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ABSTRACT
This work was carried out to investigate the effects of Burrantashi extracts on the lipoproteins Burantashi is a popular seasoning agent to barbecued meat (Suya) in Nigeria. Found in the northern parts of the country. Lipoproteins are the principal steroid or fat that is synthesized in the liver or intestines of animals. 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, 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 e.g. are discussed. The research is focused on human data and the safety and effectiveness of burantashi stem as a phosphodiesterase – 5- inhibitors (PDEs) used to treat erectile dysfunction.
CHAPTER ONE
INTRODUCTION
Erectile dysfunction, ED, is a sexual dysfunction that affects the reproductive systems of both men and women. By definition according to National Institute of Health consensus Development Panel on impotence (1993), in Males, it is a 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 (1994), it is characterized with the persistent or recurrent inability to attain, or maintain until completion of the sexual activity, an adequate Lubrication- Swelling response that otherwise is present during female sexual arousal and sexual activity is thus prevented. Hence, it is called Women impotence or female erectile dysfunction. The word impotence may also be used to describe other problems that may interfere with sexual intercourse and reproduction, such as lack of Sexual Desire and problems with ejaculation or orgasm. Using the term “erectile dysfunction,” however makes it clear that those other problems are not involved (NIH, 2005).
An erection occurs as a hydraulic effect due to blood entering and being retained in sponge-like bodies within the penis and clitoris. The process is most often than not initiated as a result of sexual arousal, when signals are transmitted from the brain to nerves in the pelvis. Erectile dysfunction is, therefore indicated when an erection is consistently difficult or impossible to produce, despite arousal (Laumann et al., 1999).
1.1 PREVALENCE OF ERECTILE DYSFUNCTION IN WOMEN
Erectile dysfunction which is known as Female erection dysfunction in women occurs in 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 Otubu et al. (1998) about 8.7% of Women suffer from this very condition in the United States while between 35.3 – 40%, according to Adequnloye (2002) and Eze (1994) of Women in Nigeria suffer from this condition. Spector and Carey (1994) reported 5-10% in the United States. In addition, Female erectile dysfunction occurs at any age but majorly in old age. Hence, the most significant age related change is menopause (Karen, 2000) and (Rod et al., 2005).
However, erectile dysfunction may be
caused by diabetes, atherosclerosis, hormonal imbalances, neurological
problems etc. (Organic causes) or stress, depression etc. Because
treating the underlying causes (Organic or Psychological), the first
line treatment of ED consists of a trial of PDES inhibitor (the first of
which was Sildenafil or Viagra). In some cases, treatment can involve
prostag-Landin tablets in the Urethra, intravenous injection with a fine
needle into the penis or clitoris that causes swelling of Penis or
Clitoris Pump or Vascular surgery, estrogen replacement therapy for the
women etc.
Although there are various methods and techniques that
are used to treat this very condition, however, for the purpose of this
project, the treatment is restricted to Yohimbe, an extract from
Pausinystalia yohimbe.
1.2 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 the United States. Again, according to the statistical
research carried out by Adegunloye (2002) and Eze (1994) respectively in
Nigeria, results shows that about 23-26.4% of men suffer from this
condition while according to Spector and Carey (1999) discovered that
about 4-9% of men suffer from the condition in the United States.
While erectile dysfunction can occur at any age, it is uncommon among
young men and more common in the elderly. By the age of 45, most men
have experienced erectile dysfunction at least some of the time.
According to the Massachusetts Male Aging Study, complete impotence
increases from 5% among Men 40 years of age to 15% among Men 70 years
and older. Population studies conducted in the Netherlands found out
that some degree of ED occurred in 20% of Men between 50 – 54 and in 50%
of men between ages 70 – 78. In 1998, the National Ambulatory Medical
care Survey counted 1,520,000 Doctor Offices visited for ED.
1.3 OBJECTIVE STUDY AND AIMS
This project focuses to give a clear picture of the effect on erectile tissues of the penis, clitoris of both men and women.
1.4 NITRIC OXIDE-CYCLIC GMP PATHWAY WITH SOME EMPHASIS ON CAVERNOSAL CONTRACTILITY
Nitric Oxide (NO) is formed from the conversion of L- arginine by nitric oxide synthase (NOS), endothelial (eNOS), and inducible (iNOS). nNOS is expressed in penile neurons innervating the corpus Cavernosum, and eNOS protein expression has been identified primarily in both Cavernosal Smooth Muscle and endothelium. NO is released from nerve endings and endothelial cells and stimulates the activity of soluble guanylate cyclase (sGC), leading to an increase in cyclic guanosine- 3‟,5‟,- Monophosphate (cGMP) and, finally, to Calcuim depletion from the cytosolic space and Cavernous Smooth muscle relaxation. The effect of cGMP are mediated by cGMP dependent Protein Kinase, cGMP-gated ion channels, and cGMP-regulated Phosphodiesterases (PDE). Thus, cGMP effect depends on the expression of a Cell-Specific cGMP-receptor protein in a given cell type.
