All issues
Volume 166 (1992)
- Issue 4 Pages 407-
- Issue 3 Pages 269-
- Issue 2 Pages 201-
- Issue 1 Pages 1-
Volume 166, Issue 1
Displaying 1-15 of 15 articles from this issue
- |<
- <
- 1
- >
- >|
-
ADRIAN I. KATZ, FUMI TAKEMOTO, MATSUHIKO HAYASHI1992 Volume 166 Issue 1 Pages 1-16
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSKATZ, A.I., TAKEMOTO, F, and HAYASHI, M. Hormone Receptors and Sites of Action in the Kidney. Tohoku J. Exp. Med., 1992, 166, (1), 1-16-Identification of hormone target sites in the nephron has been achieved in part using autoradiography, and largely with microdissection and microanalysis techniques that permit quantitative measurements of hormone binding or postbinding effects in discrete nephron segments. The nephron target sites of hormones whose intracellular second messenger is known have been located by measuring their stimulatory effect on cyclic AMP or GMP production along the nephron. These hormones include arginine vasopressin, parathyroid hormone, calcitonin, and β-adrenergic catecholamines. In contrast, the action sites of hormones whose cellular mediators are less well understood have been identified using micro modifications of conventional binding techniques scaled down to the minute (≤1 μg protein) amount of tissue available. In this group are aldosterone, corticosterone, insulin, angiotensin II, α-Adrenergic catecholamines and dopamine. Atrial natriuretic peptides and glucagon have been studied with both methods. The precise localization of hormone receptors and sites of action in the functionally heterogeneous nephron is critical for understanding the interactions between the kidney and the endocrine system in fluid volume homeostasis, blood pressure control, and in biochemical and metabolic regulation.View full abstractDownload PDF (1689K) -
TADASHI INAGAMI, KENJI MIZUNO, MINORU KAWAMURA, TOMIO OKAMURA, DANIEL ...1992 Volume 166 Issue 1 Pages 17-26
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSINAGAMI, T., MIZUNO, K., KAWAMURA, M., OKAMURA, T., CLEMENS, D.L. and HIGASHIMORI, K. Localization of Components of the Renin-Angiotensin System within the Kidney and Sustained Release of Angiotensins from Isolated and Perfused Kidney. Tohoku J. Exp. Med., 1992, 166 (1), 17-26-We found colocalization of renin, angiotensin (Ang) I and Ang II in juxtaglomerular (JG) cells of the kidney. Coexistence of Ang II in renin granules was demonstrated by electron microscopic immunogold labeling of these components. Coexistence of both Ang I and Ang II in the high density renin storage granules were also demonstrated by gradient centrifugation of renal homogenate. These findings supported the synthesis of Ang I and Ang II in juxtaglomerular cells. Isolated and cultured JG cells showed the synthesis of Ang I, Ang II and renin. Ang I and Ang II were secreted from isolated and perfused rat kidneys at steady rates over 2hr. Their secretion rates were proportional to that of renin. The rate of Ang II secretion from the kidney was higher than that from the vascular bed. Ang II was also found in renal lymph. These findings indicate that a large amount of Ang II is generated in JG cells by the intracellular action of renin and may play a significant role in the regulation of renal function.View full abstractDownload PDF (1781K) -
SADAYOSHI ITO, OSCAR A. CARRETERO, KEISHI ABE, Luis A. Juncos, KAORU Y ...1992 Volume 166 Issue 1 Pages 27-39
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSITO, S., CARRETERO, O.A., ABE, K., Juncos, L.A. and YOSHINAGA, K. Macula Densa Control of Renin Release and Glomerular Hemodynamics. Tohoku J. Exp. Med., 1992, 166 (1), 27-39 In each nephron of the mammalian kidney, the tubule returns to the hilus of the parent glomerulus, forming the juxtaglomerular apparatus (JGA). The JGA displays a unique arrangement of afferent and efferent arterioles, interstitial cells and macula densa (a specialized plaque of tubular epithelial cells). Because of this intimate anatomical relationship, it has long been suggested that the macula densa may somehow sense changes in the composition of the tubular fluid and control both the glomerular filtration rate and renin release. Despite extensive investigation, attempts to obtain direct evidence of this have been hindered by the anatomical complexity of the JGA. However, recent technical developments now permit direct assessment of the role of the macula densa in the control of both renin release and glomerular hemodynamics. These developments include microdissection/perfusion of the afferent arteriole, the macula densa or both, as well as a sensitive renin assay which permits measurement of renin release from a single JGA. Observations resulting from such developments are discussed in this article.View full abstractDownload PDF (1973K) -
