الفهرس 
Introduction and aim of the workOnly 14 pages are availabe for public view
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Abstract
Introduction: The renin-angiotensin system (RAS) is a complex and mixed enzymatic-hormonal system that controls electrolytes balance, fluid volume, and systemic blood pressure. Activation of central (AT1) receptors is required for the stress-induced hormone secretion, as well as, stimulation of the central sympathetic activity. The aim of the work: study the role of renin-angiotensin system in stress-induced hypertension. Materials and Methods: The work was divided into nonstressed and stressed groups. These groups were subdivided into 5 subgroups; each included 6 experiments to study the effect of β blocker (atenolol), α blocker (terazocin), angiotensin-converting enzyme inhibitor (captopril) and angiotensin receptor blocker (candesartan). Results: Highly significant reduction in heart rate (p< 0.001) was recorded in candesartan treated group, followed by captopril and terazocin after 30 minutes of stress, while atenolol had only highly significant effect in short term stress. This study provided an evidence that the rapid, peak increase in MAP following onset of immobilization stress is due, to a significant extent, to α- adrenergic mechanisms, whereas β -adrenergic mechanisms played a quantitatively greater role beginning ~30 minutes after the stress began. Moreover, the important role of β -adrenergic receptor activation in the blood pressure response was linked more closely with renin- angiotensin system. Conclusion: Stress triggers significant increase in heart rate, arterial blood pressure, plasma renin activity and blood glucose level. The stress induced hypertensive response can be divided into α1 receptor –dependent phase and β1–receptor–dependent phase. The β1-effect on blood pressure appears to be due to control of the renin-angiotensin system