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PubMed1998

Intracerebroventricular infusion of CRF increases extracellular concentrations of norepinephrine in the hippocampus and cortex as determined by in vivo voltammetry.

Previous studies have indicated that intracerebroventricular (i.c.v.) infusions of corticotropin-releasing factor (CRF) activate locus coeruleus (LC) noradrenergic neurons and increase the metabolism and extracellular concentrations of norepinephrine (NE) in several brain regions, suggesting increased release. To examine the temporal aspects and mechanism of the presumed release of NE, CRF was infused i.c.v. and the oxidation current was recorded using carbon fiber voltammetric electrodes placed in rat hippocampus or cortex. The CRF (1 microg, i.c.v.) caused a significant increase of oxidation current with a delay of approximately 5 min, and a peak at approximately 35 min. Similar responses were observed in the medial prefrontal cortex. The hippocampal response was markedly attenuated when CRF was infused into rats pretreated with DSP-4 to deplete NE, suggesting that the observed changes in current resulted from oxidation of NE. The increase of NE-like current did not occur when 25 microg alpha-helical CRF9-41 (ahCRF) was injected immediately before 1 microg CRF, suggesting that the response was mediated by cerebral CRF-receptors. Subcutaneous pretreatment with the ganglionic blocker, chlorisondamine, at a dose of 3 mg/kg had no effect on the voltammetric response to CRF, but a 6 mg/kg dose completely prevented the response. The beta-adrenoceptor antagonists, S-propranolol (5 mg/kg), nadolol (5 and 10 mg/kg), and timolol (5 mg/kg) attenuated the NE response to i.c.v. CRF to varying degrees. When chlorisondamine (3 microg) or nadolol (5 microg) were given i.c.v. before the CRF, the hippocampal responses were not blocked. These results suggest peripheral actions of ganglionic and beta-adrenergic blockers. We conclude that peripheral autonomic mechanisms, and probably both central and peripheral beta-adrenoceptors, contribute to the increased secretion of hippocampal NE in response to i.c.v. CRF.

Adrenergic beta-Antagonists↗

PubMed1981

Cell survival in chick embryo ciliary ganglion is reduced by chronic ganglionic blockade.

Changes in the activities of enzymes involved in the synthesis or degradation of transmitters has been used as an index of maturation in autonomic neurons. In some cases, a reduction in enzyme activity during normal development may reflect decreased cell survival rather than, or in addition to, changes in the rate of development. Similarly, changes in enzyme activity following experimental manipulation during development may also reflect cell loss. In the ciliary ganglion, biochemical indexes of development are altered after denervation, and after treatment with a ganglionic blocker, chlorisondamine. Surgical removal of afferents to the ciliary ganglion in the early chick embryo results in a virtually complete loss of ganglion cells. Chiappinelli et al. have reported that choline acetyltransferase (ChAT) is reduced in chick iris and ciliary ganglion after chronic treatment with chlorisondamine (on days 5, 8, 10 and 13 of incubation). This suggests that the development of transmitter enzymes may be regulated via interaction at the presynaptic site. Since they also report that chlorisondamine treatment reduced ganglionic dry weight, which could reflect a loss of cells, it may be that the same synaptic interaction governs cell survival as well as enzyme maturation. The present study provides evidence that treatment with chlorisondamine does, in fact, reduce cell survival in the ciliary ganglion.

Afferent Pathways↗

PubMed2006

Leptin inhibits gastric emptying in rats: role of CCK receptors and vagal afferent fibers.

