Differential Reactivity of Cortical and Juxtamedullary Glomeruli to Adenosine-1 and Adenosine-2 Receptor Stimulation and Angiotensin-Converting Enzyme Inhibition

Dietrich, Maximilian; Steinhausen, M.; Dussel, R.

doi:10.1006/mvre.1993.1012

Cited by 26 publications

(29 citation statements)

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“…Additionally, the presence of ANG II (10 Ϫ11 or 10 Ϫ14 M) did not affect adenosineinduced constriction, suggesting a lack of interaction between these agents in this preparation. Although we are unable to exclude the possibility of such an interaction in OMDVR, these results support those of Dietrich and Steinhausen who found cortical but not juxtamedullary dependence of A 1 receptor stimulation on the renin-angiotensin system in glomerular arterioles (25). In summary, our data indicate an ability for adenosine to modulate OMDVR vascular tone through both A 1 and A 2 receptors.…”

Section: Discussionsupporting

confidence: 73%

“…Those receptor subtypes mediate selective effects on the renal vasculature. Stimulation of the A 1 receptor produces afferent arteriolar vasoconstriction (11,12,24) and a reduction in glomerular filtration rate (19) while A 2 receptor stimulation yields efferent and afferent arteriolar vasodilatation (24,25). In our hands, stimulation by adenosine or CGS-21680, an A 2 receptor agonist, consistently vasodilates ANG II-preconstricted OMDVR (Figs.…”

Section: Discussionmentioning

confidence: 67%

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Adenosine modulates vasomotor tone in outer medullary descending vasa recta of the rat.

Silldorff¹,

Kreisberg²,

Pallone³

1996

J. Clin. Invest.

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Adenosine is generated within the renal medulla under hypoxic conditions and is known to induce net vasoconstriction within the renal cortex while increasing medullary blood flow and oxygenation. To test the hypothesis that vasoconstriction of outer medullary descending vasa recta (OMDVR) is modulated by adenosine, we examined the effects of adenosine and adenosine A 1 and A 2 receptor subtype agonists on in vitro perfused control and preconstricted rat OMDVR. Constriction with angiotensin II (ANG II, 10 Ϫ 9 M) was attenuated by adenosine in a concentration-dependent manner (EC 50 to 10 Ϫ 5 M) elicited a biphasic response. Additionally, cyclohexyladenosine (10 Ϫ 6 M) caused vasoconstriction and CGS-21680 (10 Ϫ 6 M) had no effect on untreated vessels. Finally, an influence of ANG II receptor stimulation on adenosine A 1 receptor-mediated vasoconstriction could not be shown. These data suggest that OMDVR possess both A 1 and A 2 adenosine receptors and that they mediate constriction and dilatation, respectively. We conclude that adenosine is a potent modulator of OMDVR vasomotor tone and that its net effect is dependent upon local concentrations. ( J. Clin. Invest. 1996. 98:18-23.)

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 67%

Adenosine modulates vasomotor tone in outer medullary descending vasa recta of the rat.

Silldorff¹,

Kreisberg²,

Pallone³

1996

J. Clin. Invest.

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“…In this experimental model adenosine induced a preglomerular constriction, when applied topically from the interstitial side, which was most prominent in the distal part of the afferent arterioles (64). With the use of adenosine agonists and antagonists with different receptor subtype specificity, the data supported the concept that activation of adenosine A 1 receptors leads to constriction mainly of afferent arterioles near the glomerulus, whereas adenosine A 2 receptor activation leads to dilation mainly of the postglomerular arteries (65,90,133). Another study in the isolated perfused hydronephrotic rat kidney preparation provided evidence for both adenosine-induced constriction and dilation of afferent arterioles, and these effects were dependent on activation of adenosine A 1 and A 2a /A 2b receptors, respectively (327).…”

Section: Adenosine Effects On Pre-and Postglomerular Arteriessupporting

confidence: 67%

“…The vasoconstrictive action of exogenous and endogenous adenosine can be antagonized by angiotensin II receptor antagonists (64,207,249,320). Likewise, inhibitors of angiotensin I converting enzyme can block adenosine-induced renal vasoconstriction (65). The assumed interaction of angiotensin II and adenosine in preglomerular vessels was confirmed in dogs (106,107).…”

