الفهرس 
AcknowledgementOnly 14 pages are availabe for public view
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Abstract
The main objective of the present study was designed to investigate the possible endothelial and smooth muscle mechanisms involved in the deleterious effects of acute CS A exposure on endothelium dependent- and -independent vasorelaxations. Endothelium-dependent relaxations were evoked via activation of endothelial cholinergic, p-adrenergic or adenosinergic receptors by acetylcholine, isoprenaline or NECA, respectively. Two different examples of endothelium-independent vasorelaxants were also investigated, the nitrovasodilator sodium nitroprusside and the DAi agonist, SKF38393. Two vascular preparations were used, the isolated perfused kidney and the rat aortic smooth muscle. Further, the present study evaluated the role of presynaptic DAi-receptors in the modulatory effect of CSA on the renal , sympathetic neurotransmission. The main results and conclusions of the present study can be summarized as follows:
1- The nature and the identity of the endothelial relaxing factors mediating the renal vasodilatory responses in the present study appear to be dependent on the receptor type and vascular tissue involved. In perfused kidneys, whereas all three principal relaxing factors of endothelium (NO, EDHF, vasodilator prostanoids) contributed to acetylcholine relaxations, responses to isoprenaline or NECA were mediated via EDHF and NO but no involvement for vasodilator prostanoids. However, in rat aortic rings the endothelial factors contributed variably to NECA or isoprenaline relaxations from those demonstrated in isolated kidneys. NECA relaxations were found to involving NO, EDHF and vasodilator prostanoids. On the other1 hand, the endothelium-dependent relaxantion of isoprenaline, in isolated aortic rings, appear to be mediated solely via NO.