Catapres and Weed

{Fulldrug} and Weed

Authored by Pin Ng PhD

Edited by Hugh Soames

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Catapres and Weed


Most people who consume marijuana do so for its mood-altering and relaxing abilities. Weed gives people a high and allows them to relax. However, heavy consumption of weed can cause unwanted results. It can increase the anxiety and depression a person experiences, and it can interact with certain other drugs including Catapres. It is important to remember that interactions do occur with all types of drugs, to a great or lesser extent and this article details the interactions of mixing Catapres and Weed.


Mixing Catapres and Weed


Clonidine, sold under the brand name Catapres among others, is an α2-adrenergic agonist medication used to treat high blood pressure, ADHD, drug withdrawal (alcohol, opioids, or nicotine), menopausal flushing, diarrhea, spasticity, and certain pain conditions. It is used orally (by mouth), by injection, or as a transdermal skin patch. Onset of action is typically within an hour with the effects on blood pressure lasting for up to eight hours.

Common side effect include dry mouth, dizziness, headaches, hypotension, and sleepiness. Severe side effects may include hallucinations, heart arrhythmias, and confusion. If rapidly stopped, withdrawal effects may occur. Use during pregnancy or breastfeeding is not recommended. Clonidine lowers blood pressure by stimulating α2 receptors in the brain, which results in relaxation of many arteries.

Clonidine was patented in 1961 and came into medical use in 1966. It is available as a generic medication. In 2020, it was the 75th most commonly prescribed medication in the United States, with more than 9 million prescriptions.

Clonidine is used to treat high blood pressure, attention deficit hyperactivity disorder (ADHD), drug withdrawal (alcohol, opioids, or smoking), menopausal flushing, diarrhea, and certain pain conditions. It also sees some use off-label for episodic insomnia, restless-legs syndrome, and anxiety, among other uses.

Clonidine may be effective for lowering blood pressure in people with resistant hypertension.

Clonidine works by slowing the pulse rate and exerts a reduction of serum concentrations of renin, aldosterone, and catecholamines.

Clonidine may improve symptoms of attention deficit hyperactivity disorder in some people but causes many adverse effects and the beneficial effect is modest. In Australia, clonidine is an accepted but not approved use for ADHD by the TGA. Clonidine, along with methylphenidate, has been studied for treatment of ADHD. While not as effective as methylphenidate in treating ADHD, clonidine does offer some benefit; it can also be useful in combination with stimulant medications. Some studies show clonidine to be more sedating than guanfacine, which may be better at bedtime along with an arousing stimulant in the morning. Clonidine has been used to reduce sleep disturbances in ADHD, including to help offset stimulant-associated insomnia.

Clonidine may be used to ease drug withdrawal symptoms associated with abruptly stopping the long-term use of opioids, alcohol, benzodiazepines and nicotine. It can alleviate opioid withdrawal symptoms by reducing the sympathetic nervous system response such as tachycardia and hypertension, hyperhidrosis (excessive sweating), hot and cold flashes, and akathisia. It may also be helpful in aiding smokers to quit. The sedation effect can also be useful. Clonidine may also reduce severity of neonatal abstinence syndrome in infants born to mothers that are using certain drugs, particularly opioids. In infants with neonatal withdrawal syndrome, clonidine may improve the neonatal intensive care unit Network Neurobehavioral Score.

Clonidine has also been suggested as a treatment for rare instances of dexmedetomidine withdrawal.

Clonidine has some role in the treatment of spasticity, acting principally by inhibiting excessive sensory transmission below the level of injury. Its use, however, is mainly as a second or third line agent, due to side effects such as hypotension, bradycardia, and drowsiness.

Clonidine also has several off-label uses, and has been prescribed to treat psychiatric disorders including stress, sleep disorders, hyperarousal caused by post-traumatic stress disorder, borderline personality disorder, and other anxiety disorders. Clonidine is also a mild sedative, and can be used as premedication before surgery or procedures. It has also been studied as a way to calm acute manic episodes. Its epidural use for pain during heart attack, and postoperative and intractable pain has also been studied extensively. Clonidine can be used in restless legs syndrome. It can also be used to treat facial flushing and redness associated with rosacea. It has also been successfully used topically in a clinical trial as a treatment for diabetic neuropathy. Clonidine can also be used for migraine headaches and hot flashes associated with menopause. Clonidine has also been used to treat refractory diarrhea associated with irritable bowel syndrome, fecal incontinence, diabetes, diarrhea associated with opioid withdrawal, intestinal failure, neuroendocrine tumors, and cholera. Clonidine can be used in the treatment of Tourette syndrome (specifically for tics). Clonidine has also had some success in clinical trials for helping to remove or ameliorate the symptoms of hallucinogen persisting perception disorder (HPPD).

