title: Cardiogenic reflexes and left ventricular hypertrophy.
abstract: Studies performed in both animal and human species have shown that receptors anatomically located in the cardiac walls and in the pulmonary vascular bed exert a powerful influence on sympathetic vasoconstrictor tone and renin release from the kidney. This paper will review recent data collected by our group on the effects on this homeostatic reflex function of two different models of cardiac hypertrophy, i.e. that associated with arterial hypertension and that induced by prolonged physical training. It will also examine whether and to what extent cardiopulmonary reflex control of circulation can be restored after an effective antihypertensive pharmacological treatment has induced a regression of the structural alterations of the heart. The results of these studies suggest that cardiopulmonary reflex control of circulation is markedly impaired in the presence of cardiac hypertrophy, with (severe hypertensive subjects) or without (athletes) high blood pressure values. In hypertensives, furthermore, therapeutic regression of cardiac hypertrophy seems to restore, although not fully normalize, this reflex function. Taken together these findings suggest that cardiac hypertrophy, per se, is a condition characterized by the loss of the reflex functions exerted by cardiac receptors, with adverse consequences on cardiovascular homeostasis.
authors: Cattedra di Semeiotica Medica, Università di Milano, Italy.
authors: G
authors: G
authors: Grassi
authors: C
authors: C
authors: Giannattasio
authors: G
authors: G
authors: Seravalle
authors: B M
authors: BM
authors: Cattaneo
authors: J
authors: J
authors: Cléroux
authors: G
authors: G
authors: Mancia
mesh_terms: D000328:Adult; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology*; D005081:Exercise Therapy; D006321:Heart / Q000294:innervation*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D011311:Pressoreceptors / Q000502:physiology*; D012018:Reflex / Q000502:physiology*