Leptin regulates energy homeostasis and body weight by balancing energy intake and expenditure. It was recently reported that leptin, released into the gut lumen during the cephalic phase of gastric secretion, is capable of initiating intestinal nutrient absorption. Vagal afferent neurons also express receptors for both CCK and leptin, which are believed to interact in controlling food intake. The present study was undertaken to investigate the central and peripheral effects of leptin on gastric emptying rate. Under anesthesia, male Sprague-Dawley rats (250-300 g) were fitted with gastric Gregory cannulas (n=12) and some had additional cerebroventricular cannulas inserted into their right lateral ventricles. Following recovery, the rate of gastric emptying of saline (300 mOsm/kg H(2)O) was determined after instillation into the gastric fistula (3 ml, 37 degrees C, containing phenol red, 60 mg/l as a non-absorbable dilution marker). Gastric emptying rate was determined from the volume and phenol red concentrations recovered after 5 min. Leptin, injected intraperitoneally (i.p.; 10, 30, 60, 100 microg/kg) or intracerebroventricularly (i.c.v.; 5, 15 microg/rat) 15 min before the emptying, delayed gastric emptying rate of saline at the dose of 30 microg/kg or 15 microg/rat (p<0.001). When CCK(1) receptor blocker L-364,718 (1 mg/kg, i.p.), CCK(2) receptor blocker L-365,260 (1 mg/kg, ip) or adrenergic ganglion blocker bretylium tosylate (15 mg/kg, i.p.) was administered 15 min before ip leptin (30 microg/kg) injections, leptin-induced delay in gastric emptying was abolished only by the CCK(1) receptor blocker (p<0.001). However, the inhibitory effect of central leptin on gastric emptying was reversed by adrenergic blockade, but not by either CCK antagonists. Our results demonstrated that leptin delays gastric emptying. The peripheral effect of leptin on gastric motility appears to be mediated by CCK(1) receptors, suggesting the release of CCK and the involvement of vagal afferent fibers. On the other hand, the central effect of leptin on gastric emptying is likely to be mediated by adrenergic neurons. These results indicate the existence of a functional interaction between leptin and CCK receptors leading to inhibition of gastric emptying and short-term suppression of food intake, providing an additional feedback control in producing satiety.

Animals↗

PubMed1996

Potential role of the autonomic nervous system in the immunosuppressive effects of acute morphine administration.

These studies investigated the role of the autonomic nervous system in mediating the immunosuppressive effect of morphine on blood lymphocyte proliferation in rats. To determine the contribution of the autonomic nervous system, rats were pretreated with the ganglionic blocker chlorisondamine (5 mg/kg) prior to morphine (7 mg/kg) administration. Ganglionic blockade with chlorisondamine completely antagonized the inhibitory actions of morphine, suggesting that intact ganglionic transmission was required for the inhibition to occur. Blockade of postganglionic parasympathetic neurotransmission with atropine methylbromide (1 mg/kg) or blockade of sympathetic neurotransmission with the alpha-adrenoceptor antagonist phentolamine (1 mg/kg) did not attenuate the suppressive effect of morphine. Blockade of beta-adrenoceptors with propranolol (2.5 mg/kg) resulted in partial antagonism, but this action was not shared by the peripherally acting beta-adrenoceptor antagonist nadolol (6 mg/kg). These results suggest that the inhibitory effect of morphine on blood lymphocyte proliferation may be mediated through activation of the autonomic nervous system; however, individual blockade of either the parasympathetic or sympathetic division of the autonomic nervous system was not sufficient to antagonize this immunosuppressive effect.

Animals↗

PubMed2001

Depletion of brown fat norepinephrine content by acute cold exposure and adrenoceptor blockade.

Experiments were conducted to characterize the effects of acute cold exposure, with and without adrenoceptor blockade, on intrascapular brown adipose tissue (IBAT) and adrenal catecholamine content in male Sprague-Dawley rats. Groups of animals with indwelling temperature transmitters were tested following treatment with saline, the alpha-adrenoceptor blocker phentolamine, the beta-adrenoceptor blocker propranolol, combined blockade with phentolamine plus propranolol, and the ganglionic blocker chlorisondamine. IBAT norepinephrine (NE) content was not affected in animals tested at 22 degrees C, but was reduced in 4 degrees C-exposed animals treated with phentolamine (-57%), phentolamine plus propranolol (-97%), and chlorisondamine (-42%). Adrenal NE and epinephrine (EPI) content were not altered by the treatments at 4 degrees C or 22 degrees C. None of the treatments affected the temperature of animals at 22 degrees C, but significant hypothermia occurred at 4 degrees C after chlorisondamine (-2.3+/-0.3 degrees C) and the combination of phentolamine and propranolol (-1.5+/-0.4 degrees C). These results suggest that cold exposure alone did not affect IBAT NE content, but when cold exposure was combined with adrenoceptor blockade, the sympathetic activation was sufficient to cause a reduction in IBAT NE content. In addition, alpha- and beta-adrenoceptor-mediated mechanisms contribute to the maintenance of core temperature. However, both alpha- and beta-receptor mechanisms had to be interrupted before a deficit in body temperature was detected.

Adipose Tissue, Brown↗

PubMed1989

Involvement of adrenergic mechanism in hyperglycemia due to SCN stimulation.