PATRICK M. SEXTON, JIALONG ZHUO, FREDERICK A.O. MENDELSOHN1992 Volume 166 Issue 1 Pages 41-56
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSSEXTON, P.M., ZHUO, J. and MENDELSOHN, F.A.O. Localization and Regulation of Renal Receptors for Angiotensin II and Atrial Natriuretic Peptide. Tohoku J. Exp. Med., 1992, 166 (1), 41-56-The anatomical distribution of receptors for angiotensin II (Ang II) and atrial natriuretic peptide (ANP) within the kidney has been investigated by in vitro autoradiography. Ang II and ANP receptor binding occurs together in several sites in the kidney, including renal vasculature, glomeruli, proximal convoluted tubule of the outer cortex, and the vasa recta bundles of the inner stripe of the outer medulla. However, in the glomeruli, Ang II receptor binding occurs predominantly in mesangial cells, while ANP receptors are localized mainly to the visceral epithelial cells. In the inner medulla, there is a moderate density of ANP receptors in marked contrast with Ang II binding which is not detected in this site. Both Ang II and ANP receptors are modulated by alterations in sodium and fluid intake, and the peptides themselves. The overlapping distribution of receptors for these two peptide hormones in several intrarenal sites may provide an anatomical basis for their physiological interaction to regulate renal hemodynamics and tubular reabsorption of sodium and water.View full abstractDownload PDF (2082K) -
PAOLO MENE, MICHAEL S. SIMONSON, MICHAEL J. DUNN1992 Volume 166 Issue 1 Pages 57-73
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSNephrology, University Hospitals of Cleveland, Cleveland, Ohio 44106, USA MENE', P., SIMONSON, M.S. and DUNN, M.J. Eicosanoids, Mesangial Contraction, and Intracellular Signal Transduction. Tohoku J. Exp. Med., 1992, 166 (1), 57-73-The glomerular mesangial cell is a specialized pericyte with multiple functional capabilities including contraction. Mesangial contraction may reduce the glomerular filtration surface area and hence the ultrafiltration coefficient, Kf. Cultured mesangial cells convert arachidonic acid into biologically active eicosanoids which are either contractile (thromboxane A2 [TxA2], prostaglandin F2α [PGE2α]) or relaxant (POE2, PGI2). The addition of TxA2 analogues, PGE2 or sulfidopeptide leukotrienes (LTC4 and LTD4) stimulated contraction of cultured mesangial cells with threshold responses at approximately 1nM and maximum responses at 1μM. PGE2 and PGI2 antagonized mesangial contraction induced by TxA2 analogues. Contraction was enhanced by inhibiting mesangial cyclooxygenase with nonsteroidal antiinflammatory drugs (NSAID). Contractile eicosanoids stimulated phospholipase C thereby elevating intracellular inositol trisphosphate and cytosolic free Ca2+ concentration ([Ca2+]i). Vasorelaxant prostanoids stimulated adenylate cyclase, increasing intracellular cyclic AMP. We conclude that eicosanoids control mesangial contractility by regulating [Ca2+]i and CAMP. NSAID increase mesangial reactivity by blocking the inhibitory effects of endogenous vasodilator eicosanoids, with potential consequences on glomerular hemodynamics.View full abstractDownload PDF (1677K) -
YOSHIAKI KONDO, KEI KUDO, YUTAKA IGARASHI, YASURO KUBA, SYUJI ARIMA, K ...1992 Volume 166 Issue 1 Pages 75-84
