হিজামার জন্য যখন স্ক্র্যাচ করা হয় তখন স্কিন এর নিচের বেসমেন্ট মেমব্রেনে অবস্থিত ছোট ছোট রক্তনালীগুলোতে ইনজুরি হয়। আর এই ইনজুরি থেকেই তৈরি হয় নাইট্রিক অক্সাইড। বিস্তাারিত মেকানিজম জানতে ক্লিক করুন এখানে।
Nitric oxide has gotten the most attention due to its cardiovascular benefits. Alfred Nobel, the founder of the Nobel Prize, was prescribed nitroglycerin over 100 years ago by his doctor to help with his heart problems. He was skeptical, knowing nitroglycerin was used in dynamite, but this chemical helped with his heart condition. Little did he know nitroglycerin acts by releasing nitric oxide which relaxes narrowed blood vessels, increasing oxygen and blood flow.
The interior surface (endothelium) of your arteries produce nitric oxide. When plaque builds up in your arteries, called atherosclerosis, you reduce your capacity to produce nitric oxide, which is why physicians prescribe nitroglycerin for heart and stroke patients.
There is increasing evidence that nitric oxide (NO) is one of the most important paracrine modulators and mediators in the control of renal functions, such as overall and regional renal blood flow (RBF), renal autoregulation, glomerular filtration, renin secretion and salt excretion. NO also plays an important role in the pathogenesis of several renal disease states, such as diabetic nephropathy, inflammatory glomerular disease, acute renal failure in septic shock, chronic renal failure and nephrotoxicity of drugs, conveying both beneficial effects via its hemodynamic functions and detrimental effects via its cytotoxicity when produced in large amounts by inducible nitric oxide synthase (iNOS). The extensive literature on these pathophysiological functions of NO will not be covered here, and the reader is referred to the pertinent chapters (Chaps. 18,.21, 22, 23) for discussion. In the kidney an unusually large diversity of cells of different types is integrated in a delfuate’ and complex architecture, forming various types of functional units. The complexity of the spatial arrangement of cells in these functional units, fmrexample in the glomerulus and the juxtaglomerular apparatus (JGA), is not only a crucial prerequisite for proper functioning but also a serious obstacle te> the analysis of these functions. This problem also extends to the analysis of the intrarenal functions of NO, and much of the interpretation of data rests on assumptions made as to both the site of formation and the target of NO in each particular experiment. For this reason, a brief survey of the distribution of NOS isoforms in the kidney is given first. For more extensive information, the reader is referred to recent reviews (BACHMANN and MUNDEL 1994; BACHMANN 1997; KONE and BAYLIS 1997; STAR 1997).