Injection of α2 receptor agonists into the knee joint space, including clonidine, may reduce the severity of knee pain after arthroscopic knee surgery.

Light-activated derivatives of clonidine (adrenoswitches) have been developed for research purposes and shown to control pupillary reflex with light in blind mice by topical application.

The reduction in circulating norepinephrine by clonidine was used in the past as an investigatory test for phaeochromocytoma, which is a catecholamine-synthesizing tumor, usually found in the adrenal medulla. In a clonidine suppression test, plasma catecholamine levels are measured before and 3 hours after a 0.3 mg oral test dose has been given to the patient. A positive test occurs if there is no decrease in plasma levels.

It is classified by the TGA of Australia as pregnancy category B3, which means that it has shown some detrimental effects on fetal development in animal studies, although the relevance of this to human beings is unknown. Clonidine appears in high concentration in breast milk; a nursing infant’s serum clonidine concentration is approximately 2/3 of the mother’s. Caution is warranted in women who are pregnant, planning to become pregnant, or are breastfeeding.

The principal adverse effects of clonidine are sedation, dry mouth, and hypotension (low blood pressure).

By frequency

Very common (>10% frequency):

Common (1–10% frequency):

Uncommon (0.1–1% frequency):

Rare (<0.1% frequency):

Because clonidine suppresses sympathetic outflow, resulting in lower blood pressure, sudden discontinuation can result in acute hypertension due to a rebound in sympathetic outflow. In extreme cases, this can result in a hypertensive crisis, which is a medical emergency.

Clonidine therapy should generally be gradually tapered when discontinuing therapy to avoid rebound effects from occurring. Treatment of clonidine withdrawal hypertension depends on the severity of the condition. Reintroduction of clonidine for mild cases, alpha and beta blockers for more urgent situations. Beta blockers never should be used alone to treat clonidine withdrawal as alpha vasoconstriction would still continue.

Clonidine crosses the blood–brain barrier.

Clonidine treats high blood pressure by stimulating α2 receptors in the brainstem, which decreases peripheral vascular resistance, lowering blood pressure. It has specificity towards the presynaptic α2 receptors in the vasomotor center in the brainstem. This binding has a sympatholytic effect, suppresses release of norepinephrine, ATP, renin, and neuropeptide Y which if released would increase vascular resistance.: 201–203 

Clonidine also acts as an agonist at imidazoline-1 (I1) receptors in the brain, and it is hypothesized that this effect may contribute to reducing blood pressure by reducing signaling in the sympathetic nervous system; this effect acts upstream of the central α2 agonist effect of clonidine.: 201–203 

Clonidine may also cause bradycardia, theoretically by increasing signaling through the vagus nerve. When given intravenously, clonidine can temporarily increase blood pressure by stimulating α1 receptors in smooth muscles in blood vessels. This hypertensive effect is not usual when clonidine is given orally or by the transdermal route.

Plasma concentration of clonidine exceeding 2.0 ng/mL does not provide further blood pressure reduction.

In the setting of attention deficit hyperactivity disorder (ADHD), clonidine’s molecular mechanism of action occurs due to its agonism at the alpha-2A adrenergic receptor, the subtype of the adrenergic receptor that is most principally found in the brain. Within the brain, the alpha-2A adrenergic receptors are found within the prefrontal cortex (PFC), among other areas. The alpha-2A adrenergic receptors are found on the presynaptic cleft of a given neuron, and, when activated by an agonist, the effect on downstream neurons is inhibitory. The inhibition is accomplished by preventing the secretion of the neurotransmitter norepinephrine. Thus, clonidine’s agonism on alpha-2A adrenergic receptors in the PFC inhibits the action of downstream neurons by preventing the secretion of norepinephrine.

This mechanism is similar to the brain’s physiological inhibition of PFC neurons by the locus ceruleus (LC), which secretes norepinephrine into the PFC. Although norepinephrine can also bind to target adrenergic receptors on the downstream neuron (otherwise inducing a stimulatory effect), norepinephrine also binds to alpha-2A adrenergic receptors (akin to clonidine’s mechanism of action), inhibiting the release of norepinephrine by that neuron and inducing an inhibitory effect. Because the PFC is required for working memory and attention, it is thought that clonidine’s inhibition of PFC neurons helps to eliminate irrelevant attention (and subsequent behaviors), improving the person’s focus and correcting deficits in attention.