Previously we found that in rats, electrical stimulation of the suprachiasmatic nucleus (SCN) of the hypothalamus elicited hyperglycemia associated with hyperglucagonemia without immediate hyperinsulinemia. To clarify the mechanism of these responses, we examined the effects of blockers of the autonomic nervous system on these responses. Hexamethonium, a ganglion blocker, suppressed the hyperglycemic and hyperglucagonemic responses to electrical stimulation of the SCN. Both bunazosin, an alpha 1-adrenergic blocker, and yohimbin, an alpha 2-adrenergic blocker, increased the level of insulin before stimulation, but only the latter suppressed the hyperglycemic and hyperglucagonemic responses. Propranolol, a beta-adrenergic blocker, partially inhibited the responses. These findings suggest that alpha 2- and beta-adrenergic mechanisms are involved in the hyperglycemic and hyperglucagonemic responses to SCN stimulation.

Adrenergic alpha-Antagonists↗

PubMed1997

Functional evidence of excitatory M1 receptors in the rabbit airway.

The effect of vagally and acetylcholine (ACh)-induced bronchoconstrictions was assessed by an increase in the slowly adapting pulmonary stretch receptor (SAR) activity during both inflation and deflation and the rise in total lung resistance (R(L)). Those responses were compared before and after pirenzepine (PZ, M1 selective) with or without propranolol (a beta adrenoreceptor blocker), gallamine (M2 selective), 4-DAMP (M3 selective), hexamethonium (C6, a ganglion blocker) and atropine (a nonselective muscarinic receptor antagonist). The SAR activity was recorded from the cut left vagus nerve, whereas the right vagus nerve was cut and stimulated electrically. Experiments were performed in anesthetized, artificially ventilated rabbits. Vagal stimulation (5-20 Hz, 13 V, 0.2 msec) for 30 sec and ACh injection (1 and 3 microg/kg) caused bronchoconstriction in a frequency- and dose-dependent manner. At the treatment with PZ (3-30 microg/kg) in both propranolol-untreated and -treated animals, vagally mediated bronchoconstriction was blocked by this M1 receptor blocker at 10 microg/kg, whereas ACh-induced bronchoconstriction was not significantly altered by any dose of PZ. Gallamine (3-30 microg/kg) had no significant effect on vagally and ACh-induced bronchoconstrictions, which were completely blocked by atropine (2 mg/kg). Three micrograms of 4-DAMP augmented the SAR and R(L) responses to vagal stimulation but inhibited those responses to ACh injection. 4-DAMP at 10 to 30 microg/kg dose-dependently inhibited both vagally and ACh-induced bronchoconstrictions. C6 (20 mg/kg) abolished vagally mediated bronchoconstriction but had no significant effect on ACh-induced bronchoconstriction. These results suggest that M1 receptors function as the excitatory receptors in the rabbit airway.

Acetylcholine↗

PubMed1994

Ligand specificity of nicotinic acetylcholine receptors in rat spinal cord: studies with nicotine and cytisine.

Administration of nicotinic agonists to the spinal cord leads to a variety of cardiovascular and behavioral responses. The discrete localization of afferent and efferent fibers presents a system in which occupation of nicotinic receptor subtypes might be correlated with specific pharmacologic responses. To this end, we examined [3H]cytisine and [3H]nicotine binding to membranes isolated from regions of the rat spinal cord. [3H]Cytisine showed saturable, noncooperative (nH congruent to 1) binding to a single-class of sites with a Kd of 0.44 +/- 0.01 nM and total saturable sites of 19.9 +/- 0.9 fmol/mg of protein. [3H]Cytisine binding to membranes from intermediolateral cell column and dorsal and ventral sections of the lumbosacral regions each revealed a single class of binding sites with virtually identical Kd values. However, the dorsal sections of the lumbar spinal cord contained a higher number of total binding sites than ventral lumbar or intermediolateral sections. The rank order potencies of the nicotinic agonists competing for [3H]cytisine binding was cytisine > I-nicotine > N-methylcarbamylcholine > dimethylphenylpiperazinium > acetylcholine > d-nicotine > carbamylcholine. Competitive antagonists also competed with high affinities (Ki as low as nanomolar) with the order of potencies being alpha-lobeline > or = dihydro-beta-erythroidine >> methyllycaconitine, whereas the channel blockers, mecamylamine and hexamethonium, only competed at concentrations > or = 100 microM. Competitive ganglionic blockers such as d-tubocurarine or trimethaphan and neurotoxins such as alpha-bungarotoxin, alpha-cobratoxin or neuronal bungarotoxin had weak affinities for cytisine sites. Similar to [3H]cytisine, [3H]nicotine also revealed a saturable single class of binding sites, but of lower affinity. The rank order of Ki values of the agonists, antagonists and neurotoxins for competing with [3H]nicotine binding was similar to the order for [3H]cytisine. Nicotinic receptors in the spinal cord membrane show a specificity for both agonists and antagonists that differ from neuronal receptors in the ganglia or the regions of the brain characterized to date. These findings, when correlated with the pharmacological responses documented in the comparison article suggests that the spinal nicotinic receptors may define a new member of the neuronal nicotinic receptor family.

