D3.633.100.197 ...
4. Antihypertensive Action of Benzothiadiazines Creator: Freis, Edward D. Date: 15 January 1968 Publisher: Medical Society of ...
Benzothiadiazines Preferred Term Term UI T004577. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1966). ... Benzothiadiazines Preferred Concept UI. M0002371. Registry Number. 0. Scope Note. Heterocyclic compounds of a ring with SULFUR ... Benzothiadiazines [D02.886.590.700.135] * Bendroflumethiazide [D02.886.590.700.135.138] * Chlorothiazide [D02.886.590.700. ... Benzothiadiazines. Tree Number(s). D02.886.590.700.135. D02.886.655.500. D03.633.100.174. Unique ID. D001581. RDF Unique ...
Benzothiadiazines Preferred Term Term UI T004577. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1966). ... Benzothiadiazines Preferred Concept UI. M0002371. Registry Number. 0. Scope Note. Heterocyclic compounds of a ring with SULFUR ... Benzothiadiazines [D02.886.590.700.135] * Bendroflumethiazide [D02.886.590.700.135.138] * Chlorothiazide [D02.886.590.700. ... Benzothiadiazines. Tree Number(s). D02.886.590.700.135. D02.886.655.500. D03.633.100.174. Unique ID. D001581. RDF Unique ...
6. Antihypertensive Action of Benzothiadiazines Creator: Freis, Edward D. Date: 15 January 1968 Publisher: Medical Society of ...
Antihypertensive Action of Benzothiadiazines Creator: Freis, Edward D. Date: 15 January 1968 Publisher: Medical Society of the ...
This term commonly refers to the BENZOTHIADIAZINES that inhibit SODIUM-POTASSIUM-CHLORIDE SYMPORTERS and are used as DIURETICS. ... This term commonly refers to the BENZOTHIADIAZINES that inhibit SODIUM-POTASSIUM-CHLORIDE SYMPORTERS and are used as DIURETICS ...
Benzothiadiazines act on the proximal and distal convoluted tubules to increase the excretion of sodium, chloride and potassium ... On the other hand, hypo- natremia or hypochloremia is relatively uncommon except when the benzothiadiazines are given to pa- ... Winer, B. M. Antihypertensive actions of benzothiadiazines. Circula- tion 23:211- 218, 1961. Oren, B. G., Rich, M., and Belle, ...
Inhibition of these symporters by BENZOTHIADIAZINES is the basis of action of some DIURETICS. AN - coordinate with DIURETICS if ... This term commonly refers to the BENZOTHIADIAZINES that inhibit SODIUM-POTASSIUM-CHLORIDE SYMPORTERS and are used as DIURETICS ...
QSAR and Docking Studies on 1,1-Dioxo-2H-benzothiadiazines Acting as HCV NS5B polymerase inhibitors. AnithaK.a, NeeluSinghb, ...
... synthesis and biological characterization of unsymmetrical dialkyl-hydroxynaphthalenoyl-benzothiadiazines. ...
Santoni M, Conti A, Porta C, Procopio G, Sternberg CN, Basso U, De Giorgi U, Bracarda S, Rizzo M, Ortega C, Massari F, Iacovelli R, Derosa L, Masini C, Milella M, Di Lorenzo G, Atzori F, Pagano M, Buti S, De Vivo R, Mosca A, Rossi M, Paglino C, Verzoni E, Cerbone L, Muzzonigro G, Falconi M, Montironi R, Burattini L, Santini D, Cascinu S. Sunitinib, pazopanib or sorafenib for the treatment of patients with late relapsing metastatic renal cell carcinoma. J Urol. 2015 Jan; 193(1):41-7 ...
Benzothiadiazines possess a stronger hydrogen-bond donor ability compared to thioureas and exhibit remarkable catalytic ... Benzothiadiazines possess a stronger hydrogen-bond donor ability compared to thioureas and exhibit remarkable catalytic ...
  • It belongs to the class of thiazide diuretics (or benzothiadiazines). (selfhacked.com)