RENAL VASCULAR REACTIVITY TO ATP IN HYPERTHYROID AND HYPOTHYROID RATS

Citation
F. Vargas et al., RENAL VASCULAR REACTIVITY TO ATP IN HYPERTHYROID AND HYPOTHYROID RATS, Experientia, 52(3), 1996, pp. 225-229
Citations number
23
Categorie Soggetti
Multidisciplinary Sciences
Journal title
ISSN journal
00144754
Volume
52
Issue
3
Year of publication
1996
Pages
225 - 229
Database
ISI
SICI code
0014-4754(1996)52:3<225:RVRTAI>2.0.ZU;2-Z
Abstract
The effects of adenosine triphosphate (ATP) on the renal vasculature o f isolated kidneys from control, hyper- and hypothyroid rats were char acterized. ATP responsiveness was evaluated in basal tone and in raise d tone (phenylephrine 10(-6) M) preparations. These responses were com pared with those obtained with barium chloride or sodium nitroprusside (SNP), used respectively as nonreceptor agonists for vasoconstriction or vasodilation. In preparations at basal tone, ATP produced dose-rel ated vasoconstriction, which was increased in hyperthyroid kidneys, an d was severely attenuated in kidneys from hypothyroid rats. In raised tone preparations from control rats ATP produced a dual response: vaso constriction at low doses, which declined with increasing doses to giv e way to vasodilator responses; biphasic responses were found in some kidneys. Hyperthroid kidneys showed increased presser responses and a vasodilator response similar to those seen in kidneys from control rat s. However, in hypothyroid kidneys the vasodilator response was abolis hed. The responses to barium chloride and to SNP were significantly in creased and decreased in hyper- and hypothyroid kidneys, respectively; vasoconstrictor responses to SNP were also found in hypothyroid kidne ys. Hence the abnormal responses to ATP observed in both thyroid dysfu nctions may be partially explained by unspecific alterations in the co ntractile machinery of the renal vasculature in these kidneys. However , ATP responsiveness (vasoconstriction at low tone and vasodilation at raised tone) was more severely affected in hypothyroid kidneys, sugge sting that purinergic (P-2X and P-2Y) receptor activity may be decreas ed in these organs.