HHajdo and Others...Battling the A2 from dieting


I am banned!
If A2 is the really BAD guy and uneffected by stimulants (for the most part)..........

1) What else can someone use to battle the A2 receptor besides yohimbine??

Yohimbine (IMO better utilized the transdermal fashion such as: "Yohimburn" for specific localized receptor antagonism) seems to be the ONLY thing that discernably counters this dilema.

2) What happens when Yohimburn use is ceased, and/or eventual attenutaion is observed-------and the A2 receptor upregulates.....doesn't this set up potential localized stubborn fat cells to become "more" saturated with the A2 receptors than before???

Most fat burners as we know them......fascilitate fat loss through stimulation of B1, B2 (and agonistic activity), Brown Adipose Tissue (BAT) essentially via thermoregulator transmission. And even discontinued use of these products can lead to MORE A2 receptor rebound=more stubborn fat!!!

IMO: all of these things are merely temporary "fixes" and potential "hazards" in the respect that stubborn fat becomes MORE stubborn....

It just seems like an otherwise futlie never-ending cycle fueled by dangerous (almost addiction-based) cycling of Fat-burners. By the way, I fall into this category as I have been cycling ECA's for years. I am attempting ALSO to put an end to this viscious cycle as well.

The sad thing------Dietary manipulaton almost always fails long-term as your body becomes "accomodated" to the new found Maintenance calorie intake. Homeostasis and thermoregulation via the Thyroid gland takes over----and you're left in a state of catabolism and forced to eat fewer calories to maintain fat %. Unless of course....T3 is used but this can only be used short term as well for obviious reasons.

Please enlighten me.........thanks
actually any Methylxanthines will block a2 receptors.... so chocolate will do it because it has theobromine in it, if u find theobromine you could just take it as a supplement, i know B-A-C sells it.

A1 and A2 receptors BOTH are in fact blocked by methylxanthines such as theophylline but I was unaware that it wass available for purchase!

Thanks :)
More on theobromine:


Title: 3,7-Dimethyl-1-propargylxanthine: a potent and selective in vivo antagonist of adenosine analogs.
Author(s): Seale TW; Abla KA; Shamim MT; Carney JM; Daly JW

Address: Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City 73190.

Source: Life Sci 1988;43(21):1671-84

Abstract: 3,7-Dimethyl-1-propargylxanthine (DMPX), a caffeine analog that exhibits in vitro selectivity for A2-adenosine receptors, compared to A1-adenosine receptors, has now been investigated with respect to in vivo potency and selectivity. DMPX potently and selectively blocked the actions of the potent A2 adenosine agonist, 5'-N-ethylcarboxamidoadenosine (NECA), in DBA/2 mice, compared to blockade of the same responses elicited by the selective A1-adenosine agonist, N6-cyclohexyladenosine (CHA). DMPX was 57-fold more potent versus NECA-induced hypothermia than versus CHA-induced hypothermia and 11-fold more potent versus NECA-induced behavioral depression than versus CHA-induced behavioral depression. The hypothermia is mediated by peripheral receptors, based on blockade by 8-(p-sulfophenyl)theophylline (PSPT), while the behavioral depression is centrally mediated, based on lack of blockade by PSPT. DMPX was 28- and 15-fold more potent than caffeine in blocking peripheral and central NECA-responses, respectively. DMPX was equipotent with caffeine versus CHA-induced hypothermia and 2.5-fold more potent than caffeine versus CHA-induced behavioral depression. The motor stimulating potency of DMPX (ED50 10 mumol/kg) was slightly greater than caffeine

Major Indexes:

Adenosine [analogs & derivatives]
Body Temperature [drug effects]
Motor Activity [drug effects]
Theobromine [analogs & derivatives]
Minor Indexes:
Adenosine [antagonists & inhibitors] [pharmacology]
Caffeine [pharmacology]
Mice, Inbred DBA
Reference Values
Theobromine [pharmacology]
Theophylline [pharmacology]
Reagent Names:
14114-46-6 (3,7-dimethyl-1-propargylxanthine)
35920-39-9 (adenosine-5'-(N-ethylcarboxamide)
36396-99-3 (N(6)
58-08-2 (Caffeine)
58-55-9 (Theophylline)
58-61-7 (Adenosine)
83-67-0 (Theobromine)
Language: English
Periodical Type: JOURNAL ARTICLE
a2 adenosine receptors is not the same as A2 adrenoceptors

there are lots of different types of a2's
ready2explode said:
DRVJ, got a lil case of gyno I take it?