Alkaloids↗

PubMed1988

Discriminative stimulus effects of cholinergic agonists and the actions of their antagonists.

Both muscarinic- and nicotinic-cholinergic agonists have been used for discrimination training, but only nicotine has been studied extensively. The limited information available suggests that the discriminative stimulus effects of drugs classified as muscarinic-cholinergic agonists are blocked competitively by atropine but not by ganglion-blockers. The discriminative effects of nicotine are blocked non-competitively by ganglion-blocking drugs that penetrate into the CNS (e.g. mecamylamine), but they are not blocked by atropine. The specificity of the block is shown by the failure of mecamylamine to block several non-nicotinic drugs. The ganglion-blocking drug chlorisondamine penetrates poorly into the CNS when injected systemically; when injected intraventricularly, it is a potent and specific nicotine antagonist with a 4-week duration of effect. Haloperidol attenuates discriminative effects of nicotine but this is not a specific block; there are marked reductions in response rate, the morphine stimulus is also attenuated, and other neuroleptics have much weaker effects. The results support the view that the discriminative effect of nicotine involves predominantly cholinoceptive sites, and they suggest that it is not mediated primarily by the dopamine system. The transduction mechanisms for the nicotine stimulus may include the receptor sites that mediate many of its other CNS effects, but more information is needed about possible subtypes of nicotinic receptors before definitive conclusions are possible.

Animals↗

PubMed1994

N-Methyl-D-aspartate receptor-mediated signaling in the supraoptic nucleus involves activation of a nitric oxide-dependent pathway.

N-Methyl-D-aspartate (NMDA) microinjection (1 mM, 0.2 microliter) into the hypothalamic supraoptic nucleus (SON) stimulated heart rate in urethane-anaesthetized rats. This effect was inhibited by coinjection of a competitive blocker of NMDA receptors, CPP (20 nmol) or by pretreatment with a sympathetic ganglionic blocker, chlorisondamine chloride (5 mg/kg i.p.), but not by prior hypophysectomy. Furthermore, the cardioexcitatory effect of intra-SON NMDA was inhibited by prior intra-SON injection of a competitive blocker of nitric oxide (NO) synthesis, NG-nitro-L-arginine methyl ester (40 nmol) or a blocker of the soluble guanylate cyclase, Methylene blue (20 nmol), and was mimicked by intra-SON injection of a calcium ionophore, A23187 (10 nmol), which stimulates NO production by raising intracellular free calcium levels. Finally, intra-SON microinjection of a membrane-permeating cGMP analog, 8-bromo-cGMP (20 nmol) stimulated heart rate in urethane-anaesthetized rats. The results point to a functional link between a sympathetically mediated cardiophysiological effect of NMDA receptor stimulation in the SON and activation of the NO/cGMP signal transduction pathway.

Animals↗

PubMedDate not supplied

Effects of chlorisondamine and restraint on cortical [3H]ketanserin binding, 5-HT2A receptor-mediated head shakes, and behaviours in models of anxiety.

