PRELIMINARY INVESTIGATION ON EFFECTS OF BURANTASHI EXTRACT ON LIVER ENZYMES OF AIBINO MALE AND FEMALE WHISTAR RATS
This work was carried out to investigate the effects of Burantashi extract on liver enzymes of albino male and female whistar rats. Burantashi is a popular seasoning agent to barbecued meat (suya) in Nigeria,mostly found in the northern part of the Nigeria. Liver Enzymes are those enzymes that plays important role in the liver both in function and regulation. Erectile dysfunction (ED) is defined as the consistent or recurrent inability of a man to attain or maintain penile erection, sufficient for sexual activity (2nd) International consultation on sexual Dysfunction Paris, June 28th July 1st, 2003). Following the discovery and introduction of Burantashi research on the mechanism underlying penile erection, has had an enormous boost and many preclinical and clinical papers have been published in the last five years on the peripheral regulation of, and the mediators involved in human penile erection. The most widely accepted risk factors for ED are discussed. The research is focused on human data and the safety and effectiveness of Burantasni Stem as a phosphodiesterase -5- Inhibitors (PDE-5) used to treat Erectile Dysfunctions.
PHYSIOLOGY OF ERECTION
Penile Erection involves an integration of complex physiological processes involving the central nervous system, peripheral nervous system, hormonal and vascular systems. Any abnormality involving these systems whether from medications or disease has a significant impact on the ability to develop and sustain erection; ejaculate and experience orgasm. (Laumann et al., 1999).
The physiological process of erection begins in the brain and involves the nervous and vascular system. The chemicals that initiate erection are neurotransmitters present in the brain. Any kind of stimulation physical or psychological, causes nerves to send message to the vascular system which result in significant blood flow to the penis. Two arteries in the penis supply blood to erectile tissues and the corpora cavernous which become engorged and expand as a result of increased blood flow and pressures. Because blood must stay in the penis to maintain rigidity. An erectile tissue is enclosed by tunicae, which is fibrous elastic sheathes cinch which prevents blood leaving he penis during electron. When muscle in the penis contract to stop the inflow of blood and open out flow channels and an electron is reserved.
HORMONAL INVOLVEMENT IN ERECTION
Oestrogen/Progesterone: (These are female hormones that cause clitoral
erection. If the body has two much oestrogen and or too little testost erone, she ca n get very wet but can not erect her clitoral and G-spot. ( Haimen et al., 2002). Estrogen tends to increase the size of the bread, labia minors (inner lips) and clitoral hood, but shrinks the glans clitoris into the clitoral hood making it invisible. It also increases the thickness of the vaginal lining making the G-spot inaccessible. The mechanism of the clitoral and G-spot erection is the same as that of the penis. It is driven by the parasympathetic sexual nerve (The neurotransmitter acetylcholine) through the neurotransmitter. Nitric oxide and the erection dilator cGMP, which is continuously powered by the burning of testosterone without a testosterone burst and burning. She cannot pop the glans Clitoris and G-spot out. If she is on birth control pills there is a chance that her body is over flooded by estrogens and low progesterone. Over loaded liver cannot produce sufficient essential enzymes to synthesize sufficient NO, cGMP and testosterone to support the clitoral and G-spot erection infact excessive estrogen or progesterone in the body will shrink the penis, clitoral and G-spot, but likely increase the breast size (under the excessive estrogen action).
MECHANISM OF ACTION OF PDE-5 INHIBITION IN ERECTILE DYSFUNCTION.
A spinal reflex and the L-arginine nitric oxide guanglyl cyclase-cyclic guanosine monophonsphate (cGMP) pathway mediate smooth muscle relaxation that results in penile erection. Nerves and endothelial cells directly release nitric oxide in the penis, where it stimulates guanylyl cyclase to produce cGMP and lowers intracellular calcium level. This triggers relaxation of arterial and trabecular smooth muscle, leading to arterial dilation, venous constriction, and erection. Phosphodiesterases (PDEs) is the predominant phosphodiesterase in the corpus cavernosum. The catalytic site of PDE-5 normally degrades cGMP and PDE-5 inhibitors such as sildenafil potentiate endogenous increase in cGMP by inhibiting its breakdown at the catalytic site. Phosphorylation of PDE-5 increases its enzymatic activity as well as the affinity of its allosteric (noncatalytic/GAF domains) sites for cGMP. Binding of cGMP to the allosteric site further stimulates enzymatic activity. Thus phosphorlation of PDE-5 and binding of cGMP to the non catalytic site mediate negative feed back regulation of the cGMP pathway.
