Mechanism of renin release following furosemide diuresis in rabbit

Meyer, Philippe; Ménard, J; Papanicolaou, N.; Alexandre, Jonas; Devaux, C; Milliez, P

doi:10.1152/ajplegacy.1968.215.4.908

Cited by 120 publications

(52 citation statements)

References 14 publications

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“…I confirm Fidone & Sato's (1970) observation that with stimulating electrodes near to the slip from which recordings were made, and with the stimulus parameters used by Neil & O'Regan (1971) Frusemide (4-chloro-2-furfurylamino-5-sulphamoyl benzoic acid) is a powerful natriuretic agent which causes a rise in plasma renin levels in rabbits (Meyer et al 1968), and dogs (Vander & Carlson, 1969). In the present study, changes in peripheral renin levels were investigated in nonpregnant ewes, pregnant ewes and their foetuses (age range 110-150 days), after i.v.…”

Section: Psupporting

confidence: 77%

Communications

1972

The Journal of Physiology

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interpreted on the above model (Fig. 2) by means of an analogue computer, assuming that k32, kL4 and M/Na3(0) terms could be neglected. The ratio of Na2(0)/Na3(0) was that predicted from autoradiographic data (Dick et al. 1970) and the rate constants for Li movements were assumed to be onetenth those for Na (Keynes & Swan, 1959). There is quite close correlation between the computed curves and the experimental points.

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Section: Psupporting

confidence: 77%

Communications

1972

The Journal of Physiology

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“…Although Gottschalk has shown that dilution of the urine is virtually complete before the tubular fluid enters the distal convolutions (28), which suggests that chlorothiazide acts, as does ethacrynic acid, proximal to the site of the macula densa, the greater reduction of CH20 produced by ethacrynic acid (29) and its additional inhibitory effect upon TCH2o both suggest that more sodium is delivered in higher concentrations to the distal convolutions by ethacrynic acid than by chlorothiazide. Furthermore, Clapp and Robinson observed, in micropuncture studies (30), that the mean distal osmolal TF/P ratio after furosemide administration, which produces effects that are comparable to those of ethacrynic acid (31) furosemide administration in their studies on rabbits in which volume changes were excluded as in our reinfusion studies with ethacrynic acid (10). The possibility that ethacrynic acid produces a stimulus for renin release as a result of its action on tubular sodium transport is further suggested by our findings in the studies performed with ureteral occlusion.…”

Section: Resultsmentioning

confidence: 58%

“…There is also some evidence that sodium balance influences renin release (4)(5)(6). In addition, several studies have recently suggested that the mechanism controlling the release of renin is responsive to changes in tubular fluid sodium (7)(8)(9)(10). However, the data from these studies have appeared to be contradictory in some aspects.…”

Section: Introductionmentioning

confidence: 99%

The effect of altered sodium concentration in the distal nephron segments on renin release

Cooke¹,

Brown²,

Zacherle³

et al. 1970

J. Clin. Invest.

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A B S T R A C T Ethacrynic acid, a potent inhibitor of sodium reabsorption in the ascending limb of Henle's loop, produces a sharp rise in renal venous renin activity within 5 min after intravenous administration in anesthetized dogs. This response persists when volume depletion is prevented by returning urinary outflow to the femoral vein. Comparable studies with chlorothiazide, a diuretic with little or no effect on the medullary portion of the ascending limb of the loop of Henle, failed to produce a significant increase in renal venous renin activity.When administered during ureteral occlusion, ethacrynic acid produced no change in renal venous renin activity until ureteral occlusion was released and flow restored. Following release of the ureters, a prompt rise in renal venous renin was again observed within 5 min of release. Control studies of ureteral occlusion yielded a fall in renal venous renin activity following release of the ureter without administration of ethacrynic acid. These studies identify a prompt stimulatory effect of ethacrynic acid on renin release that is unrelated to volume depletion but dependent upon the presence of tubular urine flow. Although further definition of the site and characteristics of the distal tubular mechanism for stimulation of renin release requires more direct study, the data presented here indicate that changes in sodium concentration in distal tubular fluid serve as a stimulus for renin release.

