Hypertension, Vol 9, 582-590, Copyright © 1987 by American Heart Association
BD King, D Sack, MR Kichuk and TH Hintze
To better define the mechanisms of blood pressure control in states of
catecholamine excess, we infused norepinephrine for 28 days using
subcutaneously implanted osmotic pumps in dogs previously instrumented for
monitoring left ventricular dynamics and cardiac output. Plasma
norepinephrine rose from 238 +/- 27 to 4346 +/- 952 pg/ml at 21 days, while
epinephrine and dopamine levels did not change. Heart rate fell from 85 +/-
4 to 63 +/- 6 beats/min, while arterial pressure was unchanged from
baseline. Total peripheral resistance rose 0.011 +/- 0.003 mm Hg/ml/min
from a control value of 0.029 +/- 0.002 mm Hg/ml/min, and cardiac output
decreased 1093 +/- 292 ml/min from a baseline level of 3575 +/- 156 ml/min.
Since stroke volume did not change, the maintenance of arterial pressure is
related to decreases in cardiac output secondary to bradycardia. Buffering
mechanisms are responsible for maintenance of systemic arterial pressure
because hexamethonium and atropine caused hypertension. Although left
ventricular end-diastolic pressure, end-diastolic diameter, shortening,
rate of change of pressure, velocity of myocardial shortening, cardiac
work, stroke work, and the double product did not change significantly
during the study, postmortem examination demonstrated biventricular
hypertrophy. Thus, despite markedly elevated catecholamine levels and no
elevation of systemic arterial pressure, myocardial hypertrophy developed.
These studies lend support to the hypothesis that norepinephrine may be a
direct myocardial tropic hormone and suggest that intense activation of
reflex buffering mechanisms maintains blood pressure in the normal range
during chronic catecholamine infusion.
ARTICLES
Absence of hypertension despite chronic marked elevations in plasma norepinephrine in conscious dogs
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