NITRIC OXIDE REGULATION OF PENILE ERECTION
Biology And Therapeutic Implications
Unique biochemical cascade invading production of the potent second messenger molecule, 3’5’ cyclic guanosine monophosphate (cGMP) and its activation of protein kinase G (PKG) which induces physiologic penile erection by regulating the state of penile smooth muscle contractility (Burnett, 1997). In fact, current data support the notion that this NO based biochemical cascade represent a convergence of cellular biochemical and molecular inputs, which on the signal transduction regulatory level, is indispensable for the mechanism of penile erection (Hedland et al., 2000). Consistent with the importance of NO radiation of penile erection, its biology in the penis is quite complex, involving multiple regulatory interactions, the molecule itself may target several biochemical mechanisms that achieve erectile tissue relaxation but is also the target of a host of modulatory influences that determines its release and mode of action in erectile tissue. At the same time, premier signal transduction mechanism has been exploited for therapeutic purposes, specifically in the clinical management of erectile dysfunction. Discoveries pertaining to the field of NO biology in the penis have, in recent years been rapidly translated into the clinical management of the first orally effective pharmacotherapy for erectile dysfunction, sildenafil citrate (Viagra) (Goldstein et al., 1998).
NO BIOLOGY IN THE PENIS
Traditional understanding of the action of NO in the penis invokes the constitutive formation of this molecule under normal physiologic conditions with the expression and activities of the enzyme, sources localized to neural and endothelial components of the corporal tissue. The verification that NO derives from the autonomic innervations supplying the penis has directly supported the description of this molecule as a peripheral neurotransmitter of non adrenergic, no cholinergic-1992 mediated penile erection (Kim et al.,1991) the confirmation that the molecule also is produced within vascular and trabecular endothelium comprising the penile vascular supply, has offered additional support for the role of NO serving as an endothelial relaxation factor of penile erection (kimoto et al., 1990, knispel et al., 1991, azadzoic et al., 1992, Hedlund et al., 2000).
ATIEOLOGY OF ERECTILE DYSFUNCTION
Erectile dysfunction (ED) is a sexual dysfunction that affects the reproductive systems of both men and women.
According to the definition by national Institute of Health consensus Development (NIHCD) panel on importance (1993) in males. It is sexual dysfunction characterized with the inability to develop or maintain an erection of the penis sufficient for satisfactory sexual performance. It is also known as male impotence or Baby D syndrome. While in women according to American psychiatric Association (APA) (1994), it is characterized with the persistant or recurrent inability to attain, or maintain until completion of the sexual activity, an adequate lubrication. Swelling response that otherwise is present during fem ale sexual arousal and sexual activity is thus prevented. Hence it is called woman impotence or female erectile dysfunction. (NIH, 2005).
PREVALENCE OF ERECTILE DYSFUNCTION IN MEN.
Erectile dysfunction ED, varies in severity; some men have a total inability to achieve an erection others have inconsistent ability to achieve an erection, and still others can sustain only brief erection. The variation in severity of erectile dysfunction makes estimating its frequency difficult. Many men also are reluctant to discuss erectile dysfunction with their doctors, and thus, the condition is under diagnosed nevertheless experts have estimated that ED affects 30 million men in united sates, Again, according to the statistical research carried out by Adegunloye and Eze in 2002 and 1994 respectively in Nigeria, results show that about 23-26.5% of men suffer from this condition while according to carey in 1990, discovered that about 4.9% of men suffer from the condition in the united states.
PREVALENCE OF ERECTILE DYSFUNCTION IN WOMEN.
Erection dysfunction which is known as female erectile dysfunction in woman occurs about 43% of American women (NIH consensus conference, 1993). And this medical condition is a persistent or recurrent inability to attain or maintain clitoral erection until completion of the sexual activity, an adequate lubrication. Swelling response that is normally present during female sexual arousal and sexual activity is therefore absent. The individual having the condition is said to experience frigidity (American Psychiatric Association, 1994). Again according to Otuba et al in 1989, about 8.7% of women suffer from this very condition in the United States while between 35.3-40%, according t o Adegunloye in 2002 and Eze in 1994 of women in Nigeria suffer from this condition. Spector and carey in 1994 reported 5-10% in the united states.
AIM OF STUDY
The aim of this research is to find out the effects of Barantashi. (pausinystalia yohimbe). Extract on the liver enzymes of albino male and female whistar rats.
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