Mg. Sanderford et Vs. Bishop, Angiotensin II acutely attenuates range of arterial baroreflex control of renal sympathetic nerve activity, AM J P-HEAR, 279(4), 2000, pp. H1804-H1812
Citations number
36
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Acutely increasing peripheral angiotensin II (ANG II) reduces the maximum r
enal sympathetic nerve activity (RSNA) observed at low mean arterial blood
pressures (MAPs). We postulated that this observation could be explained by
the action of ANG II to acutely increase arterial blood pressure or increa
se circulating arginine vasopressin (AVP). Sustained increases in MAP and i
ncreases in circulating AVP have previously been shown to attenuate maximum
RSNA at low MAP. In conscious rabbits pretreated with an AVP V1 receptor a
ntagonist, we compared the effect of a 5-min intravenous infusion of ANG II
(10 and 20 ng.kg(-1).min(-1)) on the relationship between MAP and RSNA whe
n the acute pressor action of ANG II was left unopposed with that when the
acute pressor action of ANG II was opposed by a simultaneous infusion of so
dium nitroprusside (SNP). Intravenous infusion of ANG II resulted in a dose
-related attenuation of the maximum RSNA observed at low MAP. When the acut
e pressor action of ANG II was prevented by SNP, maximum RSNA at low MAP wa
s attenuated, similar to that observed when ANG II acutely increased MAP. I
n contrast, intravertebral infusion of ANG II attenuated maximum RSNA at lo
w MAP significantly more than when administered intravenously. The results
of this study suggest that ANG II may act within the central nervous system
to acutely attenuate the maximum RSNA observed at low MAP.