Furosemide stimulates renin expression in the kidneys of salt-supplemented rats

Modena, Barbara; Holmer, Stephan; Eckardt, Kai‐Uwe; Schricker, K. Th.; Riegger, Günter A.J.; Kaissling, Brigitte; Kurtz, Armin

doi:10.1007/bf00374901

Cited by 24 publications

(21 citation statements)

References 26 publications

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“…The observation that furosemide increased PRA values and renin mRNA levels is in keeping with several previous papers [1,3,6,12,14] and suggests that inhibition of salt transport by the thick ascending limb of Henl6, including the macula densa, stimulates both renin secretion and renin gene expression. Moreover, we have recently provided evidence that inhibition of macula densa salt transport leads to a recruitment of renin producing cells in the kidneys [14].…”

Section: Discussionsupporting

confidence: 90%

“…Moreover, we have recently provided evidence that inhibition of macula densa salt transport leads to a recruitment of renin producing cells in the kidneys [14]. The observation that clipping of one renal artery increased renin secretion as indicated by the elevated PRA values confirms previous in vivo and in vitro reports [15,17].…”

Section: Discussionsupporting

confidence: 83%

“…Meanwhile it has been well established that the macula densa exerts a negative control function on renin secretion [9,11,20] and further evidence suggests that the macula densa function participates in the control of renin secretion by the renal perfusion pressure [20]. There is accumulating evidence that inhibition of macula densa function by loop diuretics such as furosemide not only stimulate renin secretion but also renin gene expression [1,3,6,12] even in salt-balanced rats [14]. These findings prompted us to examine a possible participation of the macula densa mechanism in the change of renal renin gene expression upon unilateral renal artery stenosis for the following reasons.…”

Section: Introductionmentioning

confidence: 99%

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Role of the macula densa in the control of renal renin gene expression in two-kidney/one-clip rats

et al. 1994

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Abstract. This study was designed to examine whether macula densa function is involved in the changes of renal renin gene expression upon acute hypoperfusion of one kidney. To block macula densa function, rats with free access to salt and water were subcutaneously infused with furosemide (12 mg/day) for 6 days. Then, 4 days after the start of the infusion, the left renal arteries were clipped with 0.2-ram silver clips and renin mRNA levels in ipsilateral and contralateral kidneys, as well as plasma renin activities (PRA), were determined 48 h after clipping. In non-clipped animals furosemide increased PRA from 10 to 47 ng angiotensin I 9 h -1 9 ml 1 and raised renin mRNA levels in both kidneys 2.5-fold. In vehicle-infused animals, clipping of the left renal artery increased PRA to 37 ng angiotensin I. h -l. m1-1 and led to a 5-fold rise of renin mRNA levels in the ipsilateral kidneys and to a suppression to 20% of the control values in the contralateral kidneys. PRA values in clipped and furosemide-infused animals were 45 ng angiotensin I. h 1. ml-'. In these animals renin mRNA levels increased in the ipsilateral kidneys to similar absolute values as in vehicle-infused rats, whilst contralateral renin mRNA levels fell to about 25% of the respective controls. These findings indicate that the stimulations of renin gene expression by inhibition of macula densa salt transport and by renal artery clipping are not additive, suggesting that the macula densa mechanism may participate in the stimulation of renin gene expression upon hypoperfusion. The macula densa mechanism, however, appears to be not essentially involved in the suppression of renin gene expression in the contralaterals to stenosed kidneys.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

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Role of the macula densa in the control of renal renin gene expression in two-kidney/one-clip rats

et al. 1994

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“…The Na + /K + /2Cl -cotransporter possesses a high affinity for Na + and K + , such that minimal alterations in transport occur with physiological changes of Na + or K + concentrations; however, the affinity for chloride is lower and falls within the range of loop chloride values, thereby resulting in an uptake mechanism that is very sensitive to any change in luminal chloride (12). The role of the Na + /K + /2Cl -cotransport in this macula densa sensing is further supported by the observation that loop diuretics, which inhibit Na + /K + /2Cl -cotransport, increase renin activity, even in the absence of volume depletion (8,13,14).…”

