Does angiotensin enhance the vasoconstrictor response to noradrenaline and sympathetic stimulation in cat mesenteric blood vessels?
Angiotensin potentiates vasoconstriction by inhibiting noradrenaline uptake at nerve endings and facilitating its direct action on smooth muscle cells.
The effect of angiotensin on the response to postganglionic sympathetic stimulation was studied in isolated and perfused cat mesenteric blood vessels. Angiotensin perfusion enhanced the vasoconstrictor response to sympathetic nerve stimulation and shifted to the left the dose–response curve of noradrenaline; this potentiating effect persisted even after a return to an angiotensin-free perfusion medium. In chronically denervated preparations, angiotensin increased the effect of noradrenaline, but no persistence of this effect was observed after a return to angiotensin-free medium. The effect of angiotensin was also studied on the uptake of 3 H-noradrenaline by measuring the amount of radioactive amine disappearing from the perfusion medium during its passage through the mesenteric blood vessels or by assaying the accumulated radioactive amine in the tissue after perfusion. Angiotensin significantly inhibited the uptake of 3 H-noradrenaline measured by these two methods. It is suggested that angiotensin increases the vasoconstrictor responses to noradrenaline administration as well as to sympathetic nerve stimulation (a) by an inhibitory effect on noradrenaline uptake by nerve endings, and (b) by a facilitation of noradrenaline action directly on the smooth muscle cells.
Panisset et al. (Fri,) studied this question.