Hypertension, Vol 6, 675-681, Copyright © 1984 by American Heart Association
RG Carroll, TE Lohmeier and AJ Brown
Sympathetic nerve activity and in particular renal sympathetic nerve
activity were monitored in six conscious dogs subjected to 6 days of
intravenous angiotensin (ANG II) infusion (20 ng/kg/min). This was
accomplished by measurement of both arterial and renal venous plasma
catecholamine concentration. During the initial 4 hours of ANG II infusion,
mean arterial pressure (MAP) increased 35 +/- 8 mm Hg from a control value
of 101 +/- 4 mm Hg. Although there were no significant changes in arterial
plasma norepinephrine (NE) concentration at this time (control = 148 +/- 40
pg/ml), arterial plasma epinephrine (E) concentration increased threefold
(control 42 +/- 15 pg/ml). After 24 hours of ANG II infusion, MAP remained
elevated (132 +/- 5 mm Hg), but plasma E concentration returned to control
levels. From Days 2 through 6 of ANG II infusion, MAP was elevated
approximately 40 mm Hg, but there were no chronic increases in either
arterial plasma E or NE concentrations. In contrast to arterial plasma
catecholamine concentration, renal vein plasma NE concentration (control =
216 +/- 27 pg/ml) actually decreased during both the acute (122 +/- 12
pg/ml) and chronic (103 +/- 26 pg/ml) phases of ANG II infusion. Moreover,
renal NE overflow (renal venous plasma NE concentration-arterial plasma NE
concentration X effective renal plasma flow), an index of renal sympathetic
nerve activity, was depressed during the chronic phase of ANG II
hypertension. These results, therefore, do not support the contention that
the sympathetic nervous system mediates the hypertension produced by
elevated plasma levels of ANG II.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Chronic angiotensin II infusion decreases renal norepinephrine overflow in conscious dogs
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