scholarly journals Structure and Function of Smooth Muscle with Special Reference to Mast Cells

10.5772/48566 ◽  
2012 ◽  
Author(s):  
Angel Vodenicharov
Keyword(s):  
Smooth Muscle ◽  
Mast Cells ◽  
Special Reference ◽  
Structure And Function ◽  
And Function

Structure and Function of the Receptor for Immunoglobulin E (IgE) on Mast Cells

1981 ◽  
Vol 9 (2) ◽  
pp. 60P-60P
Author(s):  
H. Metzger ◽  
C. Fewtrell ◽  
A. Goetze ◽  
D. Holowka ◽  
J. Kanellopoulos
Keyword(s):  
Mast Cells ◽  
Immunoglobulin E ◽  
Structure And Function ◽  
And Function

Effect of chronic ANG I-converting enzyme inhibition on aging processes. II. Large arteries

1994 ◽  
Vol 267 (1) ◽  
pp. R124-R135 ◽  
Author(s):  
J. B. Michel ◽  
D. Heudes ◽  
O. Michel ◽  
P. Poitevin ◽  
M. Philippe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Arterial Wall ◽  
Left Ventricular ◽  
Structure And Function ◽  
Wall Structure ◽  
Large Artery ◽  
Converting Enzyme ◽  
Wall Stiffness ◽  
And Function

The consequences of hypertension and aging on cardiovascular structure and function are reputed to be similar, suggesting that blood pressure plays a role in the aging process. However, the exact relationship between aging, blood pressure, and the arterial structure-function relationship has not been demonstrated. To test the effects of aging, renin-angiotensin system, and pressure on the arterial wall, 20 normotensive male WAG/Rij rats were killed at 6, 12, 24, and 30 mo of age and compared with similar groups treated with an angiotensin (ANG)-converting enzyme inhibitor (ACEI), perindopril. Arterial function was determined by a systemic hemodynamic study and by in situ measurement of carotid compliance. Arterial wall structure was determined by histomorphometric and biochemical methods. Aging did not significantly modify blood pressure, but ACE inhibition decreased blood pressure significantly from 6 to 30 mo. Plasma renin activity decreased with age and increased with ACEI. Plasma atrial natriuretic factor increased with age and was significantly decreased with ACEI. Absolute and relative left ventricular weight increased with age, and ACEI delayed these increases. Arterial wall stiffness increased with age, as shown by a significant decrease in systemic and local arterial compliance and by an increase in aortic characteristic impedance. The increase in carotid wall compliance after poisoning of smooth muscle contractile function (KCN) was greater in young (6- and 12-mo old) than in old (24- and 30-mo old) rats. Chronic ACEI treatment increased basal carotid compliance values slightly and did not change KCN carotid compliance. The aortic and carotid luminal size increased regularly with age. Aging was associated without any change in absolute elastin content. In contrast, collagen content increased with aging. Aging was also associated with an increase in medial thickness. Medial thickening was mainly due to smooth muscle hypertrophy. Aging was associated with intimal proliferation, which became progressively thicker and collagen rich. ACEI treatment did not prevent aortic lumen enlargement but significantly postponed the increase in medial and intimal thickening. Biochemical determinations of the aortic wall components confirmed the morphometric data. In conclusion, the age-dependent large artery enlargement and stiffening were observed both in normotensive rats and in those rats whose blood pressure was lowered by ACEI. This suggests that aging and blood pressure affect arterial wall structure and function by different mechanisms.

scholarly journals Protective Effects of Antimuscarinics on the Bladder Remodeling After Bladder Outlet Obstruction

2017 ◽  
Vol 44 (3) ◽  
pp. 907-919 ◽  
Author(s):  
Qiang Liu ◽  
Deyi Luo ◽  
Tongxin Yang ◽  
Banghua Liao ◽  
Hong Li ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Bladder Outlet Obstruction ◽  
Outlet Obstruction ◽  
Structure And Function ◽  
Bladder Function ◽  
Bladder Smooth Muscle ◽  
M3 Receptors ◽  
And Function

Background/Aims: Overactive bladder associated with bladder outlet obstruction (BOO) is a highly prevalent condition, which is usually treated with antimuscarinics. However, the potential effects of antimuscarinics on the structure and function of bladder have not been investigated thus far. Methods: Sprague-Dawley(R) rats accepted bladder neck obstruction surgery or sham surgery, and then received treatment of three different antimuscarinics (Solifenacin, Darifenacin, and Tolterodine) or vehicle. After 3, 6 and 12 weeks, the bladder function and structure were measured. The effect of antimuscarinics on cellular alteration in vitro was observed under mechanical stimulation. Bladder morphology were examined by immunohistochemistry, and the bladder function were investigated by cystometry and strip contractility test. The expression of muscarinic receptors and inflammatory cytokines were measured by PCR and Western blotting. Results: Here we demonstrate, both in vitro and in vivo, that antimuscarinics are protective regulators for the bladder structure and function. Antimuscarinics decrease the weight of bladders with BOO. Antimuscarinics improve the voiding parameter and enhance the contraction of bladder smooth muscle. The results also show that antimuscarinics inhibit the proliferation of bladder smooth muscle cells both in vivo and in vitro, it can reduce the collagen deposition and inflammatory cytokines in bladders with BOO. During this process, the expression of M2 and M3 receptors was altered by antimuscarinics. Conclusion: Antimuscarinics could reverse the structural and functional changes of BOO bladder wall at cellular and tissue level, and the alteration of M2 and M3 receptors may be involved in this biological process.

Smooth muscle filamin A is a major determinant of conduit artery structure and function at the adult stage

2016 ◽  
Vol 468 (7) ◽  
pp. 1151-1160 ◽  
Author(s):  
Kevin Retailleau ◽  
Malika Arhatte ◽  
Sophie Demolombe ◽  
Martine Jodar ◽  
Véronique Baudrie ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Adult Stage ◽  
Structure And Function ◽  
Major Determinant ◽  
Filamin A ◽  
Conduit Artery ◽  
And Function
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