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSKONDO, Y., KUDO, K., IGARASHI, Y., KUBA, Y., ARIMA, S., TADA, K. and ABE, K. Functions of Ascending Thin Limb of Henle's Loop with Special Emphasis on Mechanism of NaCl Transpost. Tohoku J. Exp. Med., 1992, 166 (1), 75-84-Major controversy concerning the ascending thin limb of Henle's loop (ATL) centers on the urine concentration mechanism based on the countercurrent multiplier system in the inner medulla of the kidney. This renal tubular segment has specific transport properties which function to dilute the urine without any movement of water across the epithelium. This segment is fundamentally impermeable to water, moderately permeable to urea, and highly permeable to Na+ and Cl-. Whether NaCl is reabsorbed actively in the ATL has long been an important question. While mathematical modelling studies have failed to explain completely how the osmotic gradient in the inner medulla is generated without active NaCl transport in the ATL, the experimental data support the view that active NaCl reabsorption is absent. Recently, we succeeded in measuring the intracellular Na+ concentration by using the fluorescent Na+ indicator sodium-binding benzofuran isophthalate in the in vitro microperfused ATL. Our data suggest that the ATL maintains a low intracellular Na+ concentration by the ouabain-sensitive Na+/K+ ATPase in the basolateral membrane, and that the luminal membrane of the ATL has furosemide-insensitive Na+ permeability. Active Na+ reabsorption estimated in our study amounts to only a few per cents of the net Na+ reabsorption in the ATL. It is therefore suggested that the major role of Na+ extrusion in the ATL cells is to maintain a low cellular Nay concentration against ambient hyperosmolarity, although small but substantial amount of Na+ is reabsorbed by the furosemide-insensitive Na+ permeability and ouabain-sensitive Na+/K+ ATPase.View full abstractDownload PDF (1060K) -
MICHAL LANIADO-SCHWARTZMAN, NADER G. ABRAHAM, DAVID SACERDOTI, BRUNO E ...1992 Volume 166 Issue 1 Pages 85-91
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSLANIADO-SCHWARTZMAN, M., ABRAHAM, N.G., SACERDOTI, D., ESCALANTE, B. and MCGIFF, J.C. Effect of Acute and Chronic Treatment of Tin on Blood Pressure in Spontaneously Hypertensive Rats. Tohoku J. Exp. Med., 1992, 166 (1), 85-91 - Cytochrome P450-dependent metabolites of arachidonic acid (AA) are increased in the kidneys of spontaneously hypertensive rats (SHR) as compared to control rats (WKY) in the period of rapid elevation of blood pressure (BP) from 5 to 13 weeks. We treated rats with stannous chloride (SnCl2) (10mg/100g body weight/day for 4 days) to decrease selectively renal cytochrome P450 content through increasing renal heme oxygenase activity. A decrease in renal cytochrome P450-dependent AA metabolites was associated with decreased BP and increased urinary Na+ excretion in 7- but not in 20-week-old SHR rats. Chronic treatment with SnCl2 (10mg/100g body weight twice a week) from 5 to 20 weeks prevented the elevation of BP in SHR rats. Further, the antihypertensive effects of tin persisted for 7 weeks beyond its discontinuation. BP in WKY rats was unaffected by tin. Both the acute and chronic treatment with tin are the first studies to demonstrate amelioration of hypertension in SHR by an intervention which is targeted at a single enzyme system.View full abstractDownload PDF (775K) -
KEN OMATA, KEISHI ABE, HSU-LANG SHEU, KAZUNORI YOSHIDA, EIKATSU TSUTSU ...1992 Volume 166 Issue 1 Pages 93-106
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSOMATA, K., ABE, K., SHEU, H.-L., YOSHIDA, K., TSUTSUMI, E., YOSHINAGA, K., ABRAHAM, N.G. and LANIADO-SCHWARTZMAN, M. Roles of Renal Cytochrome P450-Dependent Arachidonic Acid Metabolites in Hypertension. Tohoku J. Exp. Med., 1992, 166 (1), 93-106 - Cytochrome P450 represents the third metabolic pathway of arachidonic acid giving rise to several biologically active compounds, such as 19-HETE, 20-HETE and EETs and their corresponding DHETs. The kidney is the rich source of these metabolites which have some important biologic actions within the kidney. These metabolites have a wide and contrasting spectrum of biological and renal effects, from vasodilation to vasoconstriction and from inhibition to stimulation of Na-K-ATPase, their relative production rates may influence not only renal hemodynamics but also pro- and anti-hypertensive mechanisms of hypertension. There is increasing evidence that the abnormality of these metabolites in animal models of hypertension. However, sufficient evidence of the physiological and pathophysiological roles of hypertension in man is still lacking.View full abstractDownload PDF (1543K) -