No-----thank GOD I've never experienced gyno.... or I've AT LEAST been able to keep it at bay (knock on wood ;) )

I've got a decent 4 pack/ mild 6 pack........just looking for different alternatives to getting sliced.

In some studies in which the potency of different alpha 2-adrenoceptor antagonists was evaluated, yohimbine was found to be the most potent, so you can stick with it...
Whatever effect it has on the receptor it's temporary, so I wouldn't worry about it...

Eur J Pharmacol 1980 Aug 22;66(1):87-93 Related Articles, Links

Evidence for the alpha 2 nature of the alpha-adrenergic receptor inhibiting lipolysis in human fat cells.

Lafontan M, Berlan M.

Theophylline-stimulated human subcutaneous adipocytes were incubatged in vitro in the presence of selected alpha-adrenergic agents in order to characterize the alpha-adrenoceptor of human fat cells. Inhibition of theophylline-induced lipolysis occurred with the agents tested; clonidine was the most potent agonist while methoxamine had no effect. The relative order of potency of the various agonists was: clonidine > adrenaline > phenylephrine > methoxamine; this order is consistent with the classification of agonists described for the presynaptic alpha 2-receptor. Moreover, selected antagonists were used in order to antagonise clonidine inhibition of theophylline-induced lipolysis. The order of potency of the alpha-antagonists for the human alpha-adrenoceptor of adipocytes was: yohimbine > piperoxane > phenoxybenzamine > prazosin. This order is consistent with an alpha 2 type receptor. In conclusion, the results demonstrate that the alpha-adrenergic receptor which inhibits lypolysis in human fat cells is of the alpha 2 type. it is noteworthy that although localized postsynaptically this alpha-receptor can be classified as alpha 2 like the commonly known presynaptic alpha-adrenergic receptor which inhibits noradrenaline release from sympathetic neurons.


HHajdo-----thank you ;)

In some studies in which the potency of different alpha 2-adrenoceptor antagonists was evaluated, yohimbine was found to be the most potent, so you can stick with it...
Whatever effect it has on the receptor it's temporary, so I wouldn't worry about it...

Whoa!!!! Permanent?????
DRveejay11 said:
Macro--------I know YOU can do better than that!!!


perhaps when there is more time.. needless to say they are both involved in lipolysis..

with a2 adenosine affecting C amp
An older theory was ACE inhibitors can downregulate A2 receptors. I haven't heard it tossed around in awhile, was it disproven?
nox said:
An older theory was ACE inhibitors can downregulate A2 receptors. I haven't heard it tossed around in awhile, was it disproven?

i remember reading the same thing from dan duchaine in his dirty dieting newsletters. he was experimenting with captopril for people with estrogenic fat probs.
Nox and Bronco: Thanks for jogging my memory of these other DAN secrets. IMO, they are a bit extreme but, that was Dan ;)


captopril / AcenormTM , CapotenTM


Description: Captopril is an angiotensin-converting enzyme (ACE) inhibitor used in the treatment of hypertension, congestive heart failure, and various renal syndromes such as diabetic nephropathy and scleroderma. Captopril is the first ACE inhibitor to have been marketed in the United States. Although studies on the use of captopril in heart failure have been conducted since the late 1970s, it was not until 1992 that captopril was shown to significantly reduce mortality in patients with heart failure. Similarly, only recently has captopril moved to the forefront of hypertension treatment. As the shortest-acting of all ACE inhibitors, it is usually dosed two or three times a day. Captopril contains a sulfhydryl group, which may contribute to its pharmacologic action and account for some adverse reactions that occur at higher doses. Captopril was approved by the FDA in 1981. Its patent was due to expire August 8, 1995 but was delayed to February 13, 1996 as a result of new GATT trade agreement rules.

Mechanism of Action: Captopril has an extremely high affinity for ACE and competes with the natural substrate, angiotensin I, to block its conversion to angiotensin II. Angiotensin II is a potent vasoconstrictor and a negative feedback mediator for renin activity; thus, as a result of lower angiotensin II plasma levels, blood pressure decreases and plasma renin activity increases. In addition, baroreceptor reflex mechanisms are stimulated by the drop in blood pressure.

