The Role of Pericytes in Hyperemia-Induced Capillary De-Recruitment Following Stenosis
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PERICYTES (A BIRBRAIR, SECTION EDITOR)
The Role of Pericytes in Hyperemia-Induced Capillary De-Recruitment Following Stenosis Sanjiv Kaul 1 & Carmen Methner 1 & Anusha Mishra 1,2 Accepted: 14 October 2020 # Springer Nature Switzerland AG 2020
Abstract Purpose of Review The microvascular capillary network is ensheathed by cells called pericytes—a heterogeneous population of mural cells derived from multiple lineages. Pericytes play a multifaceted role in the body, including in vascular structure and permeability, regulation of local blood flow, immune and wound healing functions, induction of angiogenesis, and generation of various progenitor cells. Here, we consider the role of pericytes in capillary de-recruitment, a pathophysiologic phenomenon that is observed following hyperemic stimuli in the presence of a stenosis and attenuates the hyperemic response. Recent Findings We discuss recent observations that conclusively demonstrate pericytes to be the cellular structures that contract in response to hyperemic stimuli when an upstream arterial stenosis is present. This response constricts capillaries, which is likely aimed at maintaining capillary hydrostatic pressure, an important factor in tissue homeostasis. Nonetheless, the ensuing attenuation of the hyperemic response can lead to a decrease in energy supply and negatively impact tissue health. Summary Therapeutics aimed at preventing pericyte-mediated capillary de-recruitment may prove beneficial in conditions such as coronary stenosis and peripheral arterial disease by reducing restriction in hyperemic flow. Identification of the pericyte subtypes involved in this de-recruitment and the underlying molecular mechanisms regulating this process will greatly assist this purpose. Keywords Pericyte . Arterial stenosis . Microvascular blood flow . Capillary . Capillary de-recruitment . Myocardial ischemia . Coronary stenosis . Peripheral arterial disease
Introduction The principles of tissue homeostatis were defined by Starling in 1896 and were further refined over the years [1]. The four starling forces that govern tissue fluid homeostasis are the hydrostatic and oncotic pressures in the capillary and interstitium, respectively, and their balance defines net fluid filtration as well as cell size. Of these forces, the one most likely to fluctuate acutely is the capillary hydrostatic pressure (CHP) because it can be influenced by systemic pressure. In order to maintain a constant CHP at a mean of about 30 mm Hg, the upstream This article is part of the Topical Collection on Pericytes
resistance arterioles, 100–300 μm in diameter, change their tone in response to aortic pressure. Thus, they dilate when aortic pressure falls and constrict when the aortic pressure rises, in order to maintain constant CHP and blood flow, a phenomenon termed autoregulation [2, 3]. This phenomenon is noted in all vital organs, including the heart, and serves to maintain constant pressure within capillaries. In conditions of hyperemia under stenosis, this drive to maintain CHP results i
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