Adrenergic and non-adrenergic control of active skeletal muscle blood flow: Implications for blood pressure regulation during exercise

Single-cell profiling reveals heterogeneity and functional patterning of GPCR expression in the vascular system

“…Most of the peptide hormones in question have been shown to affect vascular tone: vasorelaxation is, for example, mediated by the gastrointestinal hormones VIP and PACAP (acting on receptors encoded by Vipr1, Vipr2 and Adcyap1r1 ), by urocortin and corticotropin releasing hormone (acting on the gene product of Crhr2 ), by parathyroid hormone (acting on the receptor encoded by Pth1r ), or by calcitonin gene-related peptide or adrenomedullin (acting on the gene product of Calcrl )4041424344; all these receptors are G s coupled45. Vasoconstriction, in contrast, is induced by peptide mediators such as endothelin-1, angiotensin II, vasopressin or neuropeptide Y acting on the G i/o -, G q/11 - or G 12/13 -coupled receptors encoded by Ednra, Ednrb, Agtr1a, Avpra1a and Npy1r 464748. The second-largest group of GPCRs with preferential expression in SMsk/SMmes are the orphan receptors, for example, Gpr19, Gpr21, Mrgprf, Gprc5b, Gprc5c, Gpr124, Gpr126 or Lphn1 .…”

Endothelium‐dependent vasodilatory signalling modulates α1‐adrenergic vasoconstriction in contracting skeletal muscle of humans

“…While recruitment of the sympathetic nervous system during exercise results in the release of a number of neurotransmitters including NA, neuropeptide Y and ATP (Holwerda et al . ), it is thought that NA is the primary neurotransmitter involved in exercise‐induced sympathetic vasoconstriction (Buckwalter & Clifford, ). Further, handgrip exercise blunts both postjunctional α 1 ‐ and α 2 ‐adrenergic vasoconstriction similarly in humans (Rosenmeier et al .…”

Ballistic stretch or aerobic warm-up evoke postexercise hypotension after maximal exercise

“…The lack of differences in LF/HF ratio between warm-up protocols indicates that blood pressure effects were independent of autonomic control; thus, hormonal or local regulators of blood pressure might have been at play. Indeed, after exercise, especially high-intensity exercise, plasmatic concentration of several vasoconstrictive hormones, such as angiotensin-II and endothelin-1, contributes to the increases in blood pressure 18 . The effect that different warm-ups achieve on these variables is yet unknown, we hypothesize that warm-up may induce an increased clearance of hypertensive metabolites, that culminates with a systolic blood pressure that drops below baseline levels.…”

“…Blood pressure is set by hormonal, neural, and metabolic control 18 . This study indirectly assessed if neural control is responsible for the effects of warm-up on blood pressure.…”

“…Blood pressure disorders are the most common cause of death worldwide; because of this, it is crucial to understand the elements that promote acute changes in blood pressure, as well as their respective mechanisms 16 . Autonomic and non-autonomic factors influence changes in blood pressure during and post-exercise 18 . Studies regarding PEH often find controversial results, since the characteristics of the exercise protocol and different populations influence the results 19 .…”