Vasopressin Release Following Microinjection of Angiotensin II into the Caudal Ventrolateral Medulla Oblongata in the Anaesthetized Rabbit.
Abstract Stimulation of the caudal ventrolateral medulla in rats and rabbits elicits secretion of vasopressin from the neurohypophysis. Inhibition of the area attenuates baroreceptor-initiated vasopressin secretion. Angiotensin II receptor binding sites and angiotensin-like immunoreactive nerve terminals are localized in the caudal ventrolateral medulla, in the region of the A1 noradrenaline-synthesizing neurons. To examine the possible functional role of angiotensin II in this region, we have microinjected angiotensin II into the A1 area in the urethane-anaesthetized rabbit. Microinjection of angiotensin II (0.1 to 100 pmol in 100 nl) stimulated vasopressin secretion (plasma vasopressin concentration increased from 24 +/- 8 pg/ml to 104 +/- 8 pg/ml following microinjection of 10 pmol angiotensin II) and produced a depressor response with bradycardia. The responsive area was confined to the region of the A1 cell group. AII responses were blocked by prior intramedullary injection of an angiotensin II receptor antagonist, [Sar(1), Thr(8)] angiotensin II (2 nmol in 200 nl), which had no effect on the response to the excitatory amino-acid N-methyl-D-aspartate. Following spinal blockade of efferent sympathetic activity, microinjections of angiotensin II into the caudal ventrolateral medulla caused a similar increase in plasma vasopressin concentration without a depressor response, demonstrating that the stimulation of vasopressin release by angiotensin II was not secondary to hypotension. Microinjection of [Sar(1), Thr(8)] angiotensin II dramatically attenuated the normal secretion of vasopressin in response to systemic haemorrhage. Following injection of vehicle into the caudal ventrolateral medulla, haemorrhage stimulated an increase in plasma vasopressin concentration from 3 +/- 1 pg/ml to 335 +/- 75 pg/ ml (n = 5). After microinjection of [Sar(1), Thr(8)] angiotensin II the haemorrhage-induced change in vasopressin concentration was only 17 +/- 6 pg/ml to 35 +/- 7 pg/ml (n = 4). Microinjection of the N-methyl-D-aspartate receptor antagonist, DL-amino-5-phosphonovaleric acid (5 nmol, n = 4), did not alter the secretion of vasopressin in response to haemorrhage. These results in the anaesthetized rabbit suggest that angiotensin II in the caudal ventrolateral medulla may have a physiological role in baroreceptor control of vasopressin release.
Allen
A M
AM
Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, 3084 Austrialia.
Mendelsohn
F A
FA
Gierobat
Z J
ZJ
Blessing
W W
WW