Functional and morphological properties of pericytes in suburothelial venules of the mouse bladder

Hashitani, Hikaru; Mitsui, Retsu; Shimizu, Yuki; Higashi, Ryuhei; Nakamura, Kei‐ichiro

doi:10.1111/j.1476-5381.2012.02125.x

Cited by 36 publications

(59 citation statements)

References 52 publications

(56 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Early in the micturition cycle, bladder perfusion can initially increase with bladder filling; however, as the micturition cycle continues, high physiological filling of the bladder can compress the blood vessels in the bladder wall (Goi et al 2013;Kershen et al 2002;Nomiya et al 2012b). The mechanisms regulating bladder perfusion beyond passive vessel compression have not been defined in great detail, but spontaneous contractions of suburothelial venule pericytes have been described (Hashitani et al 2012). Nitric oxide (NO) appears to cause vasodilatation mainly for mucosal vessels and less so for those of the detrusor (Pontari and Ruggieri 1999).…”

Section: Physiology Of Bladder Perfusionmentioning

confidence: 99%

Are blood vessels a target to treat lower urinary tract dysfunction?

Michel

Chess-Williams

Hegde

2015

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

Bladder dysfunction is common in the general population (Stewart et al. 2010) and even more so among patients seeing a physician for any reason (Goepel et al. 2002). It often manifests as lower urinary tract symptoms (LUTS), a term originally coined to describe voiding and storage symptoms in men with benign prostatic hyperplasia (BPH) but now more universally used to describe any type of voiding and storage symptoms in both sexes. Studies into possible causes of urinary bladder dysfunction have long focused on detrusor smooth muscle cells (Turner and Brading 1999). More recently, it became clear that several other types of cells and organs contribute to regulating detrusor smooth muscle function. These include the urothelium (Andersson and McCloskey 2014; Michel 2015), afferent nerves (Michel and Igawa 2015; Yoshimura et al. 2014b), and the central and autonomic nervous systems (Fowler and Griffiths 2010; Yoshimura et al. 2014a). Alterations in any of these may at least partly be responsible for detrusor dysfunction and, accordingly, be potential targets for the treatment of bladder dysfunction. As highlighted by an article in this issue of Naunyn-Schmiedeberg's Archives of Pharmacology (Bayrak et al. 2015), there is an additional suspect, the bladder vasculature. This article will discuss the currently available experimental and clinical evidence for a role of the vasculature in causing bladder dysfunction, and how existing and emerging treatments may modulate bladder function by acting on blood vessels. Due to a similarity in concept, data on prostate perfusion will also be discussed to some extent.

show abstract

Section: Physiology Of Bladder Perfusionmentioning

confidence: 99%

Are blood vessels a target to treat lower urinary tract dysfunction?

Michel

Chess-Williams

Hegde

2015

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

show abstract

“…Confocal Ca 2+ imaging has brought many advantages to the study of Ca 2+ signalling in situ. Confocal images of vessels permit the visualization of individual vascular smooth muscle cells, pericytes and endothelial cells, and so quantification of changes of Ca 2+ signals in these cells can be made and then correlated with mechanical or electrical events [12,13,14,15,16,17,18]. In this review, we attempt to summarize our results and those of other authors over the last 2 decades in the field of Ca 2+ signalling in pericytes.…”

Section: Introductionmentioning

confidence: 97%

“…1Aiv, Ciii-v). They stain positive for α-SMA [15,17,20,28,29,35] (fig. 1Div) but negative for NG2 and thus are classified as an NG2- α-SMA phenotype [32,35].…”

Section: Topology Morphology and Contractility Of Pericytesmentioning

confidence: 99%

“…Accumulated data indicate that GPCR agonists such as ET-1, AVP and Ang II, upon binding to their receptors on the plasma membrane of pericytes, activate phosphoinositide phospholipase C-β which then hydrolyses phosphatidylinositol-4,5-bisphosphate to yield IP 3 [5,14,15,17]. In turn, IP 3 initiates Ca 2+ release from the endoplasmic reticulum through binding to IP 3 Rs, the molecular identity of which has not yet been identified in pericytes [72].…”

