Plasma Norepinephrine Level in Affective Disorders

BackgroundThe sympathetic arterial baroreflex is a closed-loop feedback system for stabilizing arterial pressure (AP). Identification of unique functions of the closed system in humans is a challenge. Here we propose an analytic and integrative framework for identifying a static operating point and open-loop gain to characterize sympathetic arterial baroreflex in humans.Methods and ResultsAn equilibrium diagram with two crossing functions of mechanoneural (MN) and neuromechanical (NM) arcs was analyzed during graded tilt maneuvers in seven healthy subjects. AP and plasma norepinephrine level (PNE), as a surrogate for sympathetic nerve activity, and were recorded after vagal modulation of heart function was blocked by atropine. The MN-arc curve was described as a locus of operating points during –7, 0, 15, and 60° head-up tilting (HUT) on a PNE-AP plane. The NM-arc curve was drawn as a line between operating points before and after ganglionic blockade (trimethaphan, 0.1 mg⋅ml–1⋅kg–1) during 0° or 15° HUT. Gain values were estimated from the slopes of these functional curves. Finally, an open-loop gain, which is a most important index for performance of arterial baroreflex, was given by a product of the gain values of MN (GMN) and NM arcs (GNM). Gain values of MN was 8.92 ± 3.07 pg⋅ml−1⋅mmHg−1; and GNM at 0° and 15° HUT were 0.61 ± 0.08 and 0.36 ± 0.05 mmHg⋅ml⋅pg–1, respectively. A postural change from supine to 15° HUT significantly reduced the open-loop gain from 5.62 ± 0.98 to 3.75 ± 0.62. The effects of HUT on the NM arc and open-loop gain seemed to be similar to those of blood loss observed in our previous animal studies.ConclusionAn equilibrium-diagram analysis contributes to a quantitative and integrative understanding of function of human sympathetic arterial baroreflex.

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Effects of intense exercise training on plasma catecholamines in coronary patients

Journal of Applied Physiology ◽

10.1152/jappl.1984.57.1.154 ◽

1984 ◽

Vol 57 (1) ◽

pp. 154-159 ◽

Cited By ~ 27

Author(s):

Ali A. Ehsani ◽

Gregory W. Heath ◽

Wade H. Martin ◽

James M. Hagberg ◽

John O. Holloszy

Keyword(s):

Blood Pressure ◽

Exercise Training ◽

Maximal Exercise ◽

Plasma Catecholamines ◽

Arterial Disease ◽

Rate Pressure Product ◽

Plasma Norepinephrine ◽

Norepinephrine Level ◽

Coronary Arterial Disease ◽

Plasma Norepinephrine Level

This paper reports the effect of 12 mo of intense endurance exercise training on the plasma catecholamine response to exercise in 11 male patients [aged 50 ± 8 yr (mean ± SD)] with coronary artery disease. A substantial adaptation to training was attained as evidenced by a 42% increase in maximum O2uptake capacity. At rest, heart rate was lower after training, but resting blood pressure and plasma catecholamines were unchanged. At the same absolute work rate, plasma norepinephrine and epinephrine levels, rate pressure product, and ischemic S-T segment depression were all significantly lower aftertraining. A higher plasma norepinephrine level was attained at maximal exercise after training (2,049± 654 before vs. 3,408 ± 1,454 pg/ml after, P < 0.025); this was associated with a higher systolic blood pressure (175 ± 25 before vs. 188 ± 22 mmHg after, P < 0.025) and a higher rate-pressure product (25.3 x 103 ± 4.5 x 103 before vs. 27.6 x 103 ± 5.2 x 103 after, P < 0.025). Despite the higher plasma norepinephrine level and rate pressure product, S-T segment depression at maximal exercise was unchanged. These findings suggest that some patients with coronary arterial disease can attain a higher myocardial O2 requirement, without electrocardiographic evidence of increased ischemia, after prolonged strenuous exercise training. myocardial infarction; coronary arterial disease Submitted on July 5, 1983 Submitted on July 5, 1983

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