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The role of nitric oxide in the cardiovascular systemRees, Daryl David January 1991 (has links)
Nitric oxide is generated by the vascular endothelium from L-arginine by a constitutive, Ca2+-dependent, NO synthase. Analogues of L-arginine were characterised as inhibitors of NO synthase to investigate the biological significance of the L-arginine-NO pathway in the vessel wall and its role in the cardiovascular system. These inhibitors attenuate the endothelium-dependent vasorelaxation and hypotension induced by various agents, produce an increase in vascular tone and an increase in blood pressure. This suggests that NO is involved in endothelium-dependent relaxation and its continuous release maintains a vasodilator tone and plays a fundamental role in the regulation of blood flow and blood pressure. The removal of the NO-dependent vasodilator tone, results in an `upregulation' of its intracellular receptor, the soluble guanylate cyclase and an increased sensitivity to those vasodilators which act by stimulating this enzyme. This phenomenon of `supersensitivity' to nitrovasodilators may be an important component of their therapeutic action in certain cardiovasulcar disorders. Vascular tissue also expresses an inducible, Ca2+-independent, NO-synthase after activation by lipopolysaccharide (LPS) which results in the generation of large quantities of NO, predominantly from the smooth muscle layer, with a consequent loss of vascular tone and a hyporeactivity to the vasoconstrictor action of phenylephrine. Induction of NO synthase in the vasculature may therefore be responsible for the hypotension and hyporesponsiveness to pressor agents characteristic of endotoxin shock. The glucocorticoid, dexamethasone inhibits the expression of this enzyme but not its activity, which may explain why steroids are more effective at preventing rather than treating this condition. These results suggest that in the cardiovascular system, NO can be considered to have both a protective and a pathological role. The release of small amounts of NO from the constitutive, Ca2+-dependent NO synthase, acts as an adaptive mechanism whereby the vascular endothelium responds to changes in its environment and regulates blood flow and blood pressure to maintain organ perfusion. In contrast, following the induction of the Ca2+-independent NO synthase, after immunological stimulation, NO is released in large quantities from vascular tissue, which may result in pathological vasodilation and tissue damage.
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Cyclic GMP and calcium homeostasis in endothelial cellsZolle Lapuente, Olga C. January 1998 (has links)
No description available.
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Effects of tetrandrine on pulmonary hypertensionWang, Huailiang January 1997 (has links)
No description available.
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Biochemical and pharmacological evaluation of the role of xanthine oxidase in the catabolism of 7-nitroindazole (7-ni) in the isolated rat mesentery in vitro and in the intact rat and mouse cardiovascular and antinociceptive effectsHarb, Hisham Labib January 2001 (has links)
No description available.
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Studies on the release of kallikrein and formation of kinin from superfused disaggregated renal cortical cellsMarshall, Kwesi George January 1991 (has links)
No description available.
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A study of mathematical modelling and signal processing of cerebral autoregulationLiu, Yi January 2003 (has links)
No description available.
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Perceived supervisor interactional style and job stress : implications for psychological and cardiovascular healthWager, Nadia Marie January 2002 (has links)
No description available.
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Impact of dietary salt intake during growth on cardiovascular homeostasis and neural control of the kidney : role of brain angiotensin II (Ang II)Huang, Chunhua January 2001 (has links)
No description available.
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Glucocorticoid receptor binding characteristics in rat genetic models of hypertension and in normal subjects of known glucocorticoid receptor genotypePanarelli, Maurizio January 1995 (has links)
No description available.
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Sodium and hypertensionMcAreavey, D. January 1982 (has links)
No description available.
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