The "local" activity of ACE inhibitors may be more responsible for their clinical effects than systemic activity. ACE-inhibiting drugs may act locally (i.e., within a specific tissue) to reduce vascular tone by decreasing local angiotensin II-induced sympathetic activity and/or by decreasing local angiotensin II- induced vasoconstrictive activity. ACE inhibitors may inhibit presynaptic norepinephrine release and postsynaptic adrenergic receptor activity, decreasing vascular sensitivity to vasopressor activity. Decreases in plasma angiotensin II levels reduce aldosterone secretion, with a subsequent decrease in sodium and water retention.

Captopril dilates arterioles, thereby lowering total peripheral vascular resistance. In hypertensive patients, blood pressure is decreased with little or no change in heart rate, stroke volume, or cardiac output. However, captopril can increase cardiac output, cardiac index, stroke volume, and exercise tolerance in patients with congestive heart failure. The drug also decreases pulmonary wedge pressure, pulmonary vascular resistance, and mean arterial and right atrial pressures in these patients.

Pharmacokinetics: Captopril is rapidly absorbed from the GI tract following oral administration. If given with food, absorption decreases by 25-40%. Noticeable antihypertensive effects begin within 15 minutes; maximum beneficial effects may require several weeks of therapy. Captopril distributes into most body tissues, and approximately 25% is bound to proteins. The drug is metabolized (50%) in the liver, followed by excretion of the unchanged drug and its metabolites in the urine. The effects of a dose of captopril generally last about 2-6 hours, but the duration of action can be prolonged in patients with renal dysfunction. The half-life in patients with normal renal function is less than 2 hours but can be as long as 6 days in anuric patients.

CONTRAINDICATIONS/PRECAUTIONS: Several dozen cases of ACE inhibitor-related fetal and neonatal death have been reported. ACE inhibitors are classified as FDA category C during the first trimester of pregnancy. Risk appears to increase during the second and third trimesters and ACE inhibitors are then considered category D drugs. Every effort should be made to discontinue ACE inhibitors whenever pregnancy is discovered.

Captopril therapy can cause neutropenia or agranulocytosis. Patients with renal disease, patients with immunosuppression or receiving immunosuppressives, and patients with collagen- vascular disease or autoimmune disease are at a greater risk for developing these complications. Complete blood counts should be established prior to and during captopril therapy when administered to these patient populations. (Leukocyte count with differential should be obtained every 2 weeks during the first 3 months of therapy in all patients receiving captopril.) Captopril should be used with caution in patients with pre- existing bone marrow depression. The dose of captopril should be adjusted in patients with renal impairment.

Captopril can cause severe hypotension when administered to patients with hypovolemia or hyponatremia or to patients receiving diuretics. This effect is due at least in part to its anti-aldosterone action. Captopril should be used cautiously in patients with congestive heart failure (initial doses should be lower than in the treatment of hypertension) because of a greater risk of developing hypotension. Hypotension may aggravate ischemia in patients with coronary artery disease or cerebrovascular disease precipitating a myocardial infarction or cerebrovascular accident.

Captopril should not be administered to patients with preexisting renal artery stenosis. Because affected kidneys depend on the renin-angiotensin system to maintain GFR, inhibition of the mechanism can lead to renal failure. Since this condition may not be known prior to therapy, renal function should be monitored closely during the first 2 weeks after initiating therapy. Captopril should be discontinued if renal function worsens acutely. Other types of renal disease can actually improve during captopril therapy. The dose of captopril should be adjusted in patients with renal impairment.

Captopril should be used with caution patients with hyperkalemia. ACE inhibitors can elevate serum potassium concentrations and could worsen pre-existing condition. Hyperkalemia is associated with serious cardiac arrhythmias.

The metabolism of captopril may be decreased in patients with hepatic disease. Monitoring and dosage adjustments may be necessary in patients with hepatic impairment.

Captopril therapy can produce angioedema, which can be fatal. Captopril is contraindicated in patients with a history of ACE inhibitor-induced angioedema, hereditary angioedema, or idiopathic angioedema.

DRUG INTERACTIONS: Captopril, and possibly other ACE inhibitors, can enhance the activity of oral antidiabetic agents. Hypoglycemia has occurred when captopril was added to either glyburide or biguanide therapy. Caution should be observed when captopril is added to the regimen of patients receiving these drugs.

Captopril can enhance the effects of antihypertensive agents and diuretics on blood pressure if given concomitantly. This additive effect may be desirable, but dosages must be adjusted accordingly. Patients with hyponatremia or hypovolemia may become hypotensive and/or develop reversible renal insufficiency when given captopril and diuretics concomitantly.

