Dopamine receptors: applications in clinical cardiology.

Goldberg, Leon I.; Rajfer, Sol I.

doi:10.1161/01.cir.72.2.245

Cited by 169 publications

(40 citation statements)

References 15 publications

(4 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It is successfully used in treatment of shock as it dilates renal arteries through activation of dopamine-1 (DA1) receptors and enhances cardiac activity via activation of cardiac -adrenergic receptors [20,27]. Dopamine receptors on vascular smooth muscles are classified by [30,31] as DA1.…”

Section: Dopaminementioning

confidence: 99%

Structure and Function of Smooth Muscle with Special Reference to Mast Cells

Vodenicharov¹

2012

Current Basic and Pathological Approaches to the Function of Muscle Cells and Tissues - From Molecules to Humans

View full text Add to dashboard Cite

Section: Dopaminementioning

confidence: 99%

Structure and Function of Smooth Muscle with Special Reference to Mast Cells

Vodenicharov¹

2012

Current Basic and Pathological Approaches to the Function of Muscle Cells and Tissues - From Molecules to Humans

View full text Add to dashboard Cite

“…To study this issue, the myocardial 13-adrenoceptor agonists dobutamine and dopamine were used.3 4 Although both of these drugs affect systemic vascular tone, only dopamine is capable of modulating vascular tone through peripheral dopaminergic receptors. 4 In addition, a-receptor activation may further modify dopamine's actions. 5 We further hypothesized that vasodilating agents may decrease diastolic pressures by several mechanisms.…”

Section: Carroll Et Almentioning

confidence: 99%

The differential effects of positive inotropic and vasodilator therapy on diastolic properties in patients with congestive cardiomyopathy.

Carroll¹,

Lang²,

Neumann³

et al. 1986

Circulation

Self Cite

115

View full text Add to dashboard Cite

Symptoms of congestive heart failure frequently reflect abnormalities in both systolic and diastolic performance. While much work has been reported regarding the mechanisms by which positive inotropic and vasodilator therapy affect systolic performance, little is known about their effect on diastolic function. In 12 patients with diffuse congestive cardiomyopathy micromanometer left ventricular and aortic pressure measurements were recorded simultaneously with two-dimensionally targeted M mode echocardiograms and thermodilution-determined cardiac output. Each patient received dopamine (2, 4, and 6 gg/kg/min), and dobutamine (2, 6, and 10 ,ug/kg/min), and 10 received nitroprusside (0.125 to 2.0 gg/kg/min). Baseline hemodynamics were characterized by low cardiac index (2.1 ± 0.7 liter/min/m2, mean ± SD), high left ventricular end-diastolic pressure (24 ± 10 mm Hg), and increased end-diastolic (6.8 + 1.0 cm) and end-systolic dimensions (6.0 1.0 cm). All patients had abnormal left ventricular pressure decay with a prolonged time constant (67 ± 20 msec) and reduced peak diastolic lengthening rates. Dopamine and dobutamine decreased the time constant of relaxation and increased the peak lengthening rate. Dobutamine also reduced the minimum diastolic pressure from 14 ± 7 to 10 + 9 mm Hg (p < .01); neither drug reduced end-diastolic pressure. In fact, dopamine elevated end-diastolic pressures in seven patients, despite more rapid pressure decay. Diastolic pressure-dimension relations after dopamine and dobutamine showed a leftward shift with a reduced end-systolic chamber size, but no significant changes in passive chamber stiffness. Nitroprusside decreased left ventricular minimum diastolic pressure by 4 ± 2 mm Hg and end-diastolic pressure by 7 ± 4 mm Hg (p < .0 1). It did not consistently accelerate left ventricular pressure decay at the doses tested. The decreased end-diastolic pressure with nitroprusside was due to a reduced end-diastolic dimension in five patients. In the other patients, all of whom had elevated right atrial pressures, diastolic pressure-dimension relations showed a parallel downward shift after nitroprusside. Thus, positive inotropic therapy with /31-adrenoceptor agonists enhances early diastolic distensibility by accelerating relaxation, augmenting filling, and reducing end-systolic chamber size. Vasodilator therapy is much more effective in lowering diastolic pressures. In some patients this is due to a reduction in extrinsic restraint of the pericardium and/or right ventricular interaction, while in others it simply reflects a decrease in chamber size without alterations in ventricular passive chamber properties. Circulation 74, No. 4, 815-825, 1986. AS OUR UNDERSTANDING of the pathophysiology of the heart failure syndrome has improved, certain classes of drugs have assumed prominent roles in its treatment.

show abstract

“…At higher doses recruitment of α 1-and α 2-adrenoceptors occurs resulting in increase in vascular resistance or until excessive β 1-adrenoceptor activity leads to tachycardia or ventricular arrhythmias. 7 Genetic factors could also had played an important role in our patient. Research has demonstrated that an SCN5A promoter polymorphism common in Asians modulates the duration of the PR and QRS intervals, thereby altering the action potential.…”

Section: Discussionmentioning

confidence: 84%

Cabergoline Induced Supraventricular Tachycardia with QT Prolongation

Menon¹,

Gaddipati²,

Venkatesh³

et al. 2017

IJOPP

View full text Add to dashboard Cite

Background:Cabergoline is commonly known to cause valvular disorders. Cases of supraventricular tachycardia with QT prolongation are seen, albeit, extremely rare. Aim: We report a case of supraventricular tachycardia with QT prolongation presumed secondary to cabergoline use. Clinical Details: A 30-year-old post-partal female complained of palpitation and syncope after two days of cabergoline usage. Her past medical history was insignificant. Electrocardiogram showed QT prolongation of 489 ms. Based on her presentation, we presume that the patient's condition was the result of cabergoline. Outcomes: Causality assessment was suggestive of a probable relationship between the patient's symptoms and her use of cabergoline. Symptoms improved significantly after the offending drug was withdrawn with an objective reduction in QTc. Conclusion: Electrocardiogram should be monitored in individuals receiving more than one QT prolonging medication or with symptoms of arrhythmia or are at high risk of QT prolongation/Torsades de Pointes.

show abstract

Dopamine receptors: applications in clinical cardiology.

Cited by 169 publications

References 15 publications

Structure and Function of Smooth Muscle with Special Reference to Mast Cells

Structure and Function of Smooth Muscle with Special Reference to Mast Cells

The differential effects of positive inotropic and vasodilator therapy on diastolic properties in patients with congestive cardiomyopathy.

Cabergoline Induced Supraventricular Tachycardia with QT Prolongation

Contact Info

Product

Resources

About