A recent study has indicated that ganglionic transmission mediates acute restraint-elicited increases in brain tryptophan (5-HT precursor) levels, 5-HT synthesis and (possibly) release. Because restraint-induced release of 5-HT has been shown to be associated with a paradoxical increase in cortical 5-HT2A receptor binding, we have examined the influence of 5-HT synthesis/release upon cortical 5-HT2A receptor binding and 5-HT2A receptor-mediated head shakes in 3-hr restrained rats pretreated with the ganglionic blocker chlorisondamine. In keeping with past reports regarding the effects of restraint and ganglionic blockade upon anxiety, we have also measured the behavioural effects of restraint and/or chlorisondamine in two animal models of anxiety, the elevated plus-maze and the social interaction test. Chlorisondamine pretreatment (2.5 mg/kg, 20 min beforehand) prevented restraint-elicited defaecation and body weight decreases. Although stress amplified the head shake response to the injection of the 5-HT2A/5-HT2C receptor agonist 1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane (DOI, 1 or 2 mg/kg 2 hr after the end of restraint), cortical [3H]ketanserin binding remained unaltered. Chlorisondamine treatment was inactive, except for the amplification of the head shake response to DOI (2 mg/kg) in restrained rats. When exposed to the social interaction test, neither restraint nor chlorisondamine affected social interaction, locomotion, or rearings. In the elevated plus-maze, the percent number of open arms entered and the total number of arms entered were decreased by acute restraint, whilst chlorisondamine pretreatment was inactive.

Animals↗

PubMed1975

Effects of divalent cations and of catecholamines on the late response of the superior cervical ganglion.

The characteristics of the late response of the superior cervical ganglion of dogs were studied by close-arterial injection of catecholamines and divalent cations to the ganglion. 2. Dopamine, noradrenaline and adrenaline inhibit the late response as well as ganglionic activity induced by other means. The effect of dopamine is brief but that of adrenaline is prolonged. 3. Cd2+, Co2+, Ni2+, Zn2+, Hg2+ and Fe2+ markedly potentiate the late response, whereas Mn2+, Ca2+ and Mg2+ inhibit it. 4. may potentiate ganglionic activity triggered by other ganglionic stimulants. The Cd-augmented activity may be blocked by a ganglion-blocker which is specific to the stimulant. 5. CdCl2 may exhibit a direct ganglion-stimulating action on a ganglion which shows prominent late responses and has been conditioned by tetanic preganglionic stimulation. 6. CdCl2 and MnCl2 may inhibit ganglionic transmission by suppressing acetylcholine release from presynaptic nerve terminals. 7. It is concluded that the late response represents the late discharges of ganglion cells, which are very sensitive to inhibition by CaCl2 and MnCl2 and may be potentiated by CdCl2.

Animals↗

PubMed1970

Turnover rate of brain 5-hydroxytryptamine increased by D-amphetamine.

1. Administration of two doses of amphetamine HCl (5 mg/kg intraperitoneally) 45 min apart raised body temperature of rats by an average of 3.4 degrees C and increased the turnover rate of brain 5-hydroxytryptamine (5-HT) by almost one-half.2. Both effects were blocked by exposure to 4 degrees C or by pretreatment with the beta-blocker Kö 592 (1-(2-methylphenoxy)-3-isopropylamine-2-propanol), but not by the administration of the ganglionic blocker chlorisondamine combined with atropine.3. Since it has previously been shown that hyperthermia per se increases the turnover rate of brain 5-HT, and that amphetamine does not directly affect the uptake and release of 5-HT in brain slices, it is concluded that the amphetamine-induced increase in 5-HT turnover may be secondary to the rise in temperature produced by the drug.

Adrenergic beta-Antagonists↗

PubMed1997

Stretch-induced stimulation of lower airway nitric oxide formation in the guinea-pig: inhibition by gadolinium chloride.

The effect of stretch on lower airway nitric oxide formation was studied in normoxic tracheostomized anaesthetized guinea-pigs. Increase of level of positive end-expiratory pressure caused increased lower airway nitric oxide formation, as measured by its presence in exhaled tracheal air. The L-type calcium channel blocker, verapamil, did not decrease lower airway nitric oxide formation. Neither the local anaesthetic xylocaine nor the ganglion blocker trimetaphan affected exhaled nitric oxide, excluding local and centrally-mediated neuronal reflexes. Intravenous administration of gadolinium chloride (GdCl3, 50 mg/kg) induced a rapid and pronounced decrease (75%) in the basal level of exhaled nitric oxide. GdCl3 completely abolished lower airway nitric oxide formation induced by ventilation with positive end-expiratory pressure (7 cm H2O). GdCl3 induced hypoxaemia, but there was no indication for the development of lung oedema. The results indicate that positive end-expiratory pressure stimulates lower airway nitric oxide formation in the guinea-pig. GdCl3 inhibits lower airway nitric oxide formation in the guinea-pig in vivo, perhaps by interference with stretch-induced cellular calcium-influx.