Section: Introductionmentioning

confidence: 97%

Role of p38 in the regulation of renal cortical cyclooxygenase-2 expression by extracellular chloride

Cheng¹,

Wang²,

Zhang³

et al. 2000

J. Clin. Invest.

123

120

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“…How this intrarenal pressure-related mechanism works to determine the number of renin cells, is not understood in detail. It is conceivable that the macula densa could play a mediator function in this context (58,120,130). The macula densa cells express cyclooxygenase 2 (COX-2), and some lines of evidence suggest an involvement of COX-2 and prostaglandin E 2 (PGE 2 ), which should favor recruitment of renin cells.…”

Section: Plasticity Of Renin Productionmentioning

confidence: 99%

Plasticity of renal endocrine function

Kurt

Kurtz

2015

American Journal of Physiology-Regulatory, Integrative and Comp

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The kidneys are important endocrine organs. They secrete humoral factors, such as calcitriol, erythropoietin, klotho, and renin into the circulation, and therefore, they are essentially involved in the regulation of a variety of processes ranging from bone formation to erythropoiesis. The endocrine functions are established by cells, such as proximal or distal tubular cells, renocortical interstitial cells, or mural cells of afferent arterioles. These endocrine cells are either fixed in number, such as tubular cells, which individually and gradually upregulate or downregulate hormone production, or they belong to a pool of cells, which display a recruitment behavior, such as erythropoietin-and reninproducing cells. In the latter case, regulation of humoral function occurs via (de)recruitment of active endocrine cells. As a consequence renin-and erythropoietin-producing cells in the kidney show a high degree of plasticity by reversibly switching between distinct cell states. In this review, we will focus on the characteristics of renin-and of erythropoietin-producing cells, especially on their origin and localization, their reversible transformations, and the mediators, which are responsible for transformation. Finally, we will discuss a possible interconversion of renin and erythropoietin expression.calcitriol; erythropoietin; klotho; renin THE KIDNEYS FULFILL A VARIETY of functions, such as elimination of waste products of metabolism, regulation of fluid volume, and electrolyte concentrations and acid-base balance. Besides these excretory and homeostatic functions, the kidneys are endocrine organs essentially involved in the regulation of bone mineralization, blood pressure, and erythropoiesis. Thereto, the kidneys produce and secrete the hormones calcitriol, erythropoietin (EPO), klotho, and renin.Klotho, which exists in a membranous and a secreted form, regulates calcium and phosphate homeostasis (67, 83,129), thus contributing to bone mineralization. Membrane klotho functions mainly as a coreceptor for fibroblast growth factor (FGF) 23 (85, 178), which causes phosphaturia (85) and decreases circulating calcitriol levels (187) and renal phosphate resorption, resulting in reduced plasma phosphate levels. In its soluble form (66, 110), klotho mediates enhanced Ca 2ϩ (re)absorption in the kidney and in the intestine, by activating TRPV5 and TRPV6 (21, 23) channels. Missense mutations or deficiency of klotho result in hyperphosphatemia, hypercalcemia, and vascular calcification (64, 84,95,157).Calcitriol (34,35,138), the physiologically active form of vitamin D, contributes to bone mineralization by regulating homeostasis of calcium and phosphate through acting on the intestinal tract and the kidneys. Besides its role in regulation of calcium and phosphate homeostasis, calcitriol contributes to erythropoiesis (5, 48), as well as the activity of monocytes and macrophages (30). In contrast, proliferation and activity of T-lymphocytes and, thus, the adaptive immunity are suppressed by calcitriol (30). Vitamin D defi...

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Furosemide stimulates renin expression in the kidneys of salt-supplemented rats

Cited by 24 publications

References 26 publications

Role of the macula densa in the control of renal renin gene expression in two-kidney/one-clip rats

Role of the macula densa in the control of renal renin gene expression in two-kidney/one-clip rats

Role of p38 in the regulation of renal cortical cyclooxygenase-2 expression by extracellular chloride

Plasticity of renal endocrine function

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