Abstract

Resting beat-to-beat blood pressure variability is a powerful predictor of cardiovascular events and end-organ damage. However, its underlying mechanisms remain incompletely understood. For instance, alterations in beat-to-beat blood pressure variability are thought to be driven by changes in both the reflex control of the autonomic nervous system and peripheral vascular function. To determine the role of peripheral sympathetic vasoconstriction on the beat-to-beat blood pressure variability, beat-to-beat heart rate (HR, by electrocardiography) and blood pressure (finger photoplethysmography) were continuously measured in seven healthy men (22 ± 5 yr) at rest (supine position), with and without (Control) a systemic and selective blockade of alpha 1-adrenergic receptors through the oral administration of Prazosin (1 mg/20 kg of body weight). Stroke volume was estimated from the blood pressure waveform (ModelFlow), permitting the calculation of cardiac output and total peripheral resistance. Two hours post-Prazosin ingestion, blood pressure responses to intravenous bolus infusion of phenylephrine were robustly reduced (-80 ± 15%, P = 0.001), indicating a significant functional blockade of alpha 1-adrenergic receptors. However, all resting hemodynamic variables were unchanged after the oral ingestion of Prazosin. Compared with control, Prazosin significantly reduced the standard deviation of systolic (5.5 ± 0.9 vs. 3.7 ± 0.7 mmHg, P = 0.004), diastolic (3.3 ± 1.0 vs. 2.4 ± 0.6 mmHg, P = 0.05), and mean blood pressure (3.7 ± 0.8 vs. 2.5 ± 0.5 mmHg, P = 0.02), as well as cardiac output (652 ± 251 vs. 428 ± 78 mL/min, P = 0.02) and total peripheral resistance (1.1 ± 0.6 vs. 0.5 ± 0.4 mmHg/L/min, P = 0.03). Similar results were found using different indices of blood pressure variability. Altogether, these findings suggest that peripheral sympathetic vasoconstriction plays a pivotal role in modulating resting beat-to-beat blood pressure variability in healthy young men. National Council for Scientific and Technological Development (CNPq; grant: 307293/2019-0 and 431740/2018-6). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.