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PLASMA CATECHOLAMINES AND ADRENOCEPTORS AFTER CHRONIC SINOAORTIC DENERVATION IN DOGS
Author(s) -
VALET P.,
DAMASEMICHEL C.,
MONTASTRUC J.L.,
MONTASTRUC P.
Publication year - 1989
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.1989.tb00459.x
Subject(s) - medicine , endocrinology , blood pressure , catecholamine , yohimbine , heart rate , baroreceptor , denervation , platelet , adrenergic receptor , receptor , chemistry , antagonist
Summary— Chronic sinoaortic denervation (SAD) performed by section of both carotid and aortic nerves induced a significant and sustained increase in blood pressure and heart rate in conscious dogs; under our experimental conditions, the values of systolic blood pressure and heart rate were never lower than 190 mmHg and 120 beats/min, respectively. The present long‐term study (8 mo) investigated the time‐course of plasma catecholamine levels and circulating blood cell adrenoceptor (leukocyte beta 2 and platelet alpha 2 ) number. Catecholamine plasma levels were highly correlated with the variations of leukocyte beta adrenoceptors (measured by [ 125 I]cyanopindolol binding and characterized as a beta 2 receptor in dogs). These two parameters followed a biphasic pattern after SAD: during the first 2 mo, significant increases in noradrenaline and adrenaline levels were associated with a decrease in leukocyte beta 2 adrenoceptor number; from the 4th month, they slowly returned to normal values, although blood pressure remained elevated. By contrast, platelet alpha 2 adrenoceptor number (measured by [ 3 H]yohimbine binding) did not follow this pattern since it remained lower than before SAD during the whole experiment. Finally, the development (but not the maintenance) of SAD‐induced hypertension is associated with an increase in sympathetic tone. Only leukocyte beta 2 (and not platelet alpha 2 ) adrenoceptors are directly regulated by the endogenous levels of catecholamines.