Purinergic regulation of basal and arginine vasopressin-stimulated hydraulic conductivity in rabbit cortical collecting tubule

Dillingham, Mark A.

doi:10.1007/bf01871091

Cited by 29 publications

(10 citation statements)

References 19 publications

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“…2 In the isolated, perfused rabbit collecting tubule, NECA has been shown to stimulate hydraulic conductivity. 90 Anand-Srivastava et al 91 demonstrated that NECA increases adenylyl cyclase activity in isolated segments of dog medullary thick ascending limb and collecting tubule. Furthermore, recent preliminary data indicate that adenosine A[ receptor activation results in a decrease in transtubular voltage in isolated cortical thick ascending limb, suggesting a direct action on sodium transport.…”

Section: Excretory and Tubular Epithelial Effects Of Adenosinementioning

confidence: 99%

Adenosine receptors and signaling in the kidney.

1991

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It is now generally accepted that adenosine is capable of regulating a wide range of physiological functions. Nowhere is the diversity of this action better illustrated than in the kidney. When adenosine binds to plasma membrane receptors on a variety of cell types in the kidney, it stimulates functional responses that span the entire spectrum of renal physiology, including alterations in hemodynamics, hormone and neurotransmitter release, and tubular reabsorption. These responses to adenosine appear to represent a means by which the organ and its constituent cell types can regulate their metabolic demand such that it is maintained at an appropriate level for the prevailing metabolic supply. Extracellular adenosine, produced from the hydrolysis of adenosine 5'-monophosphate and stimulated by increased substrate availability and enzyme induction, acts on at least two types of cell surface receptors to stimulate or inhibit the production of cyclic adenosine-3',5'-monophosphate and also acts in some renal cells to stimulate the production of inositol phosphates and elevation of cytosolic calcium concentration. To understand when and why this complicated system becomes activated, how it interacts with other known extracellular effector systems, and ultimately how to manipulate the system to therapeutic advantage by selective agonists or antagonists, requires a detailed knowledge of renal adenosine receptors and their signaling mechanisms. The following discussion attempts to highlight our knowledge in this area, to present a modified hypothesis for adenosine as a feedback regulator of renal function, and to identify some important questions regarding the specific cellular mechanisms of adenosine in renal cell types. T he kidney, like many organs, is endowed with intrinsic mechanisms that allow it to self-regulate many of its functions. Two well-known examples are the relatively constant glomerular filtration rate (GFR) and renal blood flow over a wide range of arterial pressure (i.e., autoregulation) and the ability to release renin in response to changes in renal perfusion pressure independent of neural or humoral signals. It was the search to understand the renal mechanism responsible for this intrinsic regulation that prompted investigators to turn their interest toward adenosine. Previous reviews 1 -5 have dealt specifically with a proposed role for adenosine in the control of GFR and renin release. Although this may have prompted much of the original interest in intrarenal adenosine, recent investigations have revealed adenosine to have a much broader regulatory role. The present discussion focuses From the Departments of Physiology and Biochemistry, Michigan State University, East Lansing, Mich.

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Section: Excretory and Tubular Epithelial Effects Of Adenosinementioning

confidence: 99%

Adenosine receptors and signaling in the kidney.

1991

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“…Elucidation of the renal tubular effects of adenosine is complicated by hormonally induced changes in hemodynamics and glomerular filtration rate that can mask direct effects of adenosine. Nevertheless, adenosine has been shown to antagonize vasopressin-stimulated water reabsorption in the cortical collecting duct (CCD)' (2) and inner medullary collecting duct (3), to stimulate Na+-phosphate and Na+-glucose transport in opossum kidney cells (4), and to inhibit the transepithelial voltage across isolated cortical thick ascending limbs of Henle's loop (5), suggesting a direct inhibitory action on sodium chloride reabsorption.…”

Section: Introductionmentioning

confidence: 99%

Adenosine regulates a chloride channel via protein kinase C and a G protein in a rabbit cortical collecting duct cell line.

Schwiebert¹,

Karlson²,

Friedman³

et al. 1992

J. Clin. Invest.

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“…Adenosine is involved in renal haemodynamics because it reduces renal blood flow (Hall et al, 1985;Arend et al, 1987;Gouyon & Guignard, 1989), in glomerular filtration rate (Churchill, 1982;Hall et al, 1985;Arend et al, 1987;Pawloska et al, 1987), in urine flow (Churchill, 1982;Dillingham & Anderson, 1985;Collis et al, 1986) and in sodium and potassium excretion rate (Churchill, 1982;Collis et al, 1986). Adenosine promotes glomerular constriction related to the entry of calcium into glomerular cells (Lopez-Novoa et al, 1987;Olivera et al, 1989).…”

Section: Introductionmentioning

confidence: 99%