Role of spleen in integrated control of splanchnic vascular tone: physiology and pathophysiologyThis article is part of a Special Issue on Information Transfer in the Microcirculation.

Abstract

Aside from its established immunologic and hematologic functions, the spleen also plays an important role in cardiovascular regulation. This occurs through changes in intrasplenic microvascular tone, as well as through splenic neurohormonal modulation of the renal and mesenteric vascular beds. Splenic regulation of blood volume occurs predominantly through fluid extravasation from the splenic circulation into lymphatic reservoirs; this is controlled by direct modulation of splenic pre- and postcapillary resistance by established physiologic agents such as atrial natriuretic peptide (ANP), nitric oxide (NO), and adrenomedullin (ADM). In addition to physiologic fluid regulation, splenic extravasation is a key factor in the inability to maintain adequate intravascular volume in septic shock. The spleen also controls renal microvascular tone through reflex activation of the splenic afferent and renal sympathetic nerves. This splenorenal reflex not only contributes to the physiologic regulation of blood pressure, but also contributes to the cardiovascular dysregulation associated with both septic shock and portal hypertension. In septic shock, the splenorenal reflex protectively limits splenic extravasation and potentially promotes renal sodium and water reabsorption and release of the vasoconstrictor angiotensin II; this function is eventually overwhelmed as shock progresses. In portal hypertension, on the other hand, the splenorenal reflex-mediated reduction in renal vascular conductance exacerbates sodium and water retention in the kidneys and may eventually contribute to renal dysfunction. Preliminary evidence suggests that the spleen also may play a role in the hemodynamic complications of portal hypertension via neurohormonal modulation of the mesenteric vascular bed. Lastly, the spleen itself may be a source of a vasoactive factor.

Blunted cardiac response to hemorrhage in cirrhotic rats is mediated by local macrophage-released endocannabinoids

“…This mechanism is likely to be involved but a purely arterial vascular effect is an oversimplification. Indeed, many studies over the past two decades demonstrate abnormalities at several levels of the cardiovascular system in cirrhosis or portal hypertension: 1) abnormal central neural cardiovascular-regulatory areas in the brainstem and hypothalamus [28]; and 2) inability to mobilize venous blood reservoirs in the liver [29], spleen [30], and gut [31]. The present study now demonstrates that the left ventricular response to hemorrhage is also blunted.…”

Postsynaptic α 1 -Adrenergic Vasoconstriction Is Impaired in Young Patients With Vasovagal Syncope and Is Corrected by Nitric Oxide Synthase Inhibition

“…These observations are consistent with findings of nitric oxide potentiated splanchnic hyporeactivity 24 , blunted chemoreflex 25 , abnormal cerebral autoregulation 26 , and impaired cardiovagal baroreflex 27 which occur during the later presyncopal phase of VVS.…”

What are the implications of the spontaneous spleno-renal shunts in liver cirrhosis?

“…But, any crucial future research directions should consider the utility of DUS particularly when repeated measures are requested beyond liver transplantation settings [34,35]. Last but not least consideration, are we sure that splenomegaly is the consequence of PH and not one of its causes, mainly taking into consideration the spleno-renal reflex-mediated reduction in vascular conductance [50] that exacerbates sodium and water retention in the kidneys?…”