KAZUHISA TAKEUCHI, KEISHI ABE, MINORU YASUJIMA, MAKITO SATO, M. KAZUTA ...1992 Volume 166 Issue 1 Pages 107-122
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSTAKEUCHI, K., ABE, K., YASUJIMA, M., SATO, M., MAEYAMA, K., WATANABE, T., SATO, S., INABA, H. and YOSHINAGA, K. Phosphoinositide Hydrolysis and Calcium Mobilization Induced by Vasopressin and Angiotensin II in Cultured Vascular Smooth Muscle Cells. Tohoku J. Exp. Med., 1992, 166 (1), 107-122-The cellular action of vasoconstrictive hormones, angiotensin II (AII) and Arg8-vasopressin (AVP), on vascular smooth muscle (VSM) in cultured VSM cells from rat mesenteric artery was studied. Both AII and AVP specifically induce a transient increases in cytosolic free calcium independent of extracellular calcium or calcium channels activated by high potassium depolarization in VSM cells loaded with Fura-2. Vasoconstrictive hormones induce a dose-dependency with formation of inositolphosphates. Analysis using high pressure liquid chromatography has shown that AVP stimulates rapid and transient increases in inositol 1, 3, 4-trisphosphate, inositol 1, 4, 5-trisphosphate and inositol 1, 3, 4, 5-tetrakisphosphate within 1 minute. Moreover, a laser-excitation fluorescence system reveals high calcium concentration sites in subsarcolemmal region. These results indicate that, unlike voltage-dependent calcium influx across the cell membrane, AII and AVP induce receptor-mediated increases in cytosolic free calcium via phosphoinositide hydrolysis creating an intracellular messenger for calcium release from intracellular calcium stores.View full abstractDownload PDF (1458K) -
MURRAY EPSTEIN, RODGER D. LOUTZENHISER1992 Volume 166 Issue 1 Pages 123-134
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSEPSTEIN, M. and LOUTZENHISER, R.D. Calcium Antagonists and the Kidney. Tohoku J. Exp. Med., 1992, 166 (1), 123-134 - Recently, attention has focused on the effects of calcium antagonists on renal function. When administered in vitro to the isolated perfused kidney, calcium antagonist exhibit consistant actions permitting characterization of their renal effects. Calcium antagonists do not affect the vasodilated isolated perfused kidney, but they do dramatically alter the response of the kidney to vasoconstrictor agents. In the presence of norepinephrine, calcium antagonists markedly augment glomerular filtration rate but produce only a modest improvement in renal perfusion. Utilizing the isolated perfused hydronephrotic rat kidney model that permits direct visualization of afferent and efferent arterioles, we have demonstrated that this preferential augmentation of glomerular filtration rate is primarily attributable to a selective vasodilation of pre-glomerular vessels. Although the clinical implications of such observations are not yet clear, preliminary studies in experimental animal models indicate that calcium antagonists may exert salutary effects on renal function in clinical settings that are characterized by impaired renal hemodynamics. The possible benefits of calcium antagonists in ameliorating the development of renal dysfunction in patients in whom there is increased risk for the development of acute renal insufficiency remain to be evaluated.View full abstractDownload PDF (1184K) -
GIJSBERT G. GEYSKES, BERRY A.M. VAN SCHAIK, CARLO A. GAILLARD, REIN A. ...1992 Volume 166 Issue 1 Pages 135-146
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSGEYSKES, G.G., VAN SCHAIK, B.A.M., GAILLARD, C.A. and KOOMANS, HA. The Diuretic Effect of Calcium Entry Blockade in Normals and Hypertensive Patients. Tohoku J. Exp. Med., 1992, 166 (1), 135-146 - Calcium entry blockers have been shown to exert hemodynamic and diuretic effects in the kidney. The diuretic effects can be demonstrated most clearly in the isolated perfused kidney, not influenced by compensatory mechanisms such as a lower blood pressure or changes of hormones. However, they can also be shown in vivo in humans. We studied the renal effects of calcium entry blockade