Indomethacin has been shown to inhibit the antihypertensive response to captopril.¥I Other nonsteroidal antiinflammatory drugs (NSAIDs), aspirin, and other salicylates may also exert a similar effect on captopril's action, however, other ACE inhibitors may not be affected to the same degree as captopril. It is thought that the antihypertensive action of captopril is highly dependent on its ability to stimulate the synthesis of vasodilatory prostaglandins.¥ NSAIDs inhibit prostaglandin synthesis, thereby attenuating captopril's ability to lower blood pressure. Loss of antihypertensive effect should be considered if a NSAID is added to a regimen that includs captopril. In addition, patients on captopril should be cautioned about routine use of aspirin or over-the-counter NSAIDs.

Captopril decreases aldosterone secretion, leading to small increases in serum potassium. Hyperkalemia can occur if captopril is given to patients receiving drugs that also increase serum potassium concentration, including potassium- sparing diuretics such as amiloride or spironolactone, potassium salts, or heparin.

Serum digoxin concentrations can rise by 15-30% in patients with congestive heart failure who are given digoxin and captopril concomitantly. However, captopril-induced hyperkalemia can offset the increased digoxin concentrations, and captopril and digoxin have been administered to patients with congestive heart failure with no apparent adverse effects. The clinical significance of this interaction is not clear.

Antacids can decrease the GI absorption of captopril if administered simultaneously.

Probenecid decreases the renal tubular secretion of captopril, resulting in higher captopril serum concentrations. If probenecid is given to a patient stabilized on captopril, hypotension may occur. This interaction would appear to be of lesser significance if captopril is added after probenecid therapy is in place.

Captopril can decrease the renal elimination of lithium, which can lead to lithium toxicity. Plasma lithium concentrations should be monitored carefully during concomitant captopril therapy. Clinicians should note that some other antihypertensive agents may also interact with lithium.

ADVERSE REACTIONS: Serious adverse hematological effects, including neutropenia and agranulocytosis, have been reported infrequently during captopril therapy. Patients with impaired renal function, patients with collagen vascular disease, or patients receiving large daily doses are at greater risk.

Captopril can affect renal function. Renal insufficiency can occur but is usually reversible following discontinuance of captopril. (NOTE: Captopril has been used therapeutically in the treatment of diabetic proteinuriaý.) Polyuria and oliguria have also been reported, though rarely, during captopril therapy. Renal complications that occur during captopril therapy may be related to hypovolemia and/or hyponatremia, especially in patients with congestive heart failure who are receiving loop diuretics. These effects on renal function may resolve if hypovolemia and hyponatremia are corrected. If renal artery stenosis is suspected, captopril therapy should be discontinued. Although rare, serious renal effects include acute renal tubular necrosis, nephrotic syndrome, glomerulonephritis, and interstitial nephritis.

Dysgeusia (taste alteration), consisting of loss of taste perception or a persistent salty or metallic taste, can occur but is usually reversible within 2-3 months even if therapy is continued. This effect is believed to result from the pharmacologic activity of the drug's sulfhydryl group.

Hypotension and orthostatic hypotension rarely occurs in patients receiving captopril to treat hypertension, but hypotensive symptoms have required discontinuation of the drug in 3-5% of patients with congestive heart failure. Hypotension is generally well tolerated but can cause symptoms such as dizziness, syncope, lightheadedness, blurred vision, and, rarely, sinus tachycardia, angina, headache, fatigue, palpitations, and flushing.

ACE inhibition can result in the accumulation of kinins in the respiratory tract, sometimes causing a persistent, nonproductive cough. Dyspnea and bronchospasm also have been reported rarely during captopril therapy.

Approximately 4-7% of patients receiving captopril experience a maculopapular rash accompanied by pruritus and erythema, and occasionally by fever, eosinophilia, and arthralgia. The rash is generally mild and disappears within a few days following dosage reduction. In some cases, another ACE inhibitor has been subsequently administered without sequelae. Angioedema of the face, mucous membranes, tongue, lips, larynx, and glottis has occurred rarely but is reversible following discontinuance of the drug.

Patients receiving drugs that can increase serum potassium, or patients with congestive heart failure or impaired renal function, may be at an increased risk for developing hyperkalemia if given captopril concomitantly.


What do captopril tablets do?

