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AJP - Regulatory, Integrative and Comparative Physiology, Vol 261, Issue 4 1045-R1051, Copyright © 1991 by American Physiological Society
ARTICLES |
M. Lo, C. Julien, C. Barres, F. Boomsma, C. Cerutti, M. Vincent and J. Sassard
Departement de Physiologie et Pharmacologie Clinique, Centre National de la Recherche Scientifique, Unite de Recherche Associee 606, Faculte de Pharmacie, Lyon, France.
To assess the role of the sympathetic nervous system in the development of genetic hypertension, blood pressure (BP) was recorded in conscious adult Lyon hypertensive (LH) and normotensive (LN) rats that had received daily injections of saline or guanethidine at 1-13 wk of age. Guanethidine abolished the pressor response to tyramine, decreased plasma norepinephrine by greater than 70% and plasma 3,4-dihydroxyphenylglycol by approximately 90%, and did not change plasma epinephrine. Bilateral adrenalectomy further reduced plasma norepinephrine to 8 and 5% of control levels in LH and LN rats, respectively. BP was lowered (-7%) in sympathectomized rats, but the mean absolute BP difference between LH and LN rats was unaltered. Despite marked supersensitivity to alpha-adrenoreceptor stimulation, phentolamine induced only a small transient depressor response, which was abolished by adrenalectomy in sympathectomized rats. It is concluded that the sympathetic nervous system is not necessary for the development of hypertension in LH rats. After sympathectomy, circulating catecholamines, which mostly derive from the adrenal medulla, play only a minor role in BP maintenance.
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