electrolyte

Trichlormethiazide (Naqua) is a short-acting, 3-dichloromethyl derivative of hydrochlorothiazide, belonging to the class of thiazide diuretics. Trichlormethiazide appears to block the active reabsorption of chloride and possibly sodium in the ascending loop of Henle, altering electrolyte transfer in the proximal tubule.

Magnesium acetate tetrahydrate is the hydrated form of the anhydrous magnesium acetate salt.Magnesium acetate tetrahydrate is commonly used to synthesize other compounds, cocoa as an electrolyte supplement or as a reagent in molecular biology experiments.

Brain natriuretic peptide-32 (BNP-32), a fragment of the proBNP cardiovascular hormone precursor, exhibits affinity for natriuretic peptide receptors in rat vascular smooth muscle cells (IC50 = 7.3 nM) and promotes cGMP accumulation within these cells (EC50 = 170 nM). Additionally, BNP-32 effectively mediates the relaxation of norepinephrine-precontracted isolated rat aortic strips (EC50 = 6.7 nM). Upon administration at a dosage of 3 µg/kg, it elevates urine and urinary electrolyte outputs and induces hypotension in rats.

PGF1β, a biochemical compound, functions as a pivotal mediator in inflammatory processes and plays an integral role in uterine contractions. It exhibits significant regulatory effects on platelet aggregation and vasodilation, demonstrating its critical importance in cardiovascular health. Additionally, PGF1β contributes to the regulation of kidney function and electrolyte balance, illustrating its widespread impact across various physiological systems.

Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. (±)17-HETE is the racemic version of a cytochrome P450 (CYP450) metabolite of arachidonic acid that has stereospecific effects on sodium transport in the kidney. At a concentration of 2 μM the (S)-enantiomer of 17-HETE inhibits proximal tubule ATPase activity by as much as 70%, whereas the (R)-isomer is inactive.

Angiotensin Fragment 1-7 is a type 1 angiotensin II receptor agonist. In the renin-angiotensin system, angiotensin I is cleaved by the angiotensin-converting enzyme to form angiotensin II, which has effects on fluid and electrolyte, as well as homeostasis

18-Hydroxycorticosterone-d4 is a deuterated compound of 18-Hydroxycorticosterone. 18-Hydroxycorticosterone has a CAS number of 561-65-9. 18-Hydroxycorticosterone is a corticosteroid and corticosterone derivative, which can lead to serious electrolyte imbalances.

Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites.17-HETE is a cytochrome P450 (CYP450) metabolite of arachidonic acid that has stereospecific effects on sodium transport in the kidney.17(S)-HETE inhibits proximal tubule ATPase activity by as much as 70% at a concentration of 2 μM.

Endogenous peptide activator of intestinal guanylyl cyclase; secreted mainly by the gastrointestinal mucosa. Regulates water and electrolyte transport in intestinal and renal epithelia.

Guanylin (human) TFA is a 15-amino acid peptide that serves as an endogenous activator of intestinal guanylate cyclase. This compound is primarily located in the gastrointestinal tract, where it regulates electrolyte and water transport in the intestinal and renal epithelia through a mechanism dependent on cyclic GMP. [1][2]

Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. 16-HETE is a minor CYP450 metabolite of arachidonic acid released by the kidney upon angiotensin II stimulation that demonstrates stereospecific biological activity. Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. 16-HETE is a minor CYP450 metabolite of arachidonic acid released by the kidney upon angiotensin II stimulation that demonstrates stereospecific biological activity. 16(S)-HETE inhibits proximal tubule ATPase activity by as much as 60% at a concentration of 2 µM.[1]

Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. 17-HETE is a cytochrome P450 (CYP450) metabolite of arachidonic acid that has stereospecific effects on sodium transport in the kidney. 17(R)-HETE is an inactive isomer of 17-HETE, whereas the (S) enantiomer can inhibit proximal tubule ATPase activity at a concentration of 2 μM.

Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. (±)16-HETE is the racemic version of a minor CYP450 metabolite of arachidonic acid released by the kidney upon angiotensin II stimulation. The biological activity of 16-HETE is stereospecific. 16(R)-HETE dose-dependently stimulates vasodilation of the rabbit kidney, however 16(S)-HETE does not affect perfusion pressure. At a concentration of 2 μM the (S)-enantiomer of 16-HETE inhibits proximal tubule ATPase activity by as much as 60%, whereas the (R)-isomer has negligible effects on ATPase activity.

Atrial natriuretic peptide (3-28) (human) (ANP (3-28) (human)), a peptide hormone produced by the atrial myocardium, critically regulates blood pressure, fluid balance, and electrolyte homeostasis [1] [2].

Olsalazine-13C6is intended for use as an internal standard for the quantification of olsalazine by GC- or LC-MS. Olsalazine is an orally bioavailable prodrug form of the anti-inflammatory agent 5-aminosalicylic acid that is cleaved by bacterial azo reductases in the gut to generate active 5-ASA.1In vitro, olsalazine increases ion transport in isolated rabbit distal ileum when applied to the luminal side (ED50= 0.3 mM) and stimulates fluid transport in rat jejunum when used at a concentration of 5 mM.2,3Olsalazine (150 mg/kg for 8 days) improves stool consistency and decreases occult and gross bleeding as well as myeloperoxidase (MPO) activity and leukotriene B4levels in colon tissue in a mouse model of acute colitis induced by dextran sulfate .4Olsalazine also inhibits bovine xanthine oxidasein vitro(IC50= 3.4 mg/L) and lowers serum uric acid levels in a mouse model of hyperuricemia induced by oxonic acid when administered at a dose of 20 mg/kg.5Formulations containing olsalazine have been used in the treatment of inflammatory bowel disease (IBD) and ulcerative colitis. 1.Nugent, S.G., Kumar, D., Rampton, D.S., et al.Intestinal luminal pH in inflammatory bowel disease: Possible determinants and implications for therapy with aminosalicylates and other drugsGut48(4)571-577(2001) 2.Pamukcu, R., Hanauer, S.B., and Chang, E.B.Effect of disodium azodisalicylate on electrolyte transport in rabbit ileum and colon in vitro. Comparison with sulfasalazine and 5-aminosalicylic acidGastroenterology95(4)975-981(1988) 3.Mohsen, A.Q.M., Mulvey, D., Priddle, J.D., et al.Effects of olsalazine in the jejunum of the ratGut28(3)346-352(1987) 4.Murthy, S., Murthy, N.S., Coppola, D., et al.The efficacy of BAY y 1015 in dextran sulfate model of mouse colitisInflamm. Res.46(6)224-233(1997) 5.Niu, Y., Li, H., Gao, L., et al.Old drug, new indication: Olsalazine sodium reduced serum uric acid levels in mice via inhibiting xanthine oxidoreductase activityJ. Pharmacol. Sci.135(3)114-120(2017)

Electrolyte and fluid transport in the kidney are regulated in part by arachidonic acid and its metabolites. 16-HETE is a minor CYP450 metabolite of arachidonic acid released by the kidney upon angiotensin II stimulation that demonstrates stereospecific biological activity. 16(S)-HETE inhibits proximal tubule ATPase activity by as much as 60% at a concentration of 2 μM.

18-Hydroxycorticosterone, a corticosteroid and corticosterone derivative, can cause significant electrolyte imbalances.