Dallas, TX 75231 3, 9 February 2006 | Pflügers Archiv - European Journal of Physiology, Vol. Thus, in addition to the possible blunting of A1AR-induced vasoconstriction as discussed above, endothelial dilator factors generated in response to A2AR activation may enhance renal vasodilatation, thereby contributing to the waning renal constriction in the kidney during intravenous administration. B, Some arterioles (37%) exhibit a biphasic response, with dilation followed by constriction. �0@�|ō-�宩ع��K�.ѦՐ�J�H�����x�U��Ё��e4�`U�团�я0eY �''7\����(�g��څ5�0Tt$$�H��5C
���x��g0t����u���f'� During situations of hypoxia, interstitial concentrations of both adenosine and inosine rise, increasing the likelihood of vasoconstriction, since both have been shown to cause constriction in vivo.6 A vasoconstriction would further reduce blood flow to the hypoxic tissue, and such a response would be more damaging to already ischemic tissues. 29, No. Am J Physiol Regul Integr Comp Physiol 277: R1410–R1417, 1999. However, of two antibodies directed against different epitopes, only one showed positive staining, an observation that cautions against overinterpretation of antibody-based evidence. endobj Changes in arteriolar diameter were measured from the videotape using a video caliper (Colorado Video). 1, 30 March 2007 | Cell Death & Differentiation, Vol. Mast cells are stimulated in the course of the response, and the A3 adenosine receptor is involved in mediating constriction. All protocols were approved by the University of Virginia Animal Care and Use Committee. �k�n�n�QX��`4�Ov�q���@#{��Y�ek�s���t�I֟�%qX��ٍn��C��K� �U7�ypOq�:�j�Le!�T�+�.����ҏ�~��S�-�fcc��7O����1
�5� ���C$��v"D�Q7����k���Ϩ_e���f �݂������c� C~Fp4Ї). ��w3T�PI�2T0 BCcC=S3��\. Our results are apparently different from the net vasodilator effect of CHA in the isolated perfused kidney that was seen at perfusate concentrations of 10–5 M and higher (43, 46). These effects consisted of a stable diameter reduction that was dose dependent in the range between 10–8 and 10–6 M and that was most pronounced in the distal part of the arteriole where it caused a maximum effect of about –50%. endstream We conclude that adenosine can cause vasoconstriction in vivo, which is often masked by A2 receptor–mediated vasodilation. endobj <>>>/BBox[0 0 603 783]/Length 128>>stream Fig 5A shows the arteriole immediately before adenosine stimulation. 4, 5 January 2011 | Journal of the American Society of Nephrology, Vol. 3 0 obj Medullary blood flow represents only ∼10% of total renal blood flow. E-mail. 7, 1 May 2007 | American Journal of Physiology-Renal Physiology, Vol. <>stream Because this blood flow response was seen when adenosine was injected in the renal artery, it is not mediated by systemic consequences of adenosine such as a reduction in blood pressure (24, 54). The drug was delivered at a flow rate of 0.05 mL/min, through a side port, into the superfusate (flowing at 5 mL/min) using a syringe pump (model 355, Sage Instruments) to yield a final concentration on the cheek pouch of 25 μmol/L. endstream Further examination of the response in a large number of arterioles showed that although not all arterioles constricted, there was a dose-dependent increase in both the percentage of arterioles that constricted and the degree of constriction. First, previous studies indicate that uptake and metabolism of adenosine are necessary to cause vasoconstriction in isolated arterioles,5 and uptake of adenosine has been proposed as a mechanism by which adenosine facilitates mast cell mediator release.2330 Second, inosine, a metabolite of adenosine, elicits a similar response to adenosine both in vivo and in vitro.56. In view of the normal actions of CHA, the waning effect of adenosine in this preparation may reflect an increased expression of dilatory A2AR. Fig. 6 0 obj �0@�|ō-�宩ع��K�.ѦՐ�J�H�����x�U��Ё��e4�`U�团�я0eY �''7\����(�g��څ5�0Tt$$�H��5C
���x��g0t����u���f'� endstream B, Magnitude of the dilation (open bars) and constriction (stippled bars) for the arterioles shown in panel A (mean±SEM). Cheek pouches were superfused with a bicarbonate-buffered saline solution at 37°C that contained (mmol/L) NaCl 131.9, KCl 4.7, CaCl2 2.0, MgSO4 1.2, and NaHCO3 20.0. Derivatives of adenosine substituted at the N6 position with iodobenzyl, such as I-ABA, are potent agonists of A1 and A3 adenosine receptors.1617 Failure by 100 μmol/L 8-SPT to block the constrictor response indicated that the constriction was not mediated by A1 receptors. endobj Metabolism of adenosine and inosine can result in generation of superoxide radicals by the enzyme xanthine oxidase.31 Superoxide and hydrogen peroxide, which is produced during dismutation of superoxide, stimulate mast cells in vivo and in vitro.3233 It is possible that A3 adenosine receptor occupation facilitates mast cell degranulation induced by oxygen reactive species and that both of these signals could come from adenosine. 5, No. <>stream To quantify the constrictor component of the vasomotor response to adenosine, we applied adenosine (10−6 to 10−4 mol/L) to a number of arterioles and determined the percentage that constricted (Fig 2A). 8 0 obj Although the rat A3 receptor has been called xanthine resistant, high concentrations of certain xanthines will block the receptor; BW-A1433 has been reported to bind to rat A3 receptors with a Ki value of 15 μmol/L.18 In the present study, BW-A1433 (25 μmol/L) was superfused over the cheek pouch, as described, and the vasomotor response to adenosine and I-ABA was measured. ��� endobj The data reported in the present study indicate that dilation is the predominant response to adenosine. 15 0 obj 07, No. 38 0 obj ͐,.�. In addition, adenosine has been shown to play a role in allergy and asthma,911 which are known to involve mast cells. 293, No. <>stream endobj 23 0 obj If the endothelium restricts the movement of adenosine, one would expect differences in receptor accessibility dependent on the route of administration. endstream More recently, immunohistochemical evidence has suggested the presence of A1AR expression in glomerular vessels, presumably in afferent arterioles, and inside the glomerulum, presumably in mesangial cells (71). �� ��
� x�S�*�*T0T0 BCK L�UЏ�4Rp�W�*e� endstream It is also of note that at least in the in situ hydronephrotic kidney model the starting level for the adenosine addition studies are the prevailing tissue and plasma adenosine levels, not an adenosine-free condition. More definitive proof for the involvement of the A3 receptor will require more selective reagents that are not available at the present time. The small magnitude of both constrictor and dilator effects suggests rather low levels of expression for all receptor subtypes. The response to adenosine and inosine was found to be due to stimulation of periarteriolar mast cells and the subsequent release of a vasoconstrictor. Animal temperature was maintained at 37°C using convective heating. 292, No. Renal blood flow distribution measured with microspheres showed an increase in inner cortical blood flow, whereas outer cortical blood flow was unchanged (72).
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