Dilatation by angiotensin II of the rat femoral arterial bed in vivo via pressure/flow‐induced release of nitric oxide and prostaglandins

Abstract

1 The haemodynamic e ects of angiotensin II (AII) and, for comparison, arginine vasopressin (AVP) in the femoral and superior mesenteric artery of urethane-anaesthetized rats were analysed with the ultrasonic transit time shift technique. 2 I.v. bolus injection of AII (0.1 ± 3 nmol kg 71 ) and AVP (0.03 ± 1 nmol kg 71 ) increased blood pressure which was accompanied by a decrease in blood¯ow through the superior mesenteric artery and an increase in femoral blood¯ow. The femoral hyperaemia was in part due to vasodilatation as indicated by a rise of femoral vascular conductance up to 200% relative to baseline. The femoral vasodilatation caused by AVP, but not AII, was followed by vasoconstriction. 3 Blockade of angiotensin AT 1 receptors by telmisartan (0.2 ± 20 mmol kg 71 ) prevented all haemodynamic responses to AII. 4 The femoral dilator responses to AII and AVP depended on the increase in vascular perfusion pressure since vasodilatation was reversed to vasoconstriction when blood pressure was maintained constant by means of a gravity reservoir. However, the AII-evoked femoral vasodilatation was not due to an autonomic or neuroendocrine re¯ex because it was not depressed by hexamethonium (75 mmol kg 71 ), prazosin (0.25 mmol kg 71 ) or propranolol (3 mmol kg 71 ). 5 The AII-induced femoral vasodilatation was suppressed by blockade of nitric oxide (NO) synthesis with N G -nitro-L-arginine methyl ester (L-NAME, 40 mmol kg 71 ) and reversed to vasoconstriction when L-NAME was combined with indomethacin (30 mmol kg 71 ), but was left unaltered by antagonism of endothelin ET A/B receptors with bosentan (37 mmol kg 71 ). 6 These results demonstrate that the e ect of AII to increase systemic blood pressure and the resulting rise of perfusion pressure in the femoral artery stimulates the formation of NO and prostaglandins and thereby dilates the femoral arterial bed. This local vasodilator mechanism is su cient to mask the direct vasoconstrictor response to AII.

Interaction of Endothelial Nitric Oxide and Angiotensin in the Circulation

“…Heinemann et al (1997) found that an intravenous bolus injection of ANG II increased blood pressure, which was accompanied by a decrease in blood flow through the mesenteric artery and an increase in femoral blood flow; telmisartan prevented all hemodynamic responses to ANG II. The femoral vasodilator response to ANG II was reversed to vasoconstriction when blood pressure was maintained at a constant level, and it was also suppressed by L-NAME and reversed to vasoconstriction by combined treatment with L-NAME and indomethacin.…”

“…Bayraktutan and Ulker (2003) suggested that ANG II stimulates NO production in rat coronary microvascular endothelial cells in both an AT 1 -and AT 2 -receptorregulated manner. Heinemann et al (1997) noted that intravenous injections of ANG II increased blood pressure, which was accompanied by a decrease in blood flow through the superior mesenteric artery and an increase in femoral blood flow, possibly due to vasodilatation; telmisartan prevented all of the hemodynamic responses, and the ANG II-evoked femoral vasodilatation was suppressed by L-NAME. The femoral vasodilator response to ANG II depended on the increase in vascular perfusion pressure, because vasodilatation was reversed to vasoconstriction when blood pressure remained constant.…”

Characterization of a Model of an Arteriovenous Fistula in the Rat

“…22 Rats were anesthetized with an intraperitoneal injection of Inactin (100 mg/kg) and placed on a heated surface to maintain body temperature at 37°C. Following exposure of the femoral vessels via an inguinal incision and dissection of the vessels from surrounding tissues, a 0.7-mm probe was placed on the arterial limb of the AVF or femoral artery in the sham-operated rat using acoustical couplant gel to ensure proper signal capture according to the manufacturer's recommendation.…”

Vasopressin reverses mesenteric hyperemia and vasoconstrictor hyporesponsiveness in anesthetized portal hypertensive rats

“…15 First, the absolute values for MAP, MBF, and MVR at baseline and after the administration of a drug were compared between PVL and SHAM rats. Second, hemodynamic effects of the drugs were expressed as changes relative to baseline as a measure of vascular reactivity, 13,15 and then compared between the two groups.…”

“…[12][13][14][15] The flow probe was factory-calibrated and contained two ultrasonic transducers. Wide beams of ultrasound pass back and forth for the full width of the vessel, alternately intersecting the flowing blood in upstream and downstream direction.…”