Systemic and Renal Hemodynamic Effects of Dopamine and Prostaglandin A alone and in Combination

Robie, Norman W.; Goetter, William E.; Goldberg, Leon I.

doi:10.1159/000158002

Cited by 3 publications

(2 citation statements)

References 17 publications

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“…Renal blood flow increases markedly [19,23] while femoral blood flow increases to a lesser ex tent [3. 19, 20] in dogs that have been studied while conscious or under anesthesia.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Effects of Dopamine in Developing Swine

Buckley¹,

Brazeau²,

Frasier³

1983

Neonatology

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Cardiac function and peripheral blood flows were measured before and during single intravenous injections of dopamine (2–25 μg/kg) in developing and mature swine anesthetized with pentobarbital. A positive inotropic effect was observed in even the youngest swine. Renal vasoconstriction was observed even after low doses of dopamine in animals younger than 1 month of age, and femoral vasoconstriction in animals younger than 2 weeks of age, unless α-adrenergic receptors were blocked by phentolamine. We concluded that the vasodilator responses to dopamine are slower to develop in the renal than in the femoral circulation.

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“…Renal blood flow increases markedly [19,23] while femoral blood flow increases to a lesser ex tent [3. 19, 20] in dogs that have been studied while conscious or under anesthesia.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Effects of Dopamine in Developing Swine

Buckley¹,

Brazeau²,

Frasier³

1983

Neonatology

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“…The cardiovascular actions of dopamine are complex since they result from simultaneous aictivation of adrenoreceptors and dopamine cp-43 (Goldberg, 1972(Goldberg, , 1975Robie, Goetter & Goldberg, 1974;Sampson, Scroop & Louis, 1974, Setler, Pendleton & Finlay, 1975Furukawa et al, 1976). Intravenous infusion of dopamine to anaesthetized dogs causes increases in blood pressure, heart rate, cardiac contractility, cardiac output, renal blood flow and diuresis.…”

Section: A Dopaminementioning

confidence: 99%

Cardiovascular Dopamine Receptors: Physiological, Pharmacological and Therapeutic Implications

Lokhandwala

Barrett

1982

Journal of Autonomic Pharmacology

174

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Dopamine receptor activation can lead to pronounced changes in cardiovascular function. The myriad of effects produced by dopamine receptor agonists results from the activation of dopamine receptors located at different anatomical sites in the cardiovascular system. Further basic research is required to better characterize these dopamine receptors so as to allow the development of more specific dopamine receptor agonists. Endogenous dopamine may be involved in the physiological control of fluid and electrolyte balance and continuing research efforts in this area should provide for a better understanding of the role of cardiovascular dopamine receptors in the maintenance of overall circulatory homeostasis. Cardiovascular dopamine receptor stimulation represents an important and promising approach for the development of novel therapeutic agents for the treatment of hypertension, angina pectoris, congestive heart failure and acute renal failure.

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Antagonism of the renal vasodilator activity of dopamine by metoclopramide

Hahn¹,

Wardell²

1980

Naunyn-Schmiedeberg's Arch. Pharmacol.

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The interaction of metoclopramide with renal dopamine receptors has been characterized in anesthetized dogs surgically prepared with arterial blood pressure catheters and renal artery blood flowprobes. In normal dogs, i.v. dopamine (3 microgram/kg) produced consistent and selective decrements in renal vascular resistance (RVR) and increments in renal blood flow over a 220 min test period; mean arterial blood pressure and cardiac rate were minimally affected. Pretreatment with metoclopramide, 1 and 10 mg/kg i.v., resulted in dose-related inhibition (maximum inhibition 44% and 94%, respectively) of the renal vasodilator activity of dopamine without altering baseline parameters. The duration of antagonism produced by 1 mg/kg of metoclopramide was approximately 30 min, while 10 mg/kg resulted in significant attenuation for the entire test period. Decreases in RVR produced by prostaglandin A1 (0.03 and 0.3 microgram/kg, i.v.) and bradykinin (3 and 15 microgram/kg, i.v.) that were comparable to those of dopamine were unaltered by metoclopramide. Furthermore, metoclopramide did not affect the diastolic blood pressure responses to noradrenaline (0.2-3 microgram/kg, i.v.) or isoproterenol (0.03-0.3 microgram/kg, i.v.), nor did it alter dopamine-induced vasoconstriction of the iliac vasculature. In phenoxybenzamine (3 mg/kg, i.v.) treated dogs, dopamine (0.3-30 microgram/kg, i.v.) produced dose-related reductions in RVR. Administration of metoclopramide (10 mg/kg, i.v.) resulted in a 10-fold parallel displacement, to the right, of the RVR dose-response curve to dopamine. These findings demonstrate that metoclopramide is an effective antagonist of renal dopamine receptors following systemic administration in the dog. The results are not consistent with the classification of metoclopramide as a selective antagonist of D-2 receptors.

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Systemic and Renal Hemodynamic Effects of Dopamine and Prostaglandin A alone and in Combination

Cited by 3 publications

References 17 publications

Cardiovascular Effects of Dopamine in Developing Swine

Cardiovascular Effects of Dopamine in Developing Swine

Cardiovascular Dopamine Receptors: Physiological, Pharmacological and Therapeutic Implications

Antagonism of the renal vasodilator activity of dopamine by metoclopramide

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