Clonidine stimulates release of GHRH hormone from the hypothalamus, which in turn stimulates pituitary release of growth hormone. This effect has been used as part of a “growth hormone test,” which can assist with diagnosing growth hormone deficiency in children.

After being ingested, clonidine is absorbed into the blood stream rapidly with an overall bioavailability around 70 – 80%. Peak concentrations in human plasma occur within 60–90 minutes for the “Immediate Release” (IR) version of the drug, which is shorter than the “Extended Release” (ER/XR) version. Clonidine is fairly lipid soluble with the logarithm of its partition coefficient (log P) equal to 1.6; to compare, the optimal log P to allow a drug that is active in the human central nervous system to penetrate the blood brain barrier is 2.0. Less than half of the absorbed portion of an orally administered dose will be metabolized by the liver into inactive metabolites, with roughly the other half being excreted unchanged by the kidneys. About one-fifth of an oral dose will not be absorbed, and is thus excreted in the feces. Work with liver microsomes shows in the liver clonidine is primarily metabolized by CYP2D6 (66%), CYP1A2 (10-20%), and CYP3A (0-20%) with negligible contributions from the less abundant enzymes CYP3A5, CYP1A1, and CYP3A4. 4-hydroxyclonidine, the main metabolite of clonidine, is also an alpha-2A agonist but is non lipophilic and is not believed to contribute to the effects of clonidine since it does not cross the blood–brain barrier.

Measurements of the half-life of clonidine vary widely, between 6 and 23 hours, with the half-life being greatly affected by and prolonged in the setting of poor kidney function. Variations in half-life may be partially attributable to CYP2D6 genetics. Some research has suggested the half-life of clonidine is dose dependent and approximately doubles upon chronic dosing, while other work contradicts this. Following a 0.3 mg oral dose, a small study of five patients by Dollery et al (1976) found half-lives ranging between 6.3 – 23.4 hours (mean 12.7). A similar N=5 study by Davies et al. (1977) found a narrower range of half-lives, between 6.7 – 13 hours (average 8.6 hours), while an N=8 study by Keraäen et al. that included younger patients found a somewhat shorter average half-life of 7.5 hours.

Clonidine was introduced in 1966. It was first used as a hypertension treatment under the trade name of Catapres.

As of June 2017, clonidine was marketed under many brand names worldwide: Arkamin, Aruclonin, Atensina, Catapin, Catapres, Catapresan, Catapressan, Chianda, Chlofazoline, Chlophazolin, Clonid-Ophtal, Clonidin, Clonidina, Clonidinã, Clonidine, Clonidine hydrochloride, Clonidinhydrochlorid, Clonidini, Clonidinum, Clonigen, Clonistada, Clonnirit, Clophelinum, Dixarit, Duraclon, Edolglau, Haemiton, Hypodine, Hypolax, Iporel, Isoglaucon, Jenloga, Kapvay, Klofelino, Kochaniin, Lonid, Melzin, Menograine, Normopresan, Paracefan, Pinsanidine, Run Rui, and Winpress. It was marketed as a combination drug with chlortalidone as Arkamin-H, Bemplas, Catapres-DIU, and Clorpres, and in combination with bendroflumethiazide as Pertenso.


Research has found that anxiety is one of the leading symptoms created by marijuana in users, and that there is a correlation between Catapres and Weed and an increase in anxiety.


Anyone mixing Catapres and weed is likely to experience side effects. This happens with all medications whether weed or Catapres is mixed with them. Side effects can be harmful when mixing Catapres and weed. Doctors are likely to refuse a patient a Catapres prescription if the individual is a weed smoker or user. Of course, this could be due to the lack of studies and research completed on the mixing of Catapres and Weed.


Heavy, long-term weed use is harmful for people. It alters the brain’s functions and structure, and all pharmaceuticals and drugs including Catapres are designed to have an impact on the brain. There is a misplaced belief that pharmaceuticals and medication work by treating only the parts of the body affected yet this is obviously not the case in terms of Catapres. For example, simple painkiller medication does not heal the injury, it simply interrupts the brains functions to receive the pain cause by the injury. To say then that two drugs, Catapres and Weed, dol not interact is wrong. There will always be an interaction between Catapres and Weed in the brain11.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from


One of the milder side effects of mixing Catapres and Weed is Scromiting. This condition, reportedly caused by mixing Catapres and Weed, describes a marijuana-induced condition where the user experiences episodes of violent vomiting, which are often so severe and painful that they cause the person to scream. The medical term for Scromiting by mixing Catapres and Weed is cannabinoid hyperemesis syndrome, or CHS.  For these reasons, some people choose to quit smoking weed.


