Dopamine agonists adverse effects

Adverse Effects of Dopamine Agonists Gastrointestinal Effects... 

Develop a formal plan to assess response and adverse effects of dopamine agonists. When appropriate, be sure to make dose adjustments. 

D5 has slightly different properties than D4, and it does not have any estrogenic activity [289]. It does, however, also have adverse effects on the reproductive system, much like D4, but also on the adipose tissue, bile production, and even immune system due to D5 s effect of reducing the prolactin levels [291]. In addition, it was determined that D5 causes a significant increase in uterine tumors in rats after a 160 ppm exposure. However, it is proposed that the tumors occur in rats through a mechanism that would not affect humans [291]. D5 also acts as a dopamine agonist and it can cause adverse effects on the nervous system in humans [291]. For exposures to D6 in rats, an increase in liver and thyroid mass and reproductive effects were observed [292]. 

Dopamine receptor agonists. Deficient dopaminergic transmission in the striatum can be compensated by ergot derivatives (bromocriptine p. 114], lisu-ride, cabergoline, and pergolide) and nonergot compounds (ropinirole, prami-pexole). These agonists stimulate dopamine receptors (D2, D3, and D sub-types), have lower clinical efficacy than levodopa, and share its main adverse effects. 

It is an ergot preparation which has a specific dopamine receptor agonist action (acts mainly on receptors) and capable of crossing the blood brain barrier. It is less active than levodopa and used only in late cases as a supplement to levodopa. Adverse effects are vomiting hallucinations, hypotension, nasal stuffiness. 

Bromocriptine is a D2 agonist its structure is shown in Table 16-6. This drug has been widely used to treat Parkinson s disease in the past, but is now rarely used for this purpose, having been superseded by the newer dopamine agonists. Bromocriptine is absorbed to a variable extent from the gastrointestinal tract peak plasma levels are reached within 1-2 hours after an oral dose. It is excreted in the bile and feces. The usual daily dose of bromocriptine for parkinsonism varies between 7.5 and 30 mg. To minimize adverse effects, the dose is built up slowly over 2 or 3 months from a starting level of 1.25 mg twice daily after meals the daily dose is then increased by 2.5 mg every 2 weeks, depending on the response or the development of adverse reactions. 

Dopamine agonists may produce adverse side effects such as nausea and vomiting. Postural hypotension is also a problem in some patients. With prolonged use, these drugs may cause CNS-related side effects such as confusion and hallucinations. 

Apomorphine, a very potent non-selective dopamine agonist, which acts on both Di and D2 receptors, has been nsed with some snccess in Parkinson s disease, particn-larly in patients with severe long-term adverse effects of levodopa. Because of first-pass metabohsm it has to be used subcutaneously, sublingually, or intranasally. Its adverse effects resemble those of levodopa. 

Barrett AM, Crucian GP, Schwartz RL, Heilman KM. Adverse effect of dopamine agonist therapy in a patient with motor-intentional neglect. Arch Phys Med Rehabil 1999 80(5) 600-3. 

Dopexamine, which is related structurally to dopamine, is a potent beta2-adrenoceptor agonist (1). Its reported adverse effects include cases of atrial fibrillation and single instances of supraventricular tachycardia and hypotension. 

Lisuride is a dopamine receptor agonist that is used as an alternative drug in the treatment of Parkinson s disease. The pattern of adverse effects is similar to that seen with most of the ergot alkaloids (SEDA-10,118). The adverse effects that occurred after subcutaneous administration were so troublesome that the subcutaneous formulation was eventually unmarketable. 

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