DILATATION BY ANGIOTENSIN-II OF THE RAT FEMORAL ARTERIAL BED IN-VIVO VIA PRESSURE FLOW-INDUCED RELEASE OF NITRIC-OXIDE AND PROSTAGLANDINS/

1 The haemodynamic effects of angiotensin IT (AII) and, for comparison , arginine vasopressin (AVP) in the femoral and superior mesenteric ar tery of urethane-anaesthetized rats were analysed with the ultrasonic transit time shift technique. 2 I.v, bolus injection of AII (0.1-3 nmo l kg(-1)) sind AVP (0.03-1 nmol kg(-1)) increased blood pressure which was accompanied by a decrease in blood flow through the superior mese nteric artery and an increase in femoral blood flow. The femoral hyper aemia was in part due to vasodilatation as indicated by a rise of femo ral vascular conductance up to 200% relative to baseline. The femoral vasodilatation caused by AVP, but not AII, was followed by vasoconstri ction. 3 Blockade of angiotensin AT(1) receptors by telmisartan (0.2-2 0 mu mol kg(-1)) prevented all haemodynamic responses to AII. 4 The fe moral dilator responses to AII and AVP depended on the increase in vas cular perfusion pressure since vasodilatation was reversed to vasocons triction when blood pressure was maintained constant by means of a gra vity reservoir. However, the AII-evoked femoral vasodilatation was not due to an autonomic or neuroendocrine :reflex because it was not depr essed by hexamethonium (75 mu mol kg(-1)), prazosin (0.25 mu mol kg(-1 )) or prapranolol (3 mu mol kg(-1)). 5 The AII-induced femoral vasodil atation was suppressed by blockade of nitric oxide (NO) synthesis with NG-nitro-L-arginine methyl ester (L-NAME, 40 mu mol kg(-1)) and rever sed to vasoconstriction when L-NAME was combined with indomethacin (30 mu mol kg(-1)), but was left unaltered by antagonism of endothelin ET A/B receptors with bosentan (37 mu mol kg(-1)). 6 These results demons trate that the effect of AII to increase systemic blood pressure and t he resulting rise of perfusion pressure in the femoral artery stimulat es the formation of NO and prostaglandins and thereby dilates the femo ral arterial bed. This local vasodilator mechanism is sufficient to ma sk the direct vasoconstrictor response to AII.