Section: Dietary Nacl Status and Renin-angiotensin Systemmentioning

confidence: 92%

Adenosine and Kidney Function

Vallon

Mühlbauer²,

Oßwald³

2006

Physiological Reviews

401

379

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In this review we outline the unique effects of the autacoid adenosine in the kidney. Adenosine is present in the cytosol of renal cells and in the extracellular space of normoxic kidneys. Extracellular adenosine can derive from cellular adenosine release or extracellular breakdown of ATP, AMP, or cAMP. It is generated at enhanced rates when tubular NaCl reabsorption and thus transport work increase or when hypoxia is induced. Extracellular adenosine acts on adenosine receptor subtypes in the cell membranes to affect vascular and tubular functions. Adenosine lowers glomerular filtration rate (GFR) by constricting afferent arterioles, especially in superficial nephrons, and acts as a mediator of the tubuloglomerular feedback, i.e., a mechanism that coordinates GFR and tubular transport. In contrast, it leads to vasodilation in deep cortex and medulla. Moreover, adenosine tonically inhibits the renal release of renin and stimulates NaCl transport in the cortical proximal tubule but inhibits it in medullary segments including the medullary thick ascending limb. These differential effects of adenosine are subsequently analyzed in a more integrative way in the context of intrarenal metabolic regulation of kidney function, and potential pathophysiological consequences are outlined.

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“…Huang et al found that adenosine generated by both ecto-5′-nucleotidase-dependent and -independent mechanisms participated in mediation of TGF in vivo [25]. We and others have shown that adenosine constricts the Af-Art and dilates the Ef-Art via activation of the A 1 and A 2 receptor, respectively [26][27][28][29]. In vitro, using an isolated double-perfused Ef-Art and distal tubule containing the macula densa, we have shown that decreasing adenosine formation by blocking 5′-nucleotidase inhibits Ef-Art TGF, while increasing adenosine formation by enhancing ATP hydrolysis augments Ef-Art TGF.…”

mentioning

confidence: 73%

Cross-talk between arterioles and tubules in the kidney

et al. 2009

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In hypertension the pressure natriuresis set point is shifted to a higher pressure due to an increase in both renal vascular resistance and sodium (Na) reabsorption. The afferent arterioles (Af-Arts) and efferent arterioles (Ef-Arts) account for most renal vascular resistance; they control glomerular filtration rate (GFR) and peritubular pressure, and, consequently, renal function. Af-Art and Ef-Art resistance is regulated by factors similar to those in other arterioles and also by tubuloglomerular feedback (TGF). TGF operates via the macula densa, which senses increases in sodium chloride (NaCl) and sends a signal that constricts the Af-Art and dilates the Ef-Art. In the outer renal cortex, the connecting tubule (CNT) returns to the glomerular hilus and contacts the Af-Art. This morphology is compatible with cross-talk between the CNT and Af-Art, so-called connecting tubule glomerular feedback (CTGF). Our studies show that increasing NaCl delivery to the CNT results in Af-Art dilatation that can be blocked by inhibitors of Na transport. We believe cross-talk between the CNT and Af-Art is a novel mechanism that may contribute to regulation of renal blood flow and GFR. KeywordsAfferent arteriole; Macula densa; Connecting tubule; Tubuloglomerular feedback; Na transporterThe afferent arteriole (Af-Art) accounts for most renal vascular resistance. It controls glomerular filtration rate (GFR) and peritubular pressure, and consequently renal function. The hormonal and neural influences on vascular resistance that participate in the control of blood flow and GFR have been fairly well defined. Anatomical contact between the end of the thick ascending limb of the loop of Henle and its own glomerulus was described for the first time more than 100 years ago. In each nephron of the mammalian kidney, the tubule returns to the hilus of the parent glomerulus, forming the juxtaglomerular apparatus (JGA). The JGA is made up of (a) a plaque of specialized tubular epithelial cells called the macula densa; (b) the extraglomerular mesangium; and (c) the glomerular Af-Art and efferent arteriole (Ef-Art). This anatomical connection is thought to be crucial for tubuloglomerular feedback (TGF) control of GFR [1][2][3]. Therefore, Af-Art resistance is regulated not only by factors similar to those in other arterioles but also by the macula densa. TGF describes a functional connection between the tubular epithelium at the site of the macula densa and the underlying smooth muscle cells of the Af-Art and Ef-Art. An increase or decrease in sodium chloride (NaCl) concentration in the luminal fluid at the macula densa cells activates arteriolar constriction or dilation, respectively, and hence alters single-nephron GFR (SNGFR).Experimental studies of TGF began with the microinjection experiment designed and initiated by Klaus Thurau [4]. After the proximal segments belonging to the same nephron had been © IPNA 2008 Correspondence to: YiLin Ren, yren1@hfhs.org. Thomson and Blantz [9] evaluated the ability of TGF to stabilize tubula...

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Differential Reactivity of Cortical and Juxtamedullary Glomeruli to Adenosine-1 and Adenosine-2 Receptor Stimulation and Angiotensin-Converting Enzyme Inhibition

Cited by 26 publications

References 0 publications

Adenosine modulates vasomotor tone in outer medullary descending vasa recta of the rat.

Adenosine modulates vasomotor tone in outer medullary descending vasa recta of the rat.

Adenosine and Kidney Function

Cross-talk between arterioles and tubules in the kidney

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