Intratubul�rer Druck, glomerul�rer Capillardruck und Glomerulumfiltrat nach Furosemid und Hydrochlorothiazid

Krause, H.H.; Dume, Th.; Koch, K. M.; Ochwadt, Bruno

doi:10.1007/bf00363906

Cited by 31 publications

(15 citation statements)

References 13 publications

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“…The decrease in the glomerular filtration rate in the diuretic-treated animals as compared with the lowsodium group may indicate a relatively greater degree of contraction of the extracellular fluid volume. Alternatively, the decrease in the glomerular filtration rate may be attributable to a vasoactive effect of the diuretic (Fernander & Puschett, 1973;Burke et al, 1972;Krase et al, 1967;MartinezMaldonado et al, 1973). In the diuretic-treated animals there was a proportional decrease in whole kidney glomerular filtration rate and single nephron filtration rate, suggesting that redistribution of the glomerular filtrate did not play a major role in the decrease in sodium excretion (Horster & Thurau, 1968).…”

Section: Discussionmentioning

confidence: 96%

Chronic Effects of Chlorothiazide on Reabsorption by the Proximal Tubule of the Rat

Weinman

Eknoyan

1975

Clinical Science

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1. The renal response to a low-sodium diet alone and a low-sodium diet plus the daily oral administration of chlorothiazide was examined in rats. Sodium restriction resulted in a decrease in sodium excretion until day 4, after which it remained constant. The administration of chlorothiazide resulted in an initial natriuresis. By day 6, however, the natriuresis had abated and thereafter sodium excretion remained the same as that of the low sodium group. 2. After the animals were in balance on their respective regimens, clearance and micropuncture studies were performed. The glomerular filtration rate was lower in the chlorothiazide-treated rats than in control rats and/or in the low-sodium group. End proximal tubule TF/Pinulin ratios were higher in the diuretic-treated animals than in control rats. TF/Pinulin ratios in low-sodium animals were lower than in the diuretic-animals but higher than in control rats. 3. These studies demonstrate that the escape from the chronic effects of chlorothiazide is due to a decrease in the glomerular filtration rate and to an increase in fractional reabsorption in the proximal tubule, resulting in a reduction in delivery of filtrate to the cortical diluting segment where chlorothiazide exerts its major inhibitory effect.

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Section: Discussionmentioning

confidence: 96%

Chronic Effects of Chlorothiazide on Reabsorption by the Proximal Tubule of the Rat

Weinman

Eknoyan

1975

Clinical Science

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“…While some studies suggest an acute and probably direct relaxing effect of loop diuretics on venous tone, mean arterial blood pressure does not appear to be systematically altered in the short term before major salt losses have occurred (1,21,33,37). Furthermore, if the renal baroreceptor is located in the JGA region of the afferent arteriole, the renal vasodilatation typically seen with loop diuretics may cause an increase, not a decrease in pressure at the site of the baroreceptor, because it is well established that these agents cause an increase in glomerular capillary pressure (5,23,27). In addition, our studies in the isolated kidney show that the increase in perfusion flow rate caused by bumetanide is only between 5 and 10%, a change that is unlikely to be primarily responsible for the marked increase in renin release.…”

Section: Discussionmentioning

confidence: 99%

Permissive role of nitric oxide in macula densa control of renin secretion

Castrop

Schweda²,

Mizel³

et al. 2004

American Journal of Physiology-Renal Physiology

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Experiments were performed in neuronal (nNOS)-and endothelial nitric oxide synthase (eNOS)-deficient mice to study the role of nitric oxide (NO) in macula densa control of renin secretion in vivo and in the isolated, perfused mouse kidney. Acute and chronic administration of loop diuretics was used as a method to stimulate macula densa-mediated renin secretion. Increases in plasma renin concentration (PRC) in response to a 3-day infusion of bumetanide (50 mg⅐kg Ϫ1 ⅐day Ϫ1 ) or an acute injection of furosemide (50 mg/kg ip) were not markedly altered in nNOSϪ/Ϫ mice. Responses to furosemide were also maintained in eNOSϪ/Ϫ mice, but the administration of N -nitro-L-arginine methyl ester (L-NAME) markedly attenuated the PRC response to furosemide in these mice. In the isolated kidney preparation, bumetanide caused similar relative increases in renin secretion in kidneys of wild-type, nNOSϪ/Ϫ, and eNOSϪ/Ϫ mice. Bumetanide only marginally increased renin secretion in L-NAME-treated kidneys, but the bumetanide effect was normalized by S-nitroso-N-acetyl-penicillamine. Basal PRC was significantly reduced in male nNOSϪ/Ϫ mice compared with nNOSϩ/ϩ (189 Ϯ 28 vs. 355 Ϯ 57 ng ANG I ⅐ml Ϫ1 ⅐h Ϫ1 ; P ϭ 0.017). There was no significant difference in PRC between eNOSϩ/ϩ and eNOSϪ/Ϫ mice. Basal renin secretion rates in perfused kidneys isolated from nNOSϪ/Ϫ or eNOSϪ/Ϫ mice were markedly reduced compared with wild-type controls. Our data suggest that NO generated by macula densa nNOS does not play a specific mediator role in macula densa-dependent renin secretion. However, NO independent of its exact source permits the macula densa pathway of renin secretion to function normally. plasma renin; isolated, perfused kidney; neuronal nitric oxide synthase knockout; endothelial nitric oxide synthase knockout; furosemide; bumetanide THE MACULA DENSA (MD) CELLS LOCATED at the terminal end of the loop of Henle are believed to play an important role in both the regulation of preglomerular resistance and the control of renin secretion. Commensurate with their distinct function as sensor cells in these local regulatory pathways, MD cells have a number of unique characteristics that distinguish them from neighboring cells of the cortical thick ascending limb. One of the more striking of these discriminating features is the expression of substantial amounts of neuronal nitric oxide synthase (nNOS) and the ability to generate nitric oxide (NO) (31, 53).A considerable body of experimental evidence indicates that the expression of nNOS in the MD and the expression and secretion of renin by juxtaglomerular (JG) granular cells are altered in parallel by a variety of interventions. Reductions in oral salt intake (4,42,46, 50), renal hypoperfusion, and pharmacological blockade of Na-K-2Cl cotransport of the thick ascending limb (4, 43) all stimulate the expression of both proteins. Furthermore, changes in NOS activity have been demonstrated to affect renin secretion, and the majority of studies suggest a stimulatory role for NO (4,20,35,40,42). It ha...

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“…Glomerular hydrostatic and oncotic pressures representative of those found in normally hydrated rats (22)(23)(24) are summarized in Table 1. Glomerular capillary hydrostatic pressure was found to be about 45 mm Hg or 40% of mean arterial blood pressure, a value considerably lower than estimates generally obtained using more indirect, stop-flow techniques (27)(28)(29)(30). The drop in 'In the laboratory of Dr. Klaus Thurau of the Physiological Institute, Munich, Germany.…”

Section: = Tt P + R -(2)mentioning

confidence: 82%