Central command (CC) and the exercise pressor reflex (EPR) regulate blood pressure during exercise. We previously demonstrated that experimental stimulation of the CC and EPR pathways independently contribute to the exaggerated pressor response to exercise in hypertension. It is known that CC and EPR modify one another functionally. Whether their interactive relationship is altered in hypertension, contributing to the generation of this potentiated blood pressure response, remains unknown. To address this issue, the pressor response to activation of the CC pathway with and without concurrent stimulation of the EPR pathway, and vice versa, was examined in normotensive Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. In decerebrated, paralyzed animals, activation of the CC pathway was evoked by electrical stimulation of the mesencephalic locomotor region (MLR; 20-50 μA in 10-μA steps). Electrical stimulation of the sciatic nerve (SN, 3, 5, and 10 × motor threshold; MT) was used to activate hindlimb afferents known to carry EPR sensory information. In both WKY and SHR, the algebraic sum of the pressor responses to individual stimulation of the MLR and SN were greater than when both inputs were stimulated simultaneously. Although the blood pressure response to a constant level of SN stimulation was not significantly affected by concurrent MLR stimulation at variable intensities, the pressor response to a constant level of MLR simulation was significantly attenuated by concurrent SN stimulation in WKY but not in SHR. These findings suggest the interactive relationship between CC and the EPR is inhibitory in nature in both WKY and SHR. However, the neural occlusion between these central and peripheral pressor mechanisms is attenuated in hypertension.
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http://dx.doi.org/10.3389/fphys.2019.00095 | DOI Listing |
Int J Behav Med
January 2025
Department of Clinical Psychological Science, Maastricht University, Maastricht, The Netherlands.
Background: Previous studies demonstrated that task-specific stress appraisals as well as the more general belief that stress is (mal)adaptive (i.e., stress mindset) can affect the stress response.
View Article and Find Full Text PDFAnxiety Stress Coping
January 2025
Neuroendocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
Background And Objectives: Laboratory-based stress inductions are commonly used to elicit acute stress but vary widely in their procedures and effectiveness. We compared the effects of stress induction techniques on measures of two major biological stress systems: the early sympathetic-adrenal-medullary (SAM) and the delayed hypothalamic-pituitary-adrenal (HPA) axis response.
Design: A review and meta-analysis to examine the relationship between stress induction techniques on cardiorespiratory and salivary measures of SAM and HPA system activity.
Med Sci Sports Exerc
December 2024
College of Life and Health Sciences, Chubu University, Kasugai, Aichi, JAPAN.
Purpose: Sleep deprivation and elevated blood pressure (BP) increase the risk of cardiovascular diseases. However, the effects of sleep deprivation on BP response, especially at exercise onset remain unclear. We aimed to elucidate the effects of experimental sleep deprivation (ESD) on resting and exercise BPs, including that at exercise onset, and investigate whether a night-time nap during ESD changes the ESD-altered BP.
View Article and Find Full Text PDFDipeptidyl peptidase 4 (DPP4) is a transmembrane serine exopeptidase abundantly expressed in the kidneys, predominantly in the proximal tubule (PT); however, its non-enzymatic functions in this nephron segment remain poorly understood. While DPP4 physically associates with the Na /H exchanger isoform 3 (NHE3) and its inhibitors exert natriuretic effects, the DPP4 role in blood pressure (BP) regulation remains controversial. This study investigated the effects of PT-specific deletion ( ) and global deletion ( ) on systolic blood pressure (SBP), natriuresis, and NHE3 regulation under baseline and angiotensin II (Ang II)-stimulated conditions in both male and female mice.
View Article and Find Full Text PDFHypertension
December 2024
Vanderbilt Autonomic Dysfunction Center, Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, TN. (L.E.O., A.D., C.A.S., A.G., B.K.B., S.P., I.B.).
Background: The cholinesterase inhibitor pyridostigmine is used to treat orthostatic hypotension by facilitating cholinergic neurotransmission in autonomic ganglia, thereby harnessing residual sympathetic tone to increase blood pressure (BP) preferentially in the upright posture. We hypothesized that less severe autonomic impairment was associated with greater pressor responses to pyridostigmine.
Methods: To identify predictors of pressor response, linear regression analyses between the effect of pyridostigmine on upright BP and markers of autonomic impairment were retrospectively conducted on 38 patients who had a medication trial with pyridostigmine (60 mg single dose).
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