Captopril (CapotenTM ) is an antihypertensive (blood pressure lowering agent) known as an ACE inhibitor. Captopril controls high blood pressure (hypertension) by relaxing blood vessels; it is not a cure. High blood pressure levels can damage your kidneys, and may lead to a stroke or heart failure. Captopril also can help to treat heart failure (heart does not pump strongly enough) and certain kidney disorders. Generic captopril tablets are not yet available.

What should my doctor, dentist, or pharmacist know before I take captopril?

They need to know if you have any of these conditions:

autoimmune disease, or suppressed immune function
collagen-vascular disease (such as lupus)
heart or blood vessel disease
high blood levels of potassium
liver disease
low blood levels of sodium
low blood pressure
kidney disease
an unusual or allergic reaction to captopril, other ACE inhibitors. foods, dyes, or preservatives
pregnant or trying to get pregnant
How should I take this medicine?

Take captopril tablets by mouth. Follow the directions on the prescription label. Swallow the tablets with a drink of water. Take captopril on an empty stomach, at least 1 hour before or 2 hours after meals. Take your doses at regular intervals. Do not take your medicine more often than directed. Do not stop taking captopril except on your doctor's advice.

Special precautions for use in children:

This medicine is not for children.

What if I miss a dose?

If you miss a dose, take it as soon as you can. If it is almost time for your next dose, take only that dose. Do not take double or extra doses.

What other medicines can interact with captopril?

antiinflammatory drugs (NSAIDs, such as ibuprofen)
aspirin and aspirin-like medicines
medicines for diabetes
medicines for high blood pressure
potassium salts
water pills
Tell your doctor or pharmacist: about all other medicines you are taking, including non-prescription medicines; if you are a frequent user of drinks with caffeine or alcohol; if you smoke; or if you use illegal drugs. These may affect the way your medicine works. Check before stopping or starting any of your medicines.

What side effects may I notice from taking captopril?

Serious side effects with captopril include:

chest pain, uneven or fast heart beat, palpitations
decreased or increased amount of urine passed
difficulty breathing, or difficulty swallowing
dizziness, lightheadedness or fainting spells
fever or chills
numbness or tingling in your fingers or toes
skin rash, itching
swelling of your face, lips, or tongue
swelling of your legs or ankles
Call your doctor as soon as you can if you get any of these side effects.

Minor side effects with captopril include:

loss of taste
Let your doctor know about these side effects if they do not go away or if they annoy you.

What do I need to watch for while I take captopril?

Visit your doctor for regular checks on your progress. Check your blood pressure regularly while you are taking captopril. Ask your doctor what your blood pressure should be and when you should contact him or her. Call your doctor if you notice an uneven or fast heart beat. Do not treat yourself for a fever or sore throat; check with your doctor as these may be the result of a captopril side effect.

Check with your doctor if you get an attack of severe diarrhea, nausea and vomiting, or sweat a lot. The loss of body fluid can make it dangerous to take captopril.

You may get dizzy. Do not drive, use machinery, or do anything that needs mental alertness until you know how captopril affects you. To avoid dizzy or fainting spells, do not stand or sit up quickly, especially if you are an older person. Alcohol can make you more dizzy. Avoid alcoholic drinks.

If you are going to have surgery, tell your doctor or dentist that you are taking captopril.

Avoid salt substitutes or other foods or substances high in potassium salts.

Do not treat yourself for coughs, colds, or pain while you are taking captopril without asking your doctor or pharmacist for advice.

Antacid can stop captopril working. If you want to take antacid for an upset stomach, make sure there is an interval of at least 2 hours since you last took captopril, or 4 hours before your next dose.

Captopril can alter certain lab test results, giving a false-positive for urine ketone tests.

If you are diabetic captopril may affect your blood sugar, and cause hypoglycemia (low blood sugar). Check with your doctor before changing the dose of your diabetic medicine.

Where can I keep my medicine?

Keep out of the reach of children in a container that small children cannot open.

Store at room temperature below 30C (86F). Protect from moisture. Keep container tightly closed. Throw away any unused medicine after the expiration date.

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captopril was actually dharkham's. and it has been widely called a failure
macro said:
captopril was actually dharkham's. and it has been widely called a failure

It was a failure viewing from the A2-downregulation part, or for weight loss as a whole?

Angiotensin II (well, the entire system) seems to play a very large role in adipocyte physiology especially when it comes to diabetes and obesity. I'm really curious as to why blocking AT II formation/binding doesn't have some beneficial effect. I know the ARBs increase insulin sensitivity and promote differentiation (which I can't figure out if thats a bad or good thing). Please shine some light on this.