Clonidine: A new antihypertensive agent

Onesti, Gaddo; Bock, K. D.; Heimsoth, V.; Kim, Kwan Eun; Merguet, P

doi:10.1016/0002-9149(71)90037-3

Cited by 84 publications

(30 citation statements)

References 17 publications

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“…While abun dant clinical evidence indicates the deleterious effects of clonidine on sexuality in man, the inadequacy of research in this field has prevented any clear definition of the nature of such effects. Thus clonidine is reported to inhibit both erection and libido [8,18,19,[25][26][27], to inhibit emission without affecting desire or excitement [17], or to inhibit erection without altering libido or ejaculation in men [3]. The decreased libido was attributed to a central suppres sant effect of clonidine [4].…”

Section: Discussionmentioning

confidence: 99%

“…Clonidine is a cen trally acting hypotensive believed to act via stimulation of a '-adrenoceptors [14,34]. Although clinical reports suggest that clonidine treatment is associated with erectile difficul ties and decreased libido [8,18,19,25,27] its sexual effects remain obscure, because of the death of appropriate con trolled studies. Based largely on data from rats, it has been suggested that male sexual behavior is under the control of central monoaminergic systems [2,24,25].…”

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confidence: 99%

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Evidence for the Modulation of Sexual Behavior by α-Adrenoceptors in Male Rats

Clark

Smith

Davidson³

1985

Neuroendocrinology

149

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Clonidine, a commonly used antihypertensive agent believed to act by stimulation of central α- adrenoceptors, produced a dose-related suppression of ejaculatory behavior in sexually vigorous male rats throughout the range of treatment (0.0125–0.5 mg/kg). Treatment with 0.25 mg/kg virtually eliminated ejaculatory behavior, without altering the number of animals mounting and intromitting. These effects were maintained for at least 4 h after treatment. Prazosin, another antihypertensive (but acting by blockade of α₁-adrenoceptors), increased latencies to initiation of copulation, to ejaculation, and to reinstatement of copulation following ejaculation. Additionally, prazosin (1 mg/kg) pretreatment failed to attenuate or prevent the clonidine-induced suppression of ejaculation. In contrast, yohimbine, a drug which preferentially blocks α₂-adrenoceptors (2 mg/kg, 20 min prior to mating tests), caused a facilitation of copulatory behavior as evidenced by drastic decreases in ejaculation latency and intercopulatory and postejaculatory intervals. Pretreatment with yohimbine completely prevented the clonidine-induced suppression of ejaculation, while clonidine attenuated the facilitatory effects of yohimbine, suggesting a competitive interaction. These data lead to the suggestion that increased excitatory adrenergic activity results in increased sexual arousal either by blockade of α₂- or stimulation of α₁-adrenocep-tors. Alternatively, stimulation of α₂- or blockade of α₁-adrenoceptors results in diminished sexual motivation. While the precise implications of this animal research for the clinic are as yet unclear, further research could lead to important developments in the pharmacological treatment of sexual dysfunctions.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Evidence for the Modulation of Sexual Behavior by α-Adrenoceptors in Male Rats

Clark

Smith

Davidson³

1985

Neuroendocrinology

149

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“…There is a 17±30% incidence of impotence reported in patients treated with clonidine; this is associated with retrograde ejaculation. 20,21 In case of alpha blockers, a possible explanation for the development of impotence is accompanying ejaculatory incompetence.…”

Section: Introductionmentioning

confidence: 99%

Sexual dysfunction related to antihypertensive agents: results from the animal model

et al. 1999

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The present investigation elucidates the deleterious effects of three prototypical antihypertensive drugs namely, propranolol, clonidine and captopril on the erectile physiology. In order to delineate the direct drug effects from vascular insuf®ciency inherent in hypertensive states, the study was conducted on a normotensive animal model. The adverse effects of these drugs were estimated as changes in sexual behaviour and intracavernous pressure response to electrical stimulation in the treated rats compared to normal age-matched controls (n 10, each group). Copulation studies indicated signi®cant impairment of sexual function in the groups on propranolol and clonidine. The cavernous pressure response to nerve stimulation at the end of sixteen weeks further reinforced the gross compromise on sexual function in these two treated groups. In contrast, the captopril administration produced only marginal alterations to the responses recorded. The results from this study clearly indicate that propranolol and clonidine interfere with sexual behaviour and nerve mediated response to erection whereas captopril which is devoid of signi®cant effects on these parameters, may be a better therapeutic option.

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“…The mechanism of hypotensive action is thought to be due to the a 2 -agonist activity (Hoffman & Lefkowitz 1980) . Clonidine has been reported to cause failure of erection and decreased libido (Laver 1974;Mroczek , Leibel & Finnerty 1972;Onesti et al 1971;Ebringer et al 1970;Khan, Camel & Perry 1970). One small study mentioned decreased libido and impotence in seven of 10 patients (Laver 1974).…”

Section: Clonidine ( Catapres®)mentioning

confidence: 99%

Pharmacosexology: The Effects of Drugs on Sexual Function – A Review

Buffum

1982

Journal of Psychoactive Drugs

158

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The literature on the sexual side effects of drugs and chemicals has been reviewed. There are many substances which alter the human sociosexual response cycle either negatively, positively or both. Many of the drugs used therapeutically have been reported to have adverse effects on sexuality, and this must be taken into account when these drugs are used clinically. Many substances which are used for recreational purposes (or sometimes abused) also have profound effects on sexual response. Many of these substances are used in such a way that they can correct underlying sexual problems. Treatment of a drug abuser may well prove unsuccessful without consideration of preexistent sociosexual problems and concerns. From the dawn of recorded history, many substances have been used for the purpose of sexual enhancement. Some of these have known success and their reputations have been passed down through the millenia. The chapter has not yet been closed on aphrodisiacs, even though none have survived the rigors of scientific scrutiny. As long as humans place value on optimal sexual functioning, there will be a demand for sex-enhancing drugs. In order for the scientific and medical community to successfully meet these challenges, more effective and relevant study designs will have to be utilized in order to separate fact from fancy. The study of pharmacosexology is in its infancy, and in order for it to grow and contribute to the world body of knowledge, more researchers and clinicians must be trained in both pharmacology and sexology.

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Clonidine: A new antihypertensive agent

Cited by 84 publications

References 17 publications

Evidence for the Modulation of Sexual Behavior by α-Adrenoceptors in Male Rats

Evidence for the Modulation of Sexual Behavior by α-Adrenoceptors in Male Rats

Sexual dysfunction related to antihypertensive agents: results from the animal model

Pharmacosexology: The Effects of Drugs on Sexual Function – A Review

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