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Results for “Pressoreceptors/drug effects/physiology”

Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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4 records
All sourcesNASA NTRSDOE OSTI
NASA NTRS1999

Cardiopulmonary baroreceptor control of muscle sympathetic nerve activity in heat-stressed humans

Whole body heating decreases central venous pressure (CVP) while increasing muscle sympathetic nerve activity (MSNA). In normothermia, similar decreases in CVP elevate MSNA, presumably via cardiopulmonary baroreceptor unloading. The purpose of this project was to identify whether increases in MSNA during whole body heating could be attributed to cardiopulmonary baroreceptor unloading coincident with the thermal challenge. Seven subjects were exposed to whole body heating while sublingual temperature, skin blood flow, heart rate, arterial blood pressure, and MSNA were monitored. During the heat stress, 15 ml/kg warmed saline was infused intravenously over 7-10 min to increase CVP and load the cardiopulmonary baroreceptors. We reported previously that this amount of saline was sufficient to return CVP to pre-heat stress levels. Whole body heating increased MSNA from 25 +/- 3 to 39 +/- 3 bursts/min (P < 0. 05). Central blood volume expansion via rapid saline infusion did not significantly decrease MSNA (44 +/- 4 bursts/min, P > 0.05 relative to heat stress period) and did not alter mean arterial blood pressure (MAP) or pulse pressure. To identify whether arterial baroreceptor loading decreases MSNA during heat stress, in a separate protocol MAP was elevated via steady-state infusion of phenylephrine during whole body heating. Increasing MAP from 82 +/- 3 to 93 +/- 4 mmHg (P < 0.05) caused MSNA to decrease from 36 +/- 3 to 15 +/- 4 bursts/min (P < 0.05). These data suggest that cardiopulmonary baroreceptor unloading during passive heating is not the primary mechanism resulting in elevations in MSNA. Moreover, arterial baroreceptors remain capable of modulating MSNA during heat stress.

NASA Discipline Cardiopulmonary↗
NASA NTRS2003

Evidence for altered alpha-adrenoreceptor responsiveness after a single bout of maximal exercise

We studied hemodynamic responses to alpha- and beta-receptor agonists in eight men to test the hypothesis that adrenoreceptor responsiveness is altered within 24 h of the performance of maximal exercise. Adrenoreceptor responsiveness was tested under two experimental conditions (with and without maximal exercise). Adrenoreceptor tests were performed 24 h after each subject performed graded upright cycle ergometry to volitional exhaustion. The 2 test days (experimental conditions) were separated by at least 1 wk, and the order of exercise and no-exercise conditions was counterbalanced. Steady-state graded infusions of phenylephrine (PE) and isoproterenol (Iso) were used to assess alpha- and beta-adrenoreceptor responsiveness, respectively. Slopes calculated from linear regressions between Iso and PE doses and changes in heart rate, blood pressure, and leg vascular resistance for each subject were used as an index of alpha- and beta-adrenoreceptor responsiveness. The slope of the relationship between heart rate and Iso with maximal exercise was 1773 +/- 164 beats x microm-1x kg-1x min-1 compared with 1987 +/- 142 beats x microg-1x kg-1x min-1 without exercise (P = 0.158), whereas the slopes of the relationship between vascular resistance to Iso were -438 +/- 123 peripheral resistance units (PRU) x microg-1x kg-1x min-1 with maximal exercise and -429 +/- 105 x microg-1x kg-1 x min-1 without exercise (P = 0.904). Maximal exercise was associated with greater (P < 0.05) vascular resistance (15.1 +/- 2.8 PRU x microg-1 kg-1x min-1) and mean arterial blood pressure (15.8 +/- 2.1 mmHg. microg-1x kg-1x min-1) responses to PE infusion compared with no exercise (9.0 +/- 2.0 PRU x microg-1 kg-1 x min-1 and 10.9 +/- 2.0 mmHg. microg-1x kg-1x min-1, respectively). These results provide evidence that a single bout of maximal exercise increases alpha1-adrenoreceptor responsiveness within 24 h without affecting beta-cardiac and vascular adrenoreceptor responses.

Non-NASA Center↗
NASA NTRS1993

How should human baroreflexes be tested?

A new approach to the study of arterial baroreflexes was developed for use during the National Aeronautics and Space Administration Spacelab Life Sciences-1 Space Shuttle mission. This method holds promise as a means to characterize the vagal limb of human baroreflex responses comprehensively and efficiently.

Review↗
NASA NTRS1993

A diminished aortic-cardiac reflex during hypotension in aerobically fit young men

We compared the aortic-cardiac baroreflex sensitivity in eight average fit (AF: VO2max = 44.7 +/- 1.3 ml.kg-1 x min-1) and seven high fit (HF: VO2max = 64.1 +/- 1.7 ml.min-1 x kg-1) healthy young men during hypotension elicited by steady state sodium nitroprusside (SN) infusion. During SN mean arterial pressure (MAP) was similarly decreased in AF (-12.6 +/- 1.0 mm Hg) and HF (-12.1 +/- 1.1 mm Hg). However, the increases in heart rate (HR) were less (P < 0.023) in HF (15 +/- 3 bpm) than AF (25 +/- 1 bpm). When sustained neck suction (NS, -22 +/- 1 torr in AF and -20 +/- 1 torr in HF, P > 0.05) was applied to counteract the decreased carotid sinus transmural pressure during SN, thereby isolating the aortic baroreceptors, the increased HR remained less (P < 0.021) in HF (8 +/- 2 bpm) than AF (16 +/- 2 bpm). During both SN infusion and SN+NS, the calculated gains (i.e., delta HR/delta MAP) were significantly greater in AF (2.1 +/- 0.3 and 1.3 +/- 0.2 bpm.mm Hg-1) than HF (1.2 +/- 0.2 and 0.6 +/- 0.2 bpm.mm Hg-1). However, the estimated carotid-cardiac baroreflex sensitivity (i.e., the gain difference between the stage SN and SN + NS) was not different between AF (0.7 +/- 0.2 bpm.mm Hg-1) and HF (0.6 +/- 0.1 bpm.mm Hg-1). These data indicated that the aortic-cardiac baroreflex sensitivity during hypotension was significantly diminished with endurance exercise training.

NASA Discipline Number 14-10↗