after the first dosage and after continued oral dosages of 20mg nicardipine tid in patients with essential hypertension and in normotensive controls. Renal function was determined during maximal free water clearance, allowing estimation of changes in “proximal” and “distal” tubular sodium reabsorption. Results showed a natriuretic effect. In the control subjects, clearance results were compatible with a decrease of proximal and distal tubular reabsorption, but in the hypertensive group natriuresis was mainly achieved by an increase of the glomerular filtration rate and a decrease of fractional distal reabsorption. In both groups the natriuresis occurred concomitantly with a lower blood pressure. The ratio plasma renin activity/plasma aldosterone concentration increased, although nicardipine did not inhibit the increase of plasma aldosterone during angiotensin II infusion. Pre-treatment with the calcium entry blocker nitrendipine enhanced the natriuretic effect of atrial natriuretic factor (ANF) in sodium replete normal volunteers. Facilitation of sodium excretion by human ANF may be an additional diuretic mechanism of calcium entry blockers.View full abstractDownload PDF (1115K) -
BEN G. ZIMMERMAN, PAULINE C. RAICH1992 Volume 166 Issue 1 Pages 147-154
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSZIMMERMAN, B.G. and RAICH, P.C. Renal Hemodynamics in Canine DOCA-Salt Hypertension: Effect of Calcium Channel Blockade. Tohoku J. Exp. Med., 1992, 166 (1), 147-154 - Systemic arterial blood pressure (BP), renal blood flow (RBF), and renal vascular resistance (RVR) were followed for 3-4 wks during the progression of DOCA-salt hypertension in the conscious dog. Accompanying the gradual increase in BP was an increase in RBF; however, RVR was unchanged. The hypertension was totally reversed 5-7 days after cessation of DOCA-salt treatment, but the increase in RBF persisted, presumably as a result of renal hypertrophy. Renal adrenoceptor blockade with prazosin (6 dogs) and prazosin plus idazoxan (4 dogs) caused a comparable decrease in BP in the normotensive and DOCA-salt hypertensive dog; however, RVR was decreased only in the normotensive. Similar results were obtained during ganglionic blockade with hexamethonium. The i.v. infusion of diltiazem for 1wk restored BP of the hypertensive dog to a normotensive level, and hexamethonium given i.v. had little further effect on either BP or RVR. These results suggest a non-neurogenically mediated mechanism of canine DOCA-salt hypertension that is susceptible to calcium channel blockade.View full abstractDownload PDF (830K) -
B. JACKSON, L. FRANZE, M. WHITTY1992 Volume 166 Issue 1 Pages 155-166
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSJACKSON, B., FRANZE, L. and WHITTY, M. Systemic and Renovascular Hypertension. Tohoku J. Exp. Med., 1992, 166 (1), 155-164 - To ascertain the contribution of systemic hypertension in the progression of renal failure, we have studied the effects of pharmacological treatment of hypertension in rats with the remnant kidney model of renal insufficiency, streptozotocin diabetes, or nephrotoxic serum nephritis. Treatment with the angiotensin converting enzyme (ACE) inhibitor enalapril lowered systemic blood pressure in the remnant kidney and diabetic animals, but did not lower blood pressure in rats with nephrotoxic serum nephritis. Proteinuria was reduced in all three models, and creatinine clearance improved in the remnant kidney and diabetic animals, when compared with untreated controls. In the remnant kidney and diabetic models systemic blood pressure was lowered to a similar degree by treatments with a calcium blocker, with no improvement in either proteinuria, or glomerular filtration rate. Further studies of the long-term effects of enalapril have been undertaken in rats with the two kidney one clip model of hypertension. Rats treated with enalapril had a lower blood pressure and improved survival over one year of treatment, compared with untreated rats. After 1 year of treatment however the clipped kidney was small and fibrotic, and non functional. Following withdrawal of enalapril therapy there was no functional improvement of the clipped kidney. The possibility that ACE inhibitors have a specific intra-renal effect reducing the rate of progression of renal disease now needs confirmation in human studies. In renovascular hypertension however, intra-renal changes induced by ACE inhibitors may cause irreversible renal damage.View full abstractDownload PDF (1213K) -
