Aims: 

Urotensin II (U II) is known as the most potent mammalian vasoconstrictor identified and may play a role in aetiology of essential hypertension. We have investigated the possible role of this peptide in modulating vascular responses to adrenergic stimuli in normotensive and spontaneously hypertensive rats (SHR) and compared them with the action of angiotensin II (ANG II), which has similar physiological functions in blood vessels.

Methods: 

Isolated arterial rings (rat main pulmonary and superior mesenteric artery) was set up for isometric tension recording. Adrenergic contractions were elicited by endogenous noradrenaline released from electrically stimulated (4 Hz) perivascular nerves and by exogenous noradrenaline applied to incubation medium.

Results: 

The presence of U II in bathing solution caused inhibition of neurogenic contractions in similar extent as of those elicited by exogenous noradrenaline. There was no significant difference in this effect observed in normotensive and spontaneously hypertensive rats. In contrast, ANG II enhanced the contractile responses of arteries to transmural nerve stimulation. It has, however, no influence on contractions evoked by exogenous noradrenaline. Potentiation of neurogenic contractions by ANG II was less extensive in vessels from SHR compared with those from normotensive Wistar rats.

Conclusion: 

These results suggested that modulation of neurogenic contractions in main pulmonary and mesenteric artery by U II and ANG II is mediated by different mechanisms.