Endothelin mediates some of the renal actions of acutely administered angiotensin II

Citation
A. Riggleman et al., Endothelin mediates some of the renal actions of acutely administered angiotensin II, HYPERTENSIO, 38(1), 2001, pp. 105-109
Citations number
28
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
HYPERTENSION
ISSN journal
0194-911X → ACNP
Volume
38
Issue
1
Year of publication
2001
Pages
105 - 109
Database
ISI
SICI code
0194-911X(200107)38:1<105:EMSOTR>2.0.ZU;2-7
Abstract
Recent studies suggest that endogenous endothelin mediates much of the vaso constrictor activity and vascular fibrotic damage caused by chronic adminis tration of angiotensin II. The present study uses the mixed endothelin-A an d endothelin-B receptor antagonist bosentan and the endothelin-A-selective blocker BQ-123 to study the contribution of endogenous endothelin to the pr essor and renal action of acutely administered angiotensin II in conscious, chronically catheterized rats. Exposure to angiotensin II at 0.48 pmol 0.5 ng/100 g body weight per min IV (low dose) and 1.91 pmol 2.0 ng/100 g body weight per min IV (high dose) raised mean arterial blood pressure (18 +/-4 mmHg, P <0.01, and 39 +/-4 mm Hg, P <0.005, respectively) while also incre asing renal vascular resistance (4.3 +/-1 mm Hg/mL per min, P <0.001, and 1 0 +/-1 mm Hg/mL per min, P <0.001, respectively). In the presence of bosent an, pressor and renal vasoconstrictor responses to low-dose angiotensin II were blunted (P <0.02 and P <0.01, respectively), and the results with BQ-1 23 were similar. In contrast, these parameters were unaffected during high- dose angiotensin II infusion+bosentan, although BQ-123 did selectively redu ce the rise in renal vascular resistance, possibly via an endothelin B-medi ated nitric oxide effect. In contrast, high-dose angiotensin II caused natr iuretic and diuretic effects that were completely prevented by bosentan. Th ese results show that endothelin (via endothelin A) contributes to the pres sor and renal vasoconstrictor actions of acutely administered low-dose angi otensin 11. Furthermore, our data suggest that the previously described ang iotensin II-induced natriuresis and diuresis observed with a high pressor d ose of angiotensin II is mediated by endothelin.