Methods are provided for inhibiting stenosis following vascular trauma or disease in a mammalian host, comprising administering to the host a therapeutically effective dosage of a therapeutic conjugate containing a vascular smooth muscle binding protein that associates in a specific manner with a cell surface of the vascular smooth muscle cell, coupled to a therapeutic agent dosage form that inhibits a cellular activity of the muscle cell. Methods are also provided for the direct and/or targeted delivery of therapeutic agents to vascular smooth muscle cells that cause a dilation and fixation of the vascular lumen by inhibiting smooth muscle cell contraction, thereby constituting a biological stent.

Therapeutic inhibitor of vascular smooth muscle cells

Background Men with benign prostatic hyperplasia can be treated with α1-adrenergic–antagonist drugs that relax prostatic smooth muscle or with drugs that inhibit 5α-reductase and therefore reduce tissue androgen concentrations. However, the effects of the two types of drugs have not been compared. Methods We compared the safety and efficacy of placebo, terazosin (10 mg daily), finasteride (5 mg daily), and the combination of both drugs in 1229 men with benign prostatic hyperplasia. American Urological Association symptom scores and peak urinary-flow rates were determined at base line and periodically for one year. Results The mean changes from base line in the symptom scores in the placebo, finasteride, terazosin, and combination-therapy groups at one year were decreases of 2.6, 3.2, 6.1, and 6.2 points, respectively (P<0.001 for the comparisons of both terazosin and combination therapy with finasteride and with placebo). The mean changes at one year in the peak urinary-flow rates were increases of 1.4, 1...

https://www.nejm.org/doi/pdf/10.1056/NEJM199608223350801

The efficacy of terazosin, finasteride, or both in benign prostatic hyperplasia. Veterans Affairs Cooperative Studies Benign Prostatic Hyperplasia Study Group.

Prostate volume predicts outcome of treatment of benign prostatic hyperplasia with finasteride: Meta-analysis of randomized clinical trials*

1 We have systematically reviewed the presence, functional responses and regulation of alpha(1)-, alpha(2)- and beta-adrenoceptors in the bladder, urethra and prostate, with special emphasis on human tissues and receptor subtypes 2 Alpha(1)-adrenoceptors are only poorly expressed and play a limited functional role in the detrusor Alpha(1)-adrenoceptors, particularly their alpha(1A)-subtype, show a more pronounced expression and promote contraction of the bladder neck, urethra and prostate to enhance bladder outlet resistance, particularly in elderly men with enlarged prostates Alpha(1)-adrenoceptor agonists are important in the treatment of symptoms of benign prostatic hyperplasia, but their beneficial effects may involve receptors within and outside the prostate 3 Alpha(2)-adrenoceptors, mainly their alpha(2A)-subtype, are expressed in bladder, urethra and prostate They mediate pre-junctional inhibition of neurotransmitter release and also a weak contractile effect in the urethra of some species, but not humans Their overall post-junctional function in the lower urinary tract remains largely unclear 4 Beta-adrenoceptors mediate relaxation of smooth muscle in the bladder, urethra and prostate The available tools have limited the unequivocal identification of receptor subtypes at the protein and functional levels, but it appears that the beta(3)- and beta(2)-subtypes are important in the human bladder and urethra, respectively Beta(3)-adrenoceptor agonists are promising drug candidates for the treatment of the overactive bladder 5 We propose that the overall function of adrenoceptors in the lower urinary tract is to promote urinary continence Further elucidation of the functional roles of their subtypes will help a better understanding of voiding dysfunction and its treatment

/pdf/a1-a2-and-b-adrenoceptors-in-the-urinary-bladder-urethra-and-141o0muabo.pdf

α1‐, α2‐ and β‐adrenoceptors in the urinary bladder, urethra and prostate

The efficacy of terazosin, finasteride, or both in benign prostatic hyperplasia

Light Microscopic Stereological Analysis of the Normal Human Prostate and of Benign Prostatic Hyperplasia

Smooth muscle cell of the canine prostate in spontaneous benign hyperplasia, steroid induced hyperplasia and estrogen or tamoxifen treated dogs.

In an attempt to shed light on the action of endogenous androgens and estrogens on the stromal tissue of the human prostate, we studied the effect of selective androgen (cyproterone acetate), estrogen (tamoxifen), and prolactin (bromocriptine) antagonists. The application of cyproterone acetate led to a reduced relative volumetric amount of the smooth muscle cell organelles, whereas the administration of tamoxifen effected no alteration as compared to pretreatment values. The administration of bromocriptine led to further activation of the smooth muscle cells in benign prostatic hyperplasia. Hormones, such as leutinizing hormone, follicle stimulating hormone, testosterone, 17-beta-estradiol, and prolactin were measured to assess alterations of the pituitary gonadal axis.

The effect of antiestrogen, antiandrogen, and the prolactin inhibitor 2 bromo-alpha-ergocriptine on the stromal tissue of human benign prostatic hyperplasia. Correlation of stereological data and plasma hormones.

G. Bartsch

Papers

Light Microscopic Stereological Analysis of the Normal Human Prostate and of Benign Prostatic Hyperplasia

Smooth muscle cell of the canine prostate in spontaneous benign hyperplasia, steroid induced hyperplasia and estrogen or tamoxifen treated dogs.

The effect of antiestrogen, antiandrogen, and the prolactin inhibitor 2 bromo-alpha-ergocriptine on the stromal tissue of human benign prostatic hyperplasia. Correlation of stereological data and plasma hormones.

Can quantitative statements be formulated on human biopsies