Pharmacokinetic study of yohimbine and its pharmacodynamic effects on salivary secretion in patients treated with tricyclic antidepressants.

Bagheri, Haleh; Picault, P; Schmitt, Laurent; Houin, Georges; Berlan, Michel; Jl, Montastruc

doi:10.1111/j.1365-2125.1994.tb04248.x

Cited by 18 publications

(3 citation statements)

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“…In some studies agitation and anxiety have been reported (73,76). Although no signi®cant change in anxiety-and mood-inventory testing was found after different doses of yohimbine (up to 40 mg/day), in patients with psychiatric diseases, such as agoraphobia and panic attacks, it may induce panic episodes (83).…”

Section: Clinical Results With a Adrenoceptor Antagonists In Edmentioning

confidence: 99%

Erectile dysfunction: from biochemical pharmacology to advances in medical therapy

et al. 2000

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Research on penile smooth muscle physiology has increased the number of drugs available for treating erectile dysfunction (ED). Penile erection involves the relaxation of smooth muscle in the corpus cavernosum. The key mediator of smooth muscle relaxation is nitric oxide (NO), which acts by increasing the cellular level of cGMP. Another cyclic nucleotide, cAMP, is involved in smooth muscle cell relaxation; cAMP formation is stimulated by a number of compounds, such as alprostadil. An increase in cAMP and/or cGMP levels can also be induced by inhibition of phosphodiesterases (PDEs), the enzymes involved in cyclic nucleotide breakdown. Both papaverine and sildena®l are PDE inhibitors. Papaverine is a non-speci®c inhibitor of these enzymes; sildena®l is an orally active, potent and selective inhibitor of GMP-speci®c PDE5, the predominant isoenzyme metabolizing cGMP in the cells of the corpus cavernosum. Penile smooth muscle contraction, induced by adrenergic ®bers through a 1 adrenoceptors, produces detumescence, thus making a adrenoceptor antagonists suitable for maintenance of penile erection. The orally active drug yohimbine is a mixed a 1 -a 2 adrenoceptor antagonist that works by a dual mechanism; it facilitates sexual arousal by acting on a 2 adrenoceptors in the central nervous system and blocks adrenergic in¯uences at peripheral level.

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Section: Clinical Results With a Adrenoceptor Antagonists In Edmentioning

confidence: 99%

Erectile dysfunction: from biochemical pharmacology to advances in medical therapy

et al. 2000

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“…47 A dose of 4 mg of yohimbine also offset dry mouth caused by TCA without causing any adverse effects in a case series. 48 Reserpine is an alkaloid found primarily in Rauvolfia serpentina (Indian snakeroot) and related species. It is well-known as an antihypertensive, but can potentially cause depression in excess doses or in sensitive patients because of reserpine's depletion of catecholamine storage granules.…”

Section: Tca Adjunctsmentioning

confidence: 99%

Herbal Adjuncts to Antidepressants

Yarnell

2015

Alternative and Complementary Therapies

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The intentional use of herbal medicines to increase efficacy or decrease adverse effects of antidepressant drugs is reviewed, with notes about situations (mostly isolated case studies) in which such combinations might have been harmful. Hypericum perforatum (St. John's wort), a common antidepressant herb, is reviewed first, given that there are a number of concerns about possible harms that might arise from its use with various antidepressants. Although a handful of case studies suggest that there are problems, there is little definitive information, and preclinical research suggests the possibility of benefits.The safety of combining various herbs with monoamine oxidase-inhibiting drugs is reviewed next. Studies supporting the use of Crocus sativus (saffron) and Ginkgo biloba (ginkgo) to offset sexual adverse effects of selective serotonin reuptake inhibitors (SSRIs) are reviewed. Pausinystalia yohimbe (yohimbe) and its alkaloid yohimbine's ability to augment antidepressant therapy is discussed. The use of the herbal formula Rikkunshi-tō (Liù Jūn Zǐ Wán) to offset gastrointestinal adverse effects of SSRIs is reviewed. Finally, research on combining Rauvolfia serpentina (Indian snakeroot) and its alkaloid reserpine with antidepressants is mentioned. Much more research is needed in this area, given how frequently antidepressant drugs and herbs are used by patients.

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“…This was paralleled by a corresponding lack of effect on insulin levels at 120 min. We attribute this to the short half-life of the drug in circulation [the peak plasma concentration is reached at 1 to 1.5 hours, and half-life is 0.6 ± 0.3 hours (14,15)].…”

Section: Effects On Secondary Variablesmentioning

confidence: 99%

Genotype-based treatment of type 2 diabetes with an α _2A -adrenergic receptor antagonist

et al. 2014

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The feasibility of exploiting genomic information for individualized treatment of polygenic diseases remains uncertain. A genetic variant in ADRA2A, which encodes the α(2A)-adrenergic receptor (α(2A)AR), was recently associated with type 2 diabetes. This variant causes receptor overexpression and impaired insulin secretion; thus, we hypothesized that blocking α(2A)AR pharmacologically could improve insulin secretion in patients with the risk genotype. A total of 50 type 2 diabetes patients were recruited on the basis of ADRA2A genotype for a randomized placebo-controlled intervention study with the α(2A)AR antagonist yohimbine. The patients received 0, 10, or 20 mg of yohimbine at three separate visits. The primary endpoint was insulin secretion at 30 min (Ins30) during an oral glucose tolerance test (OGTT). Patients with the risk variant had 25% lower Ins30 than those without risk genotype. After administration of 20 mg of yohimbine, Ins30 was enhanced by 29% in the risk group, making secretion similar to patients carrying the low-risk allele. The corrected insulin response and disposition index in individuals with the high-risk (but not low-risk) allele were improved by 59 ± 18% and 43 ± 14%, respectively. The beneficial effect of yohimbine was not a consequence of improved insulin sensitivity. In summary, the data show that the insulin secretion defect in patients carrying the ADRA2A risk genotype can be corrected by α(2A)AR antagonism. The findings show that knowledge of genetic risk variants can be used to guide therapeutic interventions that directly target the underlying pathophysiology and demonstrate the potential of individualized genotype-specific treatment of type 2 diabetes.

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Pharmacokinetic study of yohimbine and its pharmacodynamic effects on salivary secretion in patients treated with tricyclic antidepressants.

Cited by 18 publications

References 18 publications

Erectile dysfunction: from biochemical pharmacology to advances in medical therapy

Erectile dysfunction: from biochemical pharmacology to advances in medical therapy

Herbal Adjuncts to Antidepressants

Genotype-based treatment of type 2 diabetes with an α _2A -adrenergic receptor antagonist

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Pharmacokinetic study of yohimbine and its pharmacodynamic effects on salivary secretion in patients treated with tricyclic antidepressants.

Cited by 18 publications

References 18 publications

Erectile dysfunction: from biochemical pharmacology to advances in medical therapy

Erectile dysfunction: from biochemical pharmacology to advances in medical therapy

Herbal Adjuncts to Antidepressants

Genotype-based treatment of type 2 diabetes with an α 2A -adrenergic receptor antagonist

Contact Info

Product

Resources

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Genotype-based treatment of type 2 diabetes with an α _2A -adrenergic receptor antagonist