AJP - Heart and Circulatory Physiology, Vol 258, Issue 5 1375-H1381, Copyright © 1990 by American Physiological Society
Ventricular hypertrophy and presynaptic regulation of sympathetic function
P. G. Schmid, C. A. Whiteis and D. D. Lund
Veterans Affairs Medical Center, Cardiovascular Center, Iowa City, Iowa.
In normal heart, presynaptic cholinergic muscarinic and alpha 2-adrenergic
mechanisms contribute to regional variations in the rate constant of
norepinephrine turnover (kNE), an index of sympathetic neural function. To
evaluate these mechanisms in the hypertrophied heart, pulmonary
artery-constricted and sham-operated guinea pigs were pretreated with 1)
saline vehicle (control) or 2) a combination of quinuclidinyl benzilate
(Q), a muscarinic cholinergic antagonist, and yohimbine (Y), an alpha
2-adrenergic antagonist. An increase in kNE was determined in multiple
regions of heart from incorporation of radiolabeled tyrosine into
norepinephrine during a control period at 24 degrees C and again at 4
degrees C. In sham animals, kNE during cold stress was increased
significantly (P less than 0.05) by Q + Y compared with vehicle, confirming
that muscarinic cholinergic and/or alpha 2-adrenergic receptors exert a
negative-feedback influence on sympathetic neurotransmitter synthesis. In
pulmonary artery-constricted animals, in contrast, there were smaller
increases in cardiac kNE compared with sham guinea pigs given Q + Y and
subjected to cold stress. These data support the concept that muscarinic
cholinergic and/or alpha 2-adrenergic presynaptic regulation of cardiac
sympathetic function is altered in the hearts and vasculature of pulmonary
artery-constricted guinea pigs.