Section: Ca2+ Signalling Induced By Gpcr Agonistsmentioning

confidence: 99%

“…1Div) but negative for NG2 and thus are classified as an NG2- α-SMA phenotype [32,35]. Information has been accumulated providing evidence that postcapillary pericytes are contractile cells and can perform several functions in the microcirculation including the regulation of blood flow and perfusion [15,17,36], the opening of interendothelial junctions [37] and junction protection from overstretching (‘umbrella-like' disposition over interendothelial junctions) [38]. Movies showing contractile activity in venular pericytes are available in the supplemental material provided for several recent publications [15,17].…”

Section: Topology Morphology and Contractility Of Pericytesmentioning

confidence: 99%

See 2 more Smart Citations

Calcium Signalling in Pericytes

Burdyga

Borysova²

2014

J Vasc Res

View full text Add to dashboard Cite

Recent advances in pericyte research have contributed to our understanding of the physiology and pathophysiology of microvessels. The microvasculature consists of arteriolar and venular networks located upstream and downstream of the capillaries. Arterioles are surrounded by a monolayer of spindle-shaped myocytes, while terminal branches of precapillary arterioles, capillaries and all sections of postcapillary venules are encircled by a monolayer of morphologically diverse pericytes. There are physiological differences in the response of pericytes and myocytes to vasoactive molecules, suggesting that these two vascular cell types could have different functional roles in the regulation of local blood flow. The contractile activity of pericytes and myocytes is controlled by changes of cytosolic free Ca²⁺ concentration. In this short review, we summarize our results and those of other authors on the contractility of pericytes and their Ca²⁺ signalling. We describe results regarding sources of Ca²⁺ and mechanisms of Ca²⁺ release and Ca²⁺ entry in control of the spatiotemporal characteristics of the Ca²⁺ signals in pericytes.

show abstract

Functional heterogeneity of PDGFRα (+) cells in spontaneously active urogenital tissues

Hashitani

Mitsui

Lang

2020

Neurourology and Urodynamics

Self Cite

View full text Add to dashboard Cite

Aims As PDGFRα (+) cells appear not to suppress the excitability of detrusor smooth muscle by generating SK3‐dependent hyperpolarising as proposed in the gastrointestinal tract, we further explored the functional roles of PDGFRα (+) cells in regulating the spontaneous activity of urogenital tissues. Methods Using PDGFRα‐eGFP mice, intracellular Ca2+ signaling in PDGFRα (+) cells of the bladder lamina propria, renal pelvis, and seminal vesicle were visualized using Cal‐590 fluorescence. The distribution and SK3 expression of PDGFRα (+) cells were also examined by immunohistochemistry. Results In the bladder lamina propria, SK3 (−) PDGFRα (+) cells exhibited spontaneous Ca2+ transients and responded to stimulation of P2Y1 purinoceptors with MRS2365 (100 nM) or adenosine diphosphate (ADP) (100 μM) by developing Ca2+ transients. In the proximal renal pelvis, PDGFRα (+) cells were distributed in the mucosal, muscular and serosal layers but did not express SK3 immunoreactivity. PDGFRα (+) cells in the musculature resembling atypical smooth muscle cells generated spontaneous Ca2+ transients that were partially suppressed upon P2Y1‐stimulation, while vigorously responding to human angiotensin II (100 nM). In the seminal vesicle, PDGFRα (+) cells in the musculature but not mucosa expressed SK3 immunoreactivity. In the mucosa, the P2Y1 stimulation evoked Ca2+ transients in both PDGFRα (+) cells and PDGFRα (−) cells. Conclusion PDGFRα (+) cells in spontaneously active urogenital tissues display heterogeneity in terms of their SK3 expression and P2Y1‐induced Ca2+ responses. Muscular PDGFRα (+) cells in the renal pelvis and mucosal PDGFRα (+) cells in the seminal vesicle may generate depolarizing signals to drive smooth muscle cells.

show abstract

Functional and morphological properties of pericytes in suburothelial venules of the mouse bladder

Cited by 36 publications

References 52 publications

Are blood vessels a target to treat lower urinary tract dysfunction?

Are blood vessels a target to treat lower urinary tract dysfunction?

Calcium Signalling in Pericytes

Functional heterogeneity of PDGFRα (+) cells in spontaneously active urogenital tissues

Contact Info

Product

Resources

About