Smooth muscle hyperplasia

Elevated NGF concentrations have been seen in two conditions involving altered muscle morphology. Hypertrophy and hyperplasia of bladder smooth muscle cells induced by increased in-travesicular pressure elevates NGF content 2-fold (Steers et al., 1991), while, within the mesenteric artery of the SHR, a rise in NGF concentration correlates with the onset of smooth muscle hyperplasia (Zettler and Rush, 1993). Since abnormalities also occur within the innervation of both these pathologies, it is unclear whether the altered NGF concentrations result from changes in muscle or nerve function. 

Constrictive bronchiolitis is characterized by subepithehal acellular fibrosis in the walls of membranous and respiratory bronchioles causing concentric narrowing or complete obliteration of the airway lumen (Fig. 1) smooth muscle hyperplasia may also be present. Progressive concentric narrowing is associated with distortion of the lumen, mucostasis, and patchy chronic inflammation. Cicatritial bronchiolitis may be a very subtle lesion, the only clue present in the biopsy specimen being the reduction of the number of bronchioles compared with that of centrilobular arterial branches. A peculiar form of constrictive bronchiolitis, neuroendocrine cell hyperplasia with bronchiolar fibrosis has been reported by Aguayo et al. in 1992 (6). The mildest lesion consists of linear zones of neuroendocrine cell hyperplasia in the bronchiolar mucosa with focal sub-epithelial fibrosis. In more obvious lesions, plaque of eccentric fibrous tissue partially occludes the lumen. In most severe stage there is a total occlusion of the lumen by fibrous tissue with few visible neuroendocrine cells. 

A number of studies indicate that irreversible airflow obstruction may occur in asthma, associated with structural changes consistent with an airway remodeling process (153). Morphometric studies have shown prominent smooth muscle hyperplasia and hypertrophy in both large and small airways (154), increased angiogenesis (155), prominent mucus gland hyperplasia (156), and airway wall thickening particularly in cases of fatal asthma (157). 

Mucus hypersecretion Mucous gland enlargement Smooth muscle hyperplasia Bronchial wall thickening Inflammation Emphysema... 

O The lower urinary tract symptoms and signs of benign prostatic hyperplasia are due to static, dynamic, or detrusor factors. The static factor refers to anatomic obstruction of the bladder neck caused by an enlarged prostate gland. The dynamic factor refers to excessive stimulation of a-adrenergic receptors in the smooth muscle of the prostate, urethra, and bladder neck. The detrusor factor refers to irritability of hypertrophied detrusor muscle as a result of long-standing bladder outlet obstruction. 

Alfuzosin is a selective alpha -blocker, which relaxes the smooth muscle in benign prostatic hyperplasia and hence increases the urinary outflow. 

Mecfianism of Action An alphaj antagonist that targets receptors around bladder neck and prostate capsule. Therapeutic Effect Relaxes smooth muscle and improves urinary flow and symptoms of prostatic hyperplasia. 

Genitourinary smooth muscle is partially dependent on autonomic innervation for normal function. Therefore, ganglionic blockade causes hesitancy in urination and may precipitate urinary retention in men with prostatic hyperplasia. Sexual function is impaired in that both erection and ejaculation may be prevented by moderate doses. 

Prazosin Selectively block 04 adrenoceptors Prevent sympathetic vasoconstriction reduce prostatic smooth muscle tone Hypertension benign prostatic hyperplasia Oral Toxicity Orthostatic hypotension... 

The causes of airway narrowing in acute asthmatic attacks (or "asthma exacerbations") include contraction of airway smooth muscle inspissation of viscid mucus plugs in the airway lumen and thickening of the bronchial mucosa from edema, cellular infiltration, and hyperplasia of secretory, vascular, and smooth muscle cells. Of these causes of airway obstruction, contraction of smooth muscle is most easily reversed by current therapy reversal of the edema and cellular infiltration requires sustained treatment with antiinflammatory agents. 

Perlman, H., Sata, M., Krasinski, K., Dorai, T., Buttyan, R. and Walsh, K. (2000) Adenovirus-encoded hammerhead ribozyme to Bcl-2 inhibits neointimal hyperplasia and induces vascular smooth muscle cell apoptosis. Cardiovasc. Res., 45, 570-578. 

Certain alpha-1 blockers such as doxazosin have been used extensively in treating benign prostatic hyperplasia (BPH).23,32 Alpha-1 receptors located on smooth muscle in the prostate capsule, neck of the bladder, and urethra cause muscle constriction that restricts urine flow and the ability to empty the bladder. By blocking these receptors, alpha-1 antagonists relax these smooth muscles and allow men with BPH to void urine more easily and completely.12 32... 

Carmody et al. found that the addition of homocysteine to a culture of vascular smooth muscle cells resulted in a dose-dependent increase in DNA synthesis and cell proliferation, but vitamins B6 and B 2 alone did not substantially inhibit the effect of homocysteine. However, the addition of folic acid resulted in significant inhibition of DNA synthesis (64). Rosiglitazone has been shown to reduce serum tHcy levels, smooth muscle proliferation, and intimal hyperplasia in Sprague-Dawley rats fed a diet high in methionine (65). 

Murthy SN, et al. Rosiglitazone reduces serum homocysteine levels, smooth muscle proliferation, and intimal hyperplasia in Sprague-Dawley rats fed a high methionine diet. Metabolism 2005 54 5) 645-652. 

Pemirolast Inhibition of smooth muscle cell proliferation and migration Ohsawa (55) Low restenosis and neointimal hyperplasia... 

Law RE, Meehan WR Xi XP et al, Troglitazone inhibits vascular smooth muscle cell growth and intimal hyperplasia. J Clin Invest 1996 98 1897-1905. 

Acute vessel recoil, chronic remodeling, and intimal hyperplasia were the mechanisms involved in this process (1-4). However, after the introduction of stents in the daily practice during interventional procedures, intimal hyperplasia became the mechanism associated in the pathophysiology of in-stent restenosis (5-9). Therefore, its prevention should be related with therapies that inhibit smooth muscle cell proliferation. 

Restenosis is caused by an exaggerated healing response involving smooth-muscle migration, neointimal hyperplasia, and a lack of compensatory vessel wall dilation, which result in a reduced vessel luminal diameter at the site of previous endothelial trauma or injury (12-14). Therefore, ICB attempts to attenuate this process and reduce target-vessel restenosis and repeat revascularization. 

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