EFFECTS OF [SAR(1),ILE(8)]-ANGIOTENSIN-II ON ROSTRAL VENTROLATERAL MEDULLA NEURONS AND BLOOD-PRESSURE IN SPONTANEOUSLY HYPERTENSIVE RATS

Citation
Rkw. Chan et al., EFFECTS OF [SAR(1),ILE(8)]-ANGIOTENSIN-II ON ROSTRAL VENTROLATERAL MEDULLA NEURONS AND BLOOD-PRESSURE IN SPONTANEOUSLY HYPERTENSIVE RATS, Neuroscience, 63(1), 1994, pp. 267-277
Citations number
39
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03064522
Volume
63
Issue
1
Year of publication
1994
Pages
267 - 277
Database
ISI
SICI code
0306-4522(1994)63:1<267:EO[ORV>2.0.ZU;2-7
Abstract
The present study was an attempt to determine the influence of brain a ngiotensin II, the activity of which is known to be higher in spontane ously hypertensive rat, on the spontaneous activity of the cardiovascu lar neurons in the rostral ventrolateral medulla of the spontaneously hypertensive rat. Both the spontaneous activity of the spinal projecti ng rostral ventrolateral medulla cardiovascular neurons and the arteri al blood pressure were simultaneously measured in the pentobarbital-an esthetized spontaneously hypertensive rat and its normotensive control , the Wistar Kyoto rat, following microinjection to rostral ventrolate ral medulla of an angiotensin II antagonist, [Sar(1), Ile(8)]-angioten sin II (sarile). A microinjection method was developed that enabled us to perform extracellular recording of the rostral ventrolateral medul la cardiovascular neuron during the microinjection of drug to the vici nity of the neuron. It was found that sarile reduced both the arterial blood pressure and firing rate of some rostral ventrolateral medulla cardiovascular neurons dose-dependently. The effects of sarile were si gnificantly greater in spontaneously hypertensive rat than in the Wist ar Kyoto rat. The present findings indicate that the rostral ventrolat eral medulla cardiovascular neurons of spontaneously hypertensive rat exhibit an augmented sensitivity to endogenous brain angiotensin II. S uch an increase in sensitivity to brain angiotensin II in the spontane ously hypertensive rat may contribute to the enhanced spontaneous acti vities of rostral ventrolateral medulla cardiovascular neurons, as in the sarile responsive single discharge units, even in the resting or p restimulation state. This interaction of brain angiotensin II and rost ral ventrolateral medulla cardiovascular neurons is likely to be contr ibutory to the genesis of hypertension in this strain of rats.