It was first included in scientific reports in 2004. Since then, researchers have determined that Scromiting is the result of ongoing, long-term use of marijuana—particularly when the drug contains high levels of THC, marijuana’s main psychoactive ingredient. Some experts believe that the receptors in the gut become overstimulated by THC, thus causing the repeated cycles of vomiting.


In the long run, a person can become even more depressed. There is a belief that marijuana is all-natural and not harmful to a person’s health. This is not true and Catapres and weed can cause health issues the more a person consumes it.


How does Weed effect the potency of Catapres?


The way in which the body absorbs and process Catapres may be affected by weed. Therefore, the potency of the Catapres may be less effective. Marijuana inhibits the metabolization of Catapres. Not having the right potency of Catapres means a person may either have a delay in the relief of their underlying symptoms.


A person seeking Catapres medication that uses weed should speak to their doctor. It is important the doctor knows about a patient’s weed use, so they can prescribe the right Catapres medication and strength. Or depending on level of interactions they may opt to prescribe a totally different medication. It is important for the doctor to know about their patient’s marijuana use. Weed is being legalized around the US, so doctors should be open to speaking about a patient’s use of it.


Sideffects of Catapres and Weed


Many individuals may not realize that there are side effects and consequences to mixing Catapres and Weed such as:


  • Dizziness
  • Sluggishness
  • Drowsiness
  • Shortness of breath
  • Itching
  • Hives
  • Palpitations
  • Respiratory Depression
  • Cardiac Arrest
  • Coma
  • Seizures
  • Death


Interestingly, it is impossible to tell what effect mixing this substance with Weed will have on an individual due to their own unique genetic make up and tolerance. It is never advisable to mix Catapres and Weed due to the chances of mild, moderate and severe side effects. If you are having an adverse reaction from mixing Catapres and Weed it’s imperative that you head to your local emergency room. Even mixing a small amount of Catapres and Weed is not recommended.


Taking Catapres and Weed together


People who take Catapres and Weed together will experience the effects of both substances. Technically, the specific effects and reactions that occur due to frequent use of Catapres and weed depend on whether you consume more weed in relation to Catapres or more Catapres in relation to weed.


The use of significantly more weed and Catapres will lead to sedation and lethargy, as well as the synergistic effects resulting from a mixture of the two medications.


People who take both weed and Catapres may experience effects such as:


  • reduced motor reflexes from Catapres and Weed
  • dizziness from Weed and Catapres
  • nausea and vomiting due to Catapres and Weed


Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and Catapres leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.

Mixing weed and Catapres


The primary effect of weed is influenced by an increase in the concentration of the inhibitory neurotransmitter GABA, which is found in the spinal cord and brain stem, and by a reduction in its effect on neuronal transmitters. When weed is combined with Catapres this primary effect is exaggerated, increasing the strain on the body with unpredictable results.


Weed and Catapres affects dopamine levels in the brain, causing the body both mental and physical distress. Larger amounts of Catapres and weed have a greater adverse effect yet leading medical recommendation is that smaller does of Catapres can be just as harmful and there is no way of knowing exactly how Catapres and weed is going to affect an individual before they take it.


Taking Catapres and weed together


People who take Catapres and weed together will experience the effects of both substances. The use of significantly more Catapres with weed will lead to sedation and lethargy, as well as the synergistic effects resulting from a mixture of the two medications.


People who take both weed and Catapres may experience effects such as:


  • reduced motor reflexes from Catapres and weed
  • dizziness from weed and Catapres
  • nausea and vomiting of the Catapres


Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and Catapres leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.

Weed Vs Catapres


Taking Catapres in sufficient quantities increases the risk of a heart failure. Additionally, people under the influence of Catapres and weed may have difficulty forming new memories. With weed vs Catapres in an individual’s system they become confused and do not understand their environment. Due to the synergistic properties of Catapres when mixed with weed it can lead to confusion, anxiety, depression and other mental disorders. Chronic use of Catapres and weed can lead to permanent changes in the brain22.G. Lafaye, L. Karila, L. Blecha and A. Benyamina, Cannabis, cannabinoids, and health – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from


Catapres Vs Weed


Studies investigating the effects of drugs such as Catapres and weed have shown that the potential for parasomnia (performing tasks in sleep) is dramatically increased when Catapres and weed are combined. Severe and dangerous side effects can occur when medications are mixed in the system, and sleep disorders are a common side effect of taking weed and Catapres together.