Numerous systemic vasculature diseases that
cause erectile dysfunction (ED) are highly associated with endothelial
dysfunction, which has been shown to contribute to decrease erectile
function in men and a number of animal models of penile erection. Based
on the increasing knowledge of intracellular signal propagation in
cavernous smooth muscle tone regulation, selective PDE inhibitors have
recently been introduced in the treatment of ED. Phosphodiesterase-5
(PDE5) inactivates cGMP, which terminates NO-cGMP-mediated SMooth Muscle
relaxation. Inhibition of PDE5 is expected to enhance penile erection
by preventing cGMP degradation. Development of pharmacologic agents with
this effect has closely paralleled the emerging science.
﴾International Journal of impotence Research (2004)﴿. Nitric oxide (NO)
was first described by Stuehr and Marletta (1985) as a product of
activated murine machrophages. Also, the substance known as endothelium-
derived relaxing factor (EDRF), described by Furchgott and Zawadzki
(1980), has been identified as NO.
Soluble guanylate cyclase
(sGC), responsible for the enzymatic conversion of guanosine -5-
triphosphate (GTP) to cyclic guanosine -3‟5‟- monophosphate (cGMP), was
first identified as a constituent of mammalian cells almost three
decades ago. No and cGMP together comprise an especially wide-ranging
signals transduction system when one considers the many roles of cGMP in
physiological regulation, including smooth muscle relaxation, visual
transduction, intestinal ion transport, and platelet function.
Erectile dysfunction (ED) is defined as the constituent inability to
achieve or maintain an erection sufficient for satisfactory sexual
performance and is considered to be a natural process of ageing. Studies
have shown that ED is caused by inadequate relaxing of the corpus
cavernosum with defeat in NO production.
It is clear that NO is the
predominant neurotransmitter responsible for cavernasal Smooth muscle
relaxation and hence penile erection. Its action is medicated through
the generation of the second messenger cGMP. Neutrally, derived NO has
been established as a mediator of smooth muscle relaxation in the penis
and it is thought that constitutive forms of nitric oxide synthase (NOS)
work to mediate the convesion of GTP to the intracellular second
messenger cGMP in smooth muscle cells. An increase in cGMP modulates
cellular events, such as relaxation of smooth muscle cells.
This
review will describe current knowledge of cellular events involved in
cavernosal relaxation and the range of putative factors involved in
NO-mediated relaxation.
1.5 SYNTHESIS OF Nitric Oxide (NO).
Recent observation suggest that the main site of NO biosythesis in human corpus cavernosum is within the terminal branches of cavernosal nerves supplying the erectile tissue. It is strongly suggested that NO released from nonadrenergic – noncholinergic (NANC) neurons increases the production of cGMP, which in turn relaxes the cavernous smooth muscle. Endothelial –derived NO plays a major role in the penis. Some suggest that NO is highly labile, therefore it cannot be stored as a preformed neurotransmitter. Other proerectile mediators, such as acetylcholine, calci-tonin gene related peptide (CGRP) or substance P, act via endothelialcells by prompting the synthesis and release of NO by these cells, ﴾Bivalacqua et al., 2001). Found in their study that in vivo adenoviral gene transfer of CGRP in combination with adrenomedullin (ADM) or prostaglandin E1(PGEI) induce penile erection by activating different receptors.
The combination of molecular oxygen and the amino acid arginine in the presence of reduced nicotinamide adenine dinucleotide phosphate (NADPH) and NO synthase, (NOS) yields citruline nitrogen of L- arginine. L- citrulline can be converted by arginine synthase (AS) to form L-arginine, the precursor for NO. Each of these enzymes, co-factors, or transport systems could be an eventual target of pharmacologic intervention in the NO cascade. Oral administration of L-arginine in high doses seems to cause significant subjective improvement in sexual function in men with Organic ED only if they have decreased production of plasma and urine nitrite and nitrates, which are stable metabolites of NO. There are at least three isoform of NOS (neuronal, endothelial, and macrophage). A constitutive form of NOS is found in endothelial and neurons, and is calcium dependent. The constitutive NOS-3, whereas the constitute NOS found in neutral and epithelial tissue has been named NOS-1. An inducible form of NOS, now designated iNOS, is calcium independent. It is induced within 4-24h of the appropriate stimulus and can produce NO in a 100-fold greater amount than can constitutive NOS.
