title: Cardiopulmonary reflex before and after regression of left ventricular hypertrophy in essential hypertension.
abstract: Studies that have examined the cardiopulmonary receptor control of circulation in hypertension have produced conflicting results. In 10 normotensive subjects and in age-matched essential hypertensive subjects without (n = 10) or with left ventricular hypertrophy (n = 12), as well as in seven subjects of the latter group restudied after 1 year of treatment that induced regression of cardiac hypertrophy, we examined the cardiopulmonary reflex by increasing central venous pressure and stimulating cardiopulmonary receptors through passive leg raising and by reducing central venous pressure and deactivating cardiopulmonary receptors through nonhypotensive lower body negative pressure. Reflex responses were measured as changes in forearm vascular resistance (mean blood pressure divided by plethysmographically measured blood flow), plasma norepinephrine concentration, and plasma renin activity. In hypertensive subjects without left ventricular hypertrophy, stimulation and deactivation of cardiopulmonary receptors caused changes in forearm vascular resistance, norepinephrine concentration, and plasma renin activity that were modestly reduced as compared with those in normotensive subjects. However, all these changes were markedly reduced in hypertensive subjects with left ventricular hypertrophy. Following regression of left ventricular hypertrophy, the changes in vascular resistance, plasma norepinephrine, and plasma renin activity induced by cardiopulmonary receptor manipulation all improved markedly. These results demonstrate that cardiopulmonary receptor regulation of peripheral vascular resistance and of neurohumoral variables is impaired in essential hypertension and that the impairment is much more pronounced when this condition is associated with cardiac structural alterations. Therapeutic regression of these alterations, however, leads to a marked improvement of this reflex, with consequent favorable effects on circulatory homeostasis.
authors.affiliation: Cattedra di Semeiotica Medica, Università di Milano, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Grassi
authors.forename: C
authors.initials: C
authors.lastname: Giannattasio
authors.forename: J
authors.initials: J
authors.lastname: Cléroux
authors.forename: C
authors.initials: C
authors.lastname: Cuspidi
authors.forename: L
authors.initials: L
authors.lastname: Sampieri
authors.forename: G B
authors.initials: GB
authors.lastname: Bolla
authors.forename: G
authors.initials: G
authors.lastname: Mancia
mesh_terms: D000328:Adult; D001158:Arteries / Q000294:innervation; D001794:Blood Pressure; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology*; D002496:Central Venous Pressure; D003080:Cold Temperature; D005260:Female; D005665:Furosemide; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D007866:Leg / Q000503:physiopathology; D008150:Lower Body Negative Pressure; D008168:Lung / Q000503:physiopathology*; D008297:Male; D011187:Posture; D011311:Pressoreceptors / Q000503:physiopathology; D012018:Reflex / Q000502:physiology*
chemical_list: D005665:Furosemide