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“…The increase in renin release on furosemide reportedly is inhibited in the presence of nonspecific or specific nNOS blockers (137), yet furosemide did not affect renal nNOS gene expression in healthy rats (139). Conversely, furosemide can reduce renin release by increased luminal Na ϩ concentration at the level of the macula densa (105,138). That leaves uncertainty about the net effect of furosemide on renin release.…”

Section: Are Direct Vascular Actions Of Furosemide Important and Whatmentioning

confidence: 99%

Everything we always wanted to know about furosemide but were afraid to ask

Huang

Mees

Vos

et al. 2016

American Journal of Physiology-Renal Physiology

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Huang X, Dorhout Mees E, Vos P, Hamza S, Braam B. Everything we always wanted to know about furosemide but were afraid to ask. Am J Physiol Renal Physiol 310: F958 -F971, 2016. First published February 24, 2016 doi:10.1152/ajprenal.00476.2015.-Furosemide is a widely used, potent natriuretic drug, which inhibits the Na ϩ -K ϩ -2Cl Ϫ cotransporter (NKCC)-2 in the ascending limb of the loop of Henle applied to reduce extracellular fluid volume expansion in heart and kidney disease. Undesirable consequences of furosemide, such as worsening of kidney function and unpredictable effects on sodium balance, led to this critical evaluation of how inhibition of NKCC affects renal and cardiovascular physiology. This evaluation reveals important knowledge gaps, involving furosemide as a drug, the function of NKCC2 (and NKCC1), and renal and systemic indirect effects of NKCC inhibition. Regarding renal effects, renal blood flow and glomerular filtration rate could become compromised by activation of tubuloglomerular feedback or by renin release, particularly if renal function is already compromised. Modulation of the intrarenal renin angiotensin system, however, is ill-defined. Regarding systemic effects, vasodilation followed by nonspecific NKCC inhibition and changes in venous compliance are not well understood. Repetitive administration of furosemide induces short-term (braking phenomenon, acute diuretic resistance) and long-term (chronic diuretic resistance) adaptations, of which the mechanisms are not well known. Modulation of NKCC2 expression and activity in kidney and heart failure is ill-defined. Lastly, furosemide's effects on cutaneous sodium stores and on uric acid levels could be beneficial or detrimental. Concluding, a considerable knowledge gap is identified regarding a potent drug with a relatively specific renal target, NKCC2, and renal and systemic actions. Resolving these questions would increase the understanding of NKCCs and their actions and improve rational use of furosemide in pathophysiology of fluid volume expansion. extracellular fluid volume; natriuresis; renal function; chronic kidney disease; heart failure DIURETICS BLOCKING THE Na ϩ -K ϩ -2Cl Ϫ cotransporter (NKCC) have an important place in the treatment of fluid overload, specifically in the context of kidney disease and heart failure (64). Of the drugs that inhibit the NKCC2 in the loop of Henle (furosemide, bumetanide, torsemide, ethacrynic acid), furosemide is most commonly applied (66) and Ͼ40 million prescriptions are dispensed every year in the USA (66a). However, many uncertainties remain about intrarenal and systemic actions of furosemide, including its two main targets NKCC1 and NKCC2.Clinically, there are a number of undesirable consequences of the use of furosemide, of which the pathophysiological mechanisms have not been sufficiently investigated. Furosemide has been associated with worsening of kidney function in patients treated for volume overload admitted for acute heart failure (104) and even glomerular filtration rate (GFR) ...

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Mechanism of renin release following furosemide diuresis in rabbit

Cited by 120 publications

References 14 publications

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The effect of altered sodium concentration in the distal nephron segments on renin release

Everything we always wanted to know about furosemide but were afraid to ask

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