Diuretics modify [Arg8]vasopressin-stimulated cAMP but not atrial natriuretic peptide-stimulated cGMP formation in renal cells

Kanda, Kazumi; Miyamoto, Noboru; Seo, Hisao; Ogawa, Katsuhito; Hatano, Takashi; Matsui, Nobuo

doi:10.1016/0014-2999(91)90082-2

Cited by 1 publication

(3 citation statements)

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“…Azosemide suppressed the accumulation (formation) of (À)-adenosine 3,5-cyclic monophosphate (c-AMP) following stimulation with ADH in rat kidney slice [49] and in rat and dog renal cells [50] and inhibited water transport activated by ADH in bullfrog bladder [49]. Arginine vasopressin binding to its receptors was also inhibited by azosemide [51].…”

Section: Mechanism Of Actionmentioning

confidence: 99%

“…The relationship between the log urinary excretion rate of azosemide and the urinary excretion rate of sodium was sigmoid after oral administration of the diuretic, 40 and 80 mg, to healthy subjects [22]. The values of ED 50 [86] for the urinary excretion rate of loop diuretics in relation to urinary excretion rate of sodium in healthy subjects were 9.3 [22], 69.8 [86], 12.1 [87] and 1.0 [88] mg/min for azosemide, furosemide, piretanide and bumetanide, respectively, indicating that potency ratios were approximately 70:7.5:5.5:1 for bumetanide, azosemide, piretanide and furosemide, respectively [22]. The relationships between log urinary excretion rate of azosemide and urine flow rate as well as urinary excretion rate of sodium were also sigmoid after 1 min and 4 h infusion of the diuretic, 1 mg/kg, to rabbits [69].…”

Section: Doseàresponse Relationshipmentioning

confidence: 99%

“…AAG, a 1 -acid glycoprotein; a and b, parameters of allometric equations (a: constant, b: exponent); ADH, antidiuretic hormone; ATP, adenosine 5 0 -triphosphate; AUC, total area under the plasma concentration-time curve from time zero to time infinity; azosemide, 2-chloro-5-(1H-tetrazole-5-yl)-N 4 -(2thenyl) sulfanilamide; BSA bovine serum albumin; c-AMP, (-)-adenosine 3,5-cyclic monophosphate; Cl, time-averaged total body clearance; Cl CR , creatinine clearance; Cl IN , inulin clearance; Cl nr , time-averaged nonrenal clearance; Cl PAH , para-aminohippurate clearance; Cl r , time-averaged renal clearance; CYP, hepatic microsomal cytochrome P450; DMIA, diabetes mellitus induced by alloxan; DMIS, diabetes mellitus induced by streptozotocin; DOCA, deoxycorticosterone acetate; D-5-W, 5% glucose in water; ED 50 , half-maximal response dose; F, extent of absolute oral bioavailability; f e , fraction of dose excreted unchanged in urine; GFR, glomerular filtration rate; HPLC, high-performance liquid chromatography; HSA, human serum albumin; k, association constant; LD 50 , half-maximal lethal dose; M1, 5-(2-amino-4-chloro-5-sulfamoylphenyl)-tetrazole; MEER, maximally efficient urinary excretion rate; MRT, mean residence time; n, binding site; NARs, rats with mutant Nagase analbuminemia; NSAIDs, nonsteroidal anti-inflammatory drugs; PCM, proteinÀcalorie malnutrition (4 week feed on 5% casein diet); PCMC, PCM with 1 week oral cysteine (250 mg/kg twice daily from 4th week); PGs, prostaglandins; r, correlation coefficient; RAAS, renin-angiotensin-aldosterone system; RPF, renal plasma flow; SHRs, spontaneously hypertensive rats; SIADH, syndrome of inappropriate secretion of antidiuretic hormone; T/P, tissue-to-plasma concentration ratio; U-ARF, acute renal failure induced by uranyl nitrate; V c , apparent volume distribution at central compartment; V db , apparent post-pseudodistribution volume of distribution; V ss , apparent volume of distribution at steady-state; W, body weight; 4 WE, 4-week exercise.…”

Section: Abbreviationsmentioning

confidence: 99%

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Pharmacokinetics and pharmacodynamics of azosemide

Suh¹,

Kim²,

Lee³

2003

Biopharm & Drug Disp

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Azosemide is used in the treatment of oedematous states and hypertension. The exact mechanism of action is not fully understood, but it mainly acts on both the medullary and cortical segments of the thick ascending limb of the loop of Henle. Delayed tolerance was demonstrated in humans by homeostatic mechanisms (principally an increase in aldosterone secretion and perhaps also an increase in the reabsorption of solute in the proximal tubule). After oral administration to healthy humans in the fasting state, the plasma concentration of azosemide reached its peak at 3-4 h with an absorption lag time of approximately 1 h and a terminal half-life of 2-3 h. The estimated extent of absolute oral bioavailability in humans was approximately 20.4%. After oral administration of the same dose of azosemide and furosemide, the diuretic effect was similar between the two drugs, but after intravenous administration, the effect of azosemide was 5.5-8 times greater than that in furosemide. This could be due to the considerable first-pass effect of azosemide. The protein binding to 4% human serum albumin was greater than 95% at azosemide concentrations ranging from 10 to 100 microg/ml using an equilibrium dialysis technique. The poor affinity of human tissues to azosemide was supported by the relatively small value of the apparent post-pseudodistribution volume of distribution (Vdbeta), 0.262 l/kg. Eleven metabolites (including degraded products) of azosemide including M1, glucuronide conjugates of both M1 and azosemide, thiophenemethanol, thiophencarboxylic acid and its glycine conjugate were obtained in rats. Only azosemide and its glucuronide were detected in humans. In humans, total body clearance, renal clearance and terminal half-life of azosemide were 112 ml/min, 41.6 ml/min and 2.03 h, respectively. Azosemide is actively secreted in the renal proximal tubule possibly via nonspecific organic acid secretory pathway in humans. Thus, the amount of azosemide that reaches its site of action could be significantly modified by changes in the capacity of this transport system. This capacity, in turn, could be predictably changed in disease states, resulting in decreased delivery of the diuretic to the transport site, as well as in the presence of other organic acids such as nonsteroidal anti-inflammatory drugs which could compete for active transport of azosemide. The urinary excretion rate of azosemide could be correlated well to its diuretic effects since the receptors are located in the loop of Henle. The diuretic effects of azosemide were dependent on the rate and composition of fluid replacement in rabbits; therefore, this factor should be considered in the evaluation of bioequivalence assessment.

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Section: Mechanism Of Actionmentioning

confidence: 99%