When a small to medium amount of weed is combined with Catapres, sleep disorders such as sleep apnea can occur. According to the latest data from the US Centers for Disease Control and Prevention (CDC) most ER visits and hospitalizations caused by too much weed were associated with other substances such as Catapres.


How long after taking Catapres can I smoke weed or take edibles?


To avoid any residual toxicity it is advisable to wait until the Catapres has totally cleared your system before taking weed, even in small quantities.


Overdose on Catapres and weed


In the case of Overdose on Catapres or if you are worried after mixing Catapres and weed, call a first responder or proceed to the nearest Emergency Room immediately.


If you are worried about someone who has taken too much Catapres or mixed weed with Catapres then call a first responder or take them to get immediate medical help. The best place for you or someone you care about in the case of a medical emergency is under medical supervision. Be sure to tell the medical team that there is a mix of Catapres and weed in their system.


Excessive Weed intake and result in scromiting, chs, and anxiety disorder.  It is advisable to quit vaping weed if you are feeling these symptoms.

Mixing Catapres and weed and antidepressants


Weed users feeling depressed and anxious may be prescribed antidepressant medication. There are some antidepressant users who also use Catapres and weed. These individuals may not realize that there are side effects and consequences to consuming both Catapres, marijuana and a range of antidepressants.


Studies on weed, Catapres and antidepressants is almost nil. The reason for so little information on the side effects of the two is mostly down to marijuana being illegal in most places – although a number of states in the United States have legalized the drug.


Self-medicating with Weed and Catapres


A lot of people suffer from depression caused by weed and Catapres. How many? According to Anxiety and Depression Association of America (ADAA), in any given year, it is estimated that nearly 16 million adults experience depression. Unfortunately, that number is likely to be wrong due to under reporting. Many people do not report suffering from depression because they do not want to be looked at as suffering from a mental illness. The stigmas around mental health continue and people do not want to be labeled as depressed.


Potential side effects from mixing Catapres and weed


Quitting weed to take Catapres


Medical professionals say an individual prescribed or taking Catapres should not stop using weed cold turkey.  Withdrawal symptoms can be significant. Heavy pot users should especially avoid going cold turkey. The side effects of withdrawal from weed include anxiety, irritability, loss of sleep, change of appetite, and depression by quitting weed cold turkey and starting to take Catapres.


A person beginning to use Catapres should cut back on weed slowly. While reducing the amount of weed use, combine it with mindfulness techniques and/or yoga. Experts stress that non-medication can greatly improve a person’s mood.


Weed and Catapres can affect a person in various ways. Different types of marijuana produce different side effects. Side effects of weed and Catapres may include:


  • loss of motor skills
  • poor or lack of coordination
  • lowered blood pressure
  • short-term memory loss
  • increased heart rate
  • increased blood pressure
  • anxiety
  • paranoia
  • increased energy
  • increased motivation


Mixing Catapres and weed can also produce hallucinations in users. This makes marijuana a hallucinogenic for some users. Weed creates different side effects in different people, making it a very potent drug. Now, mixing Catapres or other mental health drugs with weed can cause even more unwanted side effects.


Mixing drugs and weed conclusion


Long-term weed use can make depression and anxiety worse. In addition, using marijuana can prevent Catapres from working to their full potential33.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from Weed consumption should be reduced gradually to get the most out of prescription medication. Marijuana is a drug and it is harmful to individual’s long-term health. Weed has many side effects and the consequences are different to each person who uses it, especially when mixed with Catapres.


If you take Catapres, and also drink Alcohol or MDMA, you can research the effects of Catapres and Alcohol , Catapres and Cocaine as well as Catapres and MDMA here.


To find the effects of other drugs and weed refer to our Weed and Other Drugs Index A to L or our Weed and Other Drugs Index M-Z.

Or you could find what you are looking for in our Alcohol and Interactions with Other Drugs index A to L or Alcohol and Interactions with Other Drugs index M to Z , Cocaine and Interactions with Other Drugs index A to L or Cocaine and Interactions with Other Drugs index M to Z or our MDMA and Interactions with Other Drugs Index A to L or MDMA and Interactions with Other Drugs Index M to Z.


Catapres and Weed

Catapres and Weed

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  • 1
    1.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from
  • 2
    2.G. Lafaye, L. Karila, L. Blecha and A. Benyamina, Cannabis, cannabinoids, and health – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from
  • 3
    3.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from