Animals↗

PubMed1986

Capsaicin-induced beta-adrenergic action on energy metabolism in rats: influence of capsaicin on oxygen consumption, the respiratory quotient, and substrate utilization.

The mode of action of capsaicin on energy metabolism was investigated in rats. The oxygen consumption was higher when capsaicin (6.0 mg/kg) was intraperitoneally injected than when it was not injected. The respiratory quotient (R.Q.) increased and then decreased after the administration of capsaicin. The levels of serum glucose and immunoreactive insulin rapidly increased after the administration of capsaicin. Also, liver glycogen rapidly decreased, in contrast to the serum glucose concentration which rapidly increased. The serum-free fatty acid level gradually increased after the administration of capsaicin. These alterations in energy metabolism on the administration of capsaicin were similar to those in the metabolism of epinephrine, and were specifically inhibited by various beta-adrenergic blockers. On the other hand, the alterations were not affected by pretreatment with alpha-adrenergic or ganglion blockers. These results suggest that the mode of action of capsaicin on the enhancement of energy metabolism in rats comprises a direct (as an agonist) and/or an indirect (via catecholamine) beta-adrenergic action. Therefore, it was speculated that the adrenergic action of capsaicin resulted, at least in part, in a decrease in the perirenal adipose tissue weight and serum triglyceride concentration in rats fed a high fat diet supplemented with capsaicin (T. Kawada et al., J Nutr 116:1272-1278, 1986).

Adrenergic beta-Agonists↗

PubMed2003

Venous dilator effect of apelin, an endogenous peptide ligand for the orphan APJ receptor, in conscious rats.

Apelin is an endogenous depressor peptide for the G protein-coupled APJ receptor. Our hypothesis is that apelin is a venodilator, and it reduces mean circulatory filling pressure (MCFP; index of venous tone). Dose-response curves of apelin (10, 20 and 40 nmol/kg) or vehicle (0.9% NaCl) were constructed in two groups each of conscious, unrestrained rats: unblocked rats and rats pretreated with mecamylamine (Mec; ganglionic blocker) and noradrenaline (NA; to restore vascular tone). The vehicle had no effects in the unblocked or ganglionic-blocked rats. Apelin decreased mean arterial pressure (MAP) and increased heart rate (HR), but it did not alter mean circulatory filling pressure in the unblocked rats. In the ganglionic-blocked rats, apelin did not alter heart rate but decreased mean arterial pressure and mean circulatory filling pressure. These results show that apelin is an arterial and venous dilator in vivo. The depressor effect of apelin is accompanied by tachycardia which is abolished by ganglion blockade.

Animals↗

PubMed1984

Nicotinic stimulant, DMPP(1,1-dimethyl-4-phenylpiperazinium iodide) on the isolated bronchial smooth muscle preparation of guinea-pig.

Contractile responses of the isolated bronchial preparation of guinea-pig to DMPP, a nicotinic stimulant, were inhibited by ganglion blockers but not influenced by atropine, suggesting that DMPP did not bring about a contribution by stimulation of cholinergic ganglion cells. The fact that tetrodotoxin did not influence the response to DMPP suggests that a possible site of action of DMPP is not on the nerve cells.

Animals↗

PubMed1991

The effect of drugs on male sexual function and fertility.

Drugs may have negative effects on male libido, erection, ejaculation and orgasm, as well as on fertility, and research on these effects is increasing. Libido may be decreased by drugs that block dopamine or testosterone, or that cause dysphoria. Erection may be decreased by drugs that divert blood flow from the penis, or drugs that affect spinal reflexes. Ganglion blockers may also inhibit erection. Ejaculation may be diminished by drugs that affect spinal reflexes or be inhibited by ganglion blockage. Enervation of the vas deferens and epididymis may be blocked and cause a smaller emission. Retrograde ejaculation may occur due to blockage of the internal urethral sphincter. Orgasm is usually inhibited by the drugs that inhibit ejaculation. Fertility is impaired by drugs that affect sexual performance or spermatogenesis. Major groups of drugs that may affect male sexual function include drugs of abuse, CNS depressants, antihypertensives, anticholinergics, psychotherapeutics, hormones, and cancer therapeutics, in addition to miscellaneous other agents. Information about these drugs has been arranged in tables so that the provider has a convenient reference to use when explaining to men the effect of drugs on sexual response and fertility.

Drug-Related Side Effects and Adverse Reactions↗