Continuous production of endothelium-derived nitric oxide (NO) in peripheral vessels has been shown to modulate vascular resistance and blood pressure. NO is also formed in the brain upon activation of glutamate receptors, which are thought to mediate central autonomic reflexes. In the present study we assessed whether NO plays a role in central autonomic regulation. For this, we have investigated the effects of NG-methyl-L-arginine (NMA), a selective inhibitor of NO synthesis from L-arginine, on sympathetic renal nerve activity (RNA), blood pressure, and heart rate in the anesthetized rat. NMA elicited a dose-dependent sustained increase in blood pressure (approximately 20 and 30 mm Hg, 5 minutes after 10 and 50 mumol/kg i.v., respectively). Heart rate and RNA decreased transiently (15 beats per minute and 40%, respectively); RNA subsequently increased (100%) while blood pressure remained elevated. Baroreceptor deafferentation markedly altered these responses to NMA; the transient decreases in heart rate and RNA were abolished, whereas the increases in RNA and blood pressure were significantly potentiated. After spinal C-1-C-2 transection, there was no increase in RNA, and blood pressure increased to a smaller extent. L-Arginine blocked the NMA-induced increases in blood pressure and RNA. Thus, in addition to modulating vascular resistance by a peripheral action, NO may also play a role in the central regulation of sympathetic tone.
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The use of anaerobic threshold in assessment of aerobic capacity was evaluated in 34 normal subjects and 47 patients with various kinds of chronic heart disease. Anaerobic threshold was determined as the oxygen consumption (W02) at which a linear relationship between pulmonary ventilation (yE) and V02 was lost during progressive treadmill exercise. Anaerobic threshold determined in this manner was validated with that determined by blood lactate measurements in eight normal subjects and nine cardiac patients (r = .962, p < .001). Thereafter, anaerobic threshold was determined only by respiratory measurements. In symptom-limited, maximal exercise, anaerobic threshold was reached well before maximal effort and corresponded to 70% of maximal V02 both in normal subjects and cardiac patients. Anaerobic threshold decreased as age progressed in normal subjects (r = -.70, p < .001). Anaerobic threshold in cardiac patients was lower than that in the normal subjects and decreased progressively as New York Heart Association functional classification advanced (normal, 32
A new echo tracking device linked to real time ultrasonic B mode equipment was developed to measure non-invasively the elastic properties of the human abdominal aorta. Pulsatile diameter change and mean diameter of the abdominal aorta were measured in 61 subjects with this ultrasonic device. Strain and pressure-strain elastic modulus Ep were calculated from pulsatile diameter change, diameter, and pulse pressure obtained by the auscultatory method. Strain significantly decreased with age; 0.076(0.024) (mean(SD)) in group 1 (20 young adults below the age of 35 years); 0.048(0.024) in group 2 (21 middle aged subjects between the ages of 35 and 60 years); and 0.030(0.010) in group 3 (20 elderly subjects over the age of 60 years). Ep values were 0.99(0.34) X 10(5), 1.55(0.68) X 10(5), and 3.80(2.05) X 10(5) N X m-2 in groups 1, 2, and 3 respectively. Ep in group 3 was significantly higher than in groups 1 and 2. The regression equation relating Ep to age was Ep = (-0.72 + 0.058 X age) X 10(5) N X m-2 (r = 0.73). The Ep value and its age related increase agreed with the findings in postmortem arteries. The elastic properties of the abdominal aorta could, therefore, be determined non-invasively by this ultrasonic method.
We conclude that angiotensinogen was synthesized in the human heart. It was evident that the localization of angiotensinogen was not ubiquitous in the cardiac muscles, showing its predilection for the atrial muscles, muscles of the conduction system, and subendocardial layer of the left ventricle.
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