Reflex control of coronary vascular tone by cardiopulmonary receptors in humans.
To examine whether cardiopulmonary receptors participate in the reflex control of coronary vascular resistance, systemic and coronary hemodynamics were assessed before and during -10 mm Hg lower body negative pressure in eight normal subjects and eight hypertensive patients with left ventricular hypertrophy. In both study groups, lower body negative pressure induced a significant decrease in right atrial pressure, left ventricular filling pressure and cardiac output, an increase in systemic vascular resistance and no change in mean arterial pressure and heart rate. In normal subjects, there was also a significant increase in plasma norepinephrine concentration (from 294 +/- 39 to 421 +/- 47 pg/ml, p less than 0.01). This increase was accompanied by a reduction in coronary blood flow, assessed by the continuous thermodilution method (from 101 +/- 5 to 79 +/- 4 ml/min, p less than 0.05). An increase in coronary vascular resistance (from 0.865 +/- 0.1 to 1.107 +/- 0.1 mm Hg/ml per min, p less than 0.05) and in myocardial oxygen consumption was detected in normal subjects during cardiopulmonary baroreceptor unloading. In contrast, in hypertensive patients, -10 mm Hg lower body negative pressure failed to induce any change in plasma norepinephrine, coronary blood flow or vascular resistance. Intravenous propranolol administration caused no significant change in the systemic hemodynamic response to -10 mm Hg lower body negative pressure in either study group, but it did abolish the decrease in coronary flow and the increase in plasma norepinephrine, coronary vascular resistance and myocardial oxygen consumption observed in normal subjects in control conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
Trimarco
B
B
First Institute of Clinical Medicine, Second Faculty of Medicine, University of Naples, Italy.
Vigorito
C
C
Cuocolo
A
A
Ricciardelli
B
B
De Luca
N
N
Volpe
M
M
Lembo
G
G
Condorelli
M
M
D000328:Adult; D000344:Afferent Pathways / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects; D002312:Cardiomyopathy, Hypertrophic / Q000097:blood / Q000150:complications / Q000503:physiopathology; D002339:Carotid Arteries / Q000294:innervation; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000294:innervation*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000097:blood; D010101:Oxygen Consumption / Q000187:drug effects; D011311:Pressoreceptors / Q000187:drug effects / Q000502:physiology*; D011433:Propranolol / Q000494:pharmacology; D012018:Reflex / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014160:Transducers, Pressure; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects
D011433:Propranolol; D009638:Norepinephrine