JUDITH A. WHITWORTH, BENNO U. IHLE, GAVIN J. BECKER, PRISCILLA S. KINC ...1992 Volume 166 Issue 1 Pages 165-183
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSWHITWORTH, J.A., IHLE, B.U., BECKER, G.J. and KINCAID-SMITH, P.S. Preservation of Renal Function in Chronic Renal Failure. Tohoku J. Exp. Med., 1992, 166 (1), 165-183 - Mechanisms of progression of chronic renal failure (CRF) have been well documented in the rat but may not be relevant in man. Factors which may modify clinical CRF include underlying disease, diet, hypertension, intercurrent events, and adverse or beneficial effects of drug therapy. It has been argued that progression in many forms of renal disease is inexorable below a certain level of renal function. In other diseases, eg primary malignant hypertension, analgesic nephropathy, function frequently improves in both the short and long term with appropriate management. Thus knowledge of the nature of the underlying disease is essential in assessing progression. The value of diet in preserving renal function has been debated, particularly the relative roles of protein and phosphate control. In our own unit, a prospective randomized study showed a benefit of protein restriction. Development of accelerated hypertension is an important cause of progression of renal disease and clinical and experimental evidence supports the view that non-accelerated hypertension is also a factor in progression, amenable to treatment. Various intercurrent events may accelerate progression and function may be lost permanently following sepsis, urinary tract obstruction, renal arterial or venous obstruction, hypotension and in some cases pregnancy. Numerous drugs can have deleterious effects on the kidney. The possibility that converting enzyme inhibitors might preserve renal function is attracting attention but in view of their side effects their place in therapy should be determined by prospective controlled studies in which the above factors are carefully considered.View full abstractDownload PDF (2255K) -
MAKITO SATO, KEISHI ABE, KAZUHISA TAKEUCHI, MINORU YASUJIMA, NAOKI AKI ...1992 Volume 166 Issue 1 Pages 185-200
Published: 1992
Released on J-STAGE: August 31, 2006
JOURNAL FREE ACCESSSATO, M., ABE, K., TAKEUCHI, K., YASUJIMA, M., AKIU, N., SAITO, T, and YOSHINAGA, K. Effect of Sulindac on Prostaglandin Synthesis in Human and in Cultured Rat Renal and Vascular Smooth Muscle Cells. Tohoku J. Exp. Med., 1992, 166 (1), 185-200 - To examine the hypothesis that Sulindac does not inhibit renal prostaglandin (PG) synthesis, we investigated the effects of Sulindac and other nonsteroidal anti-inflammatory drugs on PG synthesis in human and in cultured rat renal and vascular smooth muscle (VSM) cells. In 7 patients with chronic glomerular disease, creatinine clearance and proteinuria were not changed by Sulindac but were significantly reduced by diclofenac sodium. However, urinary excretion of PGE2 was decreased by both drugs. In cultured glomerular mesangial (GM), renal papillary collecting tubule (RPCT) and VSM cells from mesenteric artery, indomethacin, tiaprofenic acid, aspirin and ibuprofen inhibited both basal and arachidonic acid (AA)-stimulated PG synthesis dose-dependently. Although sulindac sulfoxide, at the same concentrations, inhibited both basal and AA-stimulated PGE2 synthesis in RPCT cells, it was less potent to inhibit PGI2 synthesis in VSM cells or PGE2 synthesis in GM cells. Active form sulindac sulfide inhibited PG synthesis in all types of cells but its inactive form sulfone did not. We conclude that sulindac inhibits renal PG synthesis but has little effect on renal function. This may be explained by its relatively weak potency on glomerular or vascular PG synthesis inhibition possibly due to the different biotransformation of the sulfoxide to the active sulfide in these cells.View full abstractDownload PDF (1461K)
- |<
- <
- 1
- >
- >|