Angiotensin nerve endings

Some compensatory responses that occur during congestive heart failure. In addition to the effects shown, sympathetic discharge facilitates renin release, and angiotensin II increases norepinephrine release by sympathetic nerve endings (dashed arrows). 

Figure 6-3. Lcx al integration of ANS control via modulation of transmitter release. In the example shown, release of norepinephrine from a sympathetic nerve ending is modulated by norepinephrine itself, acting on presynaptic autoreceptors, and by acetylcholine and angiotensin II. Many other modulators (see text) influence the release process.

B. Effects Angiotensin II is a potent arteriolar vasoconstrictor and stimulant of aldosterone release. All directly incTeases peripheral vascular resistance and, through aldosterone, causes renal sodium retention. All also facilitates the release of norepinephrine from adrenergic nerve endings via presynaptic heteroreceptor action. All of these effects are mediated by the angiotensin AT, receptor, a G, -coupled receptor. 

Actions of angiotensin are mimetic of the motor actions of either acetylcholine or catecholamines. As discussed below, such actions are due to a direct effect of the peptide on the effector organ or to an indirect action through stimulation of the motor nerves or liberation of chemical transmitters at nerve endings. A brief description of these actions shall be given here. 

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