Neutral NOS has multiple regulator sites,
including binding sites for nicotinamide adenine dinucleotide phosphate
(NADPH), Flavin adenine dinucleotide (FAD), and flavin Monoucleotide
(FMN). All of these are (O factors for the synthesis of NO. these
cofactors bind to a reductase domain to process election transfer. This
is then linked to heme and tetrahydrobiopterin (BH4) – containing
catalytic oxygenenase domain by calcium-calmodulin complex (figure 2).
The complete enzyme converts L-arginine to L- citrulline and NO in the
presence of molecular Oxygen. In addition to the various protein modules
or domains of neuronal NOS, which are involved in electron transfer,
substrate binding, oxygen activation and calcium binding, a four amino
–acid motif (glycine- Leucine-glycine- Phenylalanine, GLGF) has been
identified in amino terminal region of NOS-1. Although the function of
this amino-acid motif in NOS-2 has not been established, a study on
other proteins containing this motif indicates that it may serve to
target proteins to specific sites in the cell. nNOS has a recognition
site for calmodulin that is also present in eNOS and macrophages NOS.
The constitutive isoforms are generally regulated by Ca2+ -calmodulin,
whereas inducible forms are not.
nNOS in the penis is expressed primarily as a variant of the brain form of nNOS and has been termed PnNOS. It has an additional 102-bp alternative exon located between exons 16 and 17. The function of this additional coding region is unknown. PnNOS is thought to be responsible for trigging the nitregic mechanism responsible for cavernosal relaxation. A similar variant, nNO-SU is present in the neuromuscular plates of skeletal muscles, including the perineal muscles involved in erectile rigidity and ejaculation in rats. The control of NO synthesis in the Cavernosal nerve, whether due to sexual stimulation emanating. Centrally, from the brain, or peripherally by means of the dorsal nerve spinal reflex is assumed to be exerted through the activation of PnNOS activity. This mechanism occurs mainly by Ca2+ binding to calmodulin by means of Ca2+ flux through the N-methyl-D-aspartate receptor (NMDAR). Both the NMDAR and inhibitors of nNOS activity, such as protein inhibitors of nNOS activity, such as protein inhibitors of NOS(PIN) and carboxy terminal POZ Ligand of nNOS (CAPON), also bind to nNOS .
The nitrognic activation of penile erection is not restricted to peripheral nerves of the corpora cavernosa but is also dependent on central nervous system (CNS) regulated. It was found that PnNOS, the brain type nNOS, and PIN were expressed in the hypothalamus in contrast, NMDAR1-T was expressed only in the penis, whereas the brain –type- NMDARI was present in the brain and sacral spinal cord and not in the Penis. PnNOS was found in the media preoptic area, posterior magnocellular, and the Parvocellular regions of paraventriccular nucleus, Supraoptic nucleus, septohypothalamic nucleus, medial septum, Cortex, and in some of the nNOS staining neurone through the brain. It was absent in organum vasculosum of the lamina terminalis. PIN staining was present in neurons of the medial septum and cortex, but not in the supraoptic nucleus septohypothalamic nucleus or organum vasculosym of the Laminal terminals.
Inhibitors of NOS are substrate analogues of
L-arginine, such as N-Monomethyl -L- arginine (L- NMMA), nitro-L-
arginine methyl ester (L-NAME). and N-amino –L- arginine.Drugs that
inhibit the dephosphorylation of eNOS might alleviate ED. eNOS
abnormalities may play a role in diabetic ED. Hyperglycemia decreases NO
production by eNOS via O-Linked glycossylation of eNOS at the targets
S1177 in hyperglycemic cell culture conditions and in animal models of
diabetes. ED in diabetes is associated with peripheral nerve damage but
may involve diminished endothelial-production of NO as well. Numerous
systemic vasculature, diseases (hypertension, atherosclerosis,
hyperoholesterolemia, diabetes mellitus, etc) that cause ED are highly
associated with endothelial dysfunction, which has been shown to
contribute to decreased erectile function in men and a number of animal
models of penile erection.
The activity of nNOS is controlled by a number of mechanisms.
A
balance of various inhibitory and stimulatory transcription factors
determines gene transcription of the enzyme. Enzyme activity can be
halted by phosphorylation by a cyclic adenosine Monophosphate (cAMP) –
dependent protein kinase (PKA) or cGMP- dependent protein kinase (PKG),
providing a negative feed back loop. The enzyme is activated by
increased intracellular calcium, which binds to calmodulin to form the
essential cofactor. It is also likely that co- transmitters influence
nNOS activity perhaps by altering calcium concentration by activation of
prejunctional receptors. VIP
is a probable stimulatory co-transmitter, while noradrenaline acting on x-2 adrenoceptors inhibits NO formation.
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