الفهرس 
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Abstract
Essential hypertension is a very dangerous diseases should more study done on. Apelin a novel multifunction peptide implicated in regulation of the cardiovascular system, including blood pressure and cardiac function control has been postulated to be involved in the pathophysiology of hypertension and hypertensive heart disease. Nitric oxide (NO) occurring from the endothelium was designated as an endothelium-derived relaxing factor (EDRF).a role for the apelin-APJ system as a regulator of vascular tone. Apelin causes NO-dependent vaso-relaxation of human arteries both in vitro and in vivo.
Aim of our study: Assement the following:
• Study the role of apelin and nitric oxide in the pathogenesis of essential hypertension.
• Correlate the levels of apelin to nitric oxide in both genders (male/female).
• Study the relation between of apelin and nitric oxide level and serum electrolytes in both genders.
Patients and methods: Ninety patients were enrolled in the study and divided into seventy hypertensive group and twenty normotensive group Apelin level measured by ELISA and nitrous oxide measured by griess reagent. Serum electrolytes measured by Easy lyte apparatus. Lipid profile parameter measured by Beckman AU Apparatus.
The results of the present study lead us to the following conclusions:
• Decrease in level of apelin in hypertensive patients.
• There is relation between apelin and nitrous oxide in hypertensive patients
• There is no relation between apelin and nitrous oxide in both gender
• There is no relation between apelin ,lipid profile parameter and serum electrolytes
• There is no relation between nitrous oxide ,lipid profile parameter and serum electrolytes
• There is relation between blood pressure and serum electrolytes regard serum calcium level where no relation between them.
• An increase of serum NOx levels
• High blood pressure is not solely responsible for NOx occurring
• NOx levels and there is relation between blood pressure and apelin and nitrous oxide.
• Serum NOx levels may be linked to the developing stages of hypertension in hypertensive patients with comorbidities, measurement of NOx levels in the serum would be helpful in determining when the pathological progress begins in hypertensive patients with comorbid diseases, such as diabetes mellitus, hyperlipidemia and renal disorder.
In conclusion, Essential hypertension is a major risk factor for many common causes of morbidity and mortality including stroke, myocardial infarction, heart failure, and end-stage renal Disease. Approximately, 30–50% of blood pressure variation in the general population Hypertension is one of the most common complex disorders. The discovery of the apelin/APJ axis is an exciting affair in cardiovascular research. Experimental and clinical investigations performed both in vivo and in vitro have suggested apelin/APJ as a critical mediator of cardiovascular homeostasis involved in the pathogenesis of several main cardiovascular diseases including atherosclerosis, CHD, heart failure, hypertension, PAH,MIRI and atrial fibrillation. However, the impact of apelin/APJ on atherosclerosis and hypertension is still controversial, and thus the contribution of the molecular pathway to disease protection in humans remains to be further explored. Although some synthetic agonists of APJ have therapeutic potential for reducing the risk of cardiovascular diseases, the safety and long term effect of these agonists needs to be more fully characterized and better defined. In addition to these, there are still many problems left to be solved. How are apelin and APJ regulated in vivo? Are there any other components required for their function? Are there efficient approaches to enhance their cardiovascular physiological actions besides APJ agonists? What is the exact diagnostic and prognostic role of apelin/APJ in cardiovascular disease patients? In answering these and many other questions, we will assuredly strengthen our chances of developing apelin/APJ-based therapies to help. Hypertension is increasingly understood to be a complex disorder that is strongly associated with other risk factors for CV disease. Clinical studies have demonstrated that patients with hypertension have a reduced vasodilatory response to endothelium-dependent vasodilators, such as acetylcholine, and that blockade of NOS also blunts endothelium-dependent vasodilation. In addition, there is evidence for a role of eNOS polymorphisms, and experimental studies suggest a possible genetic Component to impaired NO bioavailability and hypertension. The etiology of the association between impaired NO bioactivity and hypertension is complex, however, and has not been fully elucidated. Important mechanisms of hypertension and CV disease, in which impaired NO bioactivity plays a major role, include arterial stiffness and increased PWV, and possibly chronic SNS activation. Further clarification of the role of impaired NO bioactivity in these pathogenic mechanisms could have important implications for the management of hypertension.
In the end of study we find that: patients with essential hypertension, circulating apelin levels are reduced, and lower plasma apelin is independently associated with more profound left ventricular systolic and diastolic function impairment. Plasma NOx concentrations are highest in those patients with EH Furthermore, because plasma NOx concentrations were as high in the EH it could be speculated that plasma NOx concentrations are also modulated by EH, perse.
The results of the present study lead us to the following conclusions:
(1) High blood pressure is not solely responsible for NOx occurring
(2) in the serum, nor does high blood pressure directly affect the serum
(3) NOx levels and there is relation between blood pressure and apelin and nitrous oxide.
(4) Decrease in level of apelin in hypertensive patients
(5) There is relation between apelin and nitrous oxide in hypertensive patients
(6) There is no relation between apelin and nitrous oxide in both gender
(7) There is no relation between apelin ,nitrous oxide ,lipid profile parameter and serum electrolytes
(8) There is relation between blood pressure and serum electrolytes regard serum calcium level where no relation between them.
(9) an increase of serum NOx levels
(10) Serum NOx levels may be linked to the developing stages of hypertension in hypertensive patients with comorbidities, measurement of NOx levels in the serum would be helpful in determining when the pathological progress begins in hypertensive patients with comorbid diseases, such as diabetes mellitus, hyperlipidemia and renal disorder.
Recommendation
There have only been three studies that have compared the use of apelin and other biomarkers to aid in the diagnosis of heart failure (Miettinen et al., 2007). However, in patients with severe left ventricular dysfunction or idiopathic pulmonary hypertension apelin was still decreased but BNP was raised suggesting that apelin may be a marker for chronic pulmonary disease. In patients presenting to an emergency room with dyspnea, apelin did not reliably predict acute heart failure and was not a prognostic marker in those with confirmed heart failure (Miettinen et al., 2007). In patients with chronic heart failure secondary to idiopathic dilated cardiomyopathy, plasma apelin was no different to normal controls unlike the other biomarkers which included NT-pro BNP, IL-6, TNF-α and norepinephrine (Tasci et al., 2007). Unlike the biomarker BNP, which can be used as a diagnostic screening test and prognostic marker for heart failure.
An understanding of the homeostatic function of the vascular endothelium is important for the modern cardiologist. The role of nitric oxide in mediating many of the regulatory properties of the endothelium is now recognized, as is a growing understanding of how conditions and diseases considered to be “risk factors” for atherosclerosis cause endothelial dysfunction with loss of nitric oxide bioactivity. The potential consequences of endothelial dysfunction are numerous, including coronary constriction or inadequate dilation during physical or mental stress, producing myocardial ischemia; plaque rupture and thrombosis, causing unstable angina or myocardial infarction; and reperfusion injury after thrombolysis.