title: Cardiopulmonary receptor regulation of renin release.
abstract: Cardiopulmonary receptors have been shown to modulate renin release in animals. However, their involvement in reflex control of renin in humans has never been unequivocally established. This report reviews data on the effects on plasma renin activity of maneuvers (lower body negative pressure and passive leg raising) that reduce and increase central venous pressure and cardiac diameter without affecting blood pressure and heart rate, thereby deactivating and stimulating cardiopulmonary receptors with little or no involvement of the arterial baroreceptors. In normotensive subjects, reduction in central venous pressure was accompanied by an increase in plasma renin activity that was similar to the increase observed during tilt that reduced central venous pressure to a similar extent. Conversely, an increase in central venous pressure was accompanied by a reduction in plasma renin activity. The increase in plasma renin activity that followed the reduction in central venous pressure was drastically attenuated in four patients who had undergone cardiac transplantation, along with other reflex effects (changes in forearm vascular resistance and plasma norepinephrine) of cardiopulmonary receptor manipulations. There was a modest reduction in the overall reflex changes in plasma renin activity in patients with mild to moderate essential hypertension compared with normotensive subjects. However, patients with essential hypertension and cardiac hypertrophy showed marked attenuation of all reflex influences of the cardiopulmonary receptors. In five subjects, therapeutic regression of this structural alteration was associated with a clear improvement in the cardiopulmonary reflex. Thus, in humans, cardiopulmonary receptors exert an important reflex control of renin release. This control (which is due in part to receptors located in the cardiac walls) is moderately affected by a mild to moderate blood pressure elevation but is markedly impaired when the elevation produces structural alterations in the heart. Preliminary evidence, however, suggests that the cardiopulmonary reflex may be improved by a reduction in cardiac hypertrophy.
authors.affiliation: Instituto di Clinica Medica Generale e Terapia 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: C
authors.initials: C
authors.lastname: Cuspidi
authors.forename: G B
authors.initials: GB
authors.lastname: Bolla
authors.forename: J
authors.initials: J
authors.lastname: Cléroux
authors.forename: P
authors.initials: P
authors.lastname: Ferrazzi
authors.forename: R
authors.initials: R
authors.lastname: Fiocchi
authors.forename: G
authors.initials: G
authors.lastname: Mancia
mesh_terms: D000818:Animals; D001794:Blood Pressure; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology; D002496:Central Venous Pressure; D006321:Heart / Q000502:physiology; D006339:Heart Rate; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology; D008150:Lower Body Negative Pressure; D009638:Norepinephrine / Q000097:blood; D011187:Posture; D011311:Pressoreceptors / Q000502:physiology*; D012083:Renin / Q000097:blood*
chemical_list: D012083:Renin; D009638:Norepinephrine