PARTICIPATION OF ADENOSINE IN THE RENAL HEMODYNAMIC ABNORMALITIES OF HYPOTHYROIDISM

To investigate the participation of adenosine (ADO) in the abnormaliti es of renal function associated with hypothyroidism, glomerular hemody namics were evaluated in normal (N1) and 2-wk thyroidectomized (Htx) r ats. Studies were performed before and during intravenous infusion of the ADO blocker 1,3-dipropyl-8-p-sulfophenyl xanthine (PSPX, 20 mM, 1. 2 ml/h), intra-aortic ADO (100 nmol . kg(-1). min(-1)), or vehicle. In addition, single-nephron glomerular filtration rate (SNGFR) was measu red during the infusion of different intrarenal ADO doses (1, 10, and 35 nmol . kg(-1). min(-1)); plasma and renal content of ADO were measu red by high-performance liquid chromatography in additional groups. De creased SNGFR, glomerular blood flow (Q(A)), and ultrafiltration coeff icient (K-f) were found in Htx rats. PSPX did not modify glomerular he modynamics in N1 rats; in contrast, in Htx rats, the antagonist increa sed SNGFR, Q(A), and K-f, with a fall in afferent (R(A)) and efferent (R(E)) resistances. ADO infusion in N1 rats produced. renal vasoconstr iction characterized by a fall in SNGFR, Q(A), and K-f, with an increa sed R(A) and R(E). Paradoxically, in Htx rats, ADO increased SNGFR, Q( A), and K-f, decreasing R(A) and R(E). However, when ADO was infused t hrough the renal artery, it induced a 20% reduction of SNGFR at 1 nmol . kg(-1). min(-1) that rose to control values at 10 nmol . k(-1). min (-1) and increased to 38.3% at 35 . k(-1). min(-1). Renal ADO content was markedly low in Htx rats (4.37 +/- 0.79 and 115.46 +/- 14.9 nmol/g wet wt for Htx and N1 rats, respectively). Renal vasodilation induced by PSPX in Htx rats suggests predominant activation of A(1) receptors in this condition. The vasodilatory response to exogenous ADO suggest s additional activation of A(2) receptors.