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- W975329970 abstract "This chapter states that vasodilator substances increase renal blood flow (RBF) and augment sodium excretion. The exact mechanism of this natriuresis is not fully delineated but may be because of hemodynamic changes or direct tubular effects. It has been found that changes in the resistance within either of these vessels will alter the RBF. The presence of specific postsynaptic dopaminergic receptors in the kidney distinguishes it from most other vascular beds. These postsynaptic receptors on stimulation directly induce renal vasodilation. Structurally, distinct presynaptic dopaminergic receptors present in peripheral sympathetic nerve endings attenuate norepinephrine release. The existence of vascular dopamine receptors has been generally accepted since the in vivo demonstration of a specific vasodilator effect of Dopamine. These receptors occur principally in the renal and mesenteric vessels. In addition to Dopamine analogs, several types of bicyclic systems have been tested as renal vasodilators. The dihydroxy- 2-aminotetralins represent semi-rigid analogs of the α- and β-rotamers of Ddopamine. At lower doses, renal blood flow increases; when the dose is increased, cardiac output increases. Finally, vasoconstriction occurs. Excessive vasoconstriction is one of the adverse effects of Dopamine, and thus, compounds with reduced alpha-adrenergic activity would have application in the treatment of shock. Agents that improve RBF have potential therapeutic indications for prevention and treatment of acute renal failure. Dopamine markedly improves renal function in hypotensive patients and in patients with cirrhosis." @default.
- W975329970 created "2016-06-24" @default.
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- W975329970 date "1981-01-01" @default.
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- W975329970 title "Chapter 11. Renal Blood Flow and Dopaminergic Agonists" @default.
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- W975329970 doi "https://doi.org/10.1016/s0065-7743(08)61278-6" @default.
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