There are a variety of drugs which can result in hyperkalemia, via a variety of mechanisms. Here are a list of some of the common offenders, categorized loosely based on mechanism, though admittedly there is some overlap between categories:1. Drugs which cause translocation of K from the intracellular to the extracellular fluid: these include succinylcholine , isoflurane , minoxidil , and beta-blockers. 2. Potassium-Sparing Diuretics : drugs such as spironolactone (mineralocorticoid receptor antagonists) and amiloridine/triamterene (blockers of the ENaC) are common causers of . Inhibitors of renin-angiotensin-aldosterone axis: ACE-inhibitors , angiotensin receptor blockers .4. Hyperosmolarity: hyperosmolarity induces water efflux out of cells, and by solvent drag increases intravascular potassium concentrations. Drugs such as mannitol can therefore cause translocational . NSAIDs : NSAIDs can lower renin secretion, which is normally mediated in part by locally-produced . Bactrim : the hyperkalemia induced by Bactrim is via an ENaC inhibitory effect exerted by the trimethoprim moiety. Pentamidine induced hyperkalemia via a similar . calcineurin inhibitors (., cyclosporine, tacrolimus): it is postulated that these medications inhibit renal tubular responsiveness to . heparin & ketoconazole : these drugs may be associated by hyperkalemia by inhibiting aldosterone . digitalis : digitalis inhibits the Na-K ATPase (which pumps 3 Na out of the cell and 2 K in); as such, it can result in hyperkalemia and a variety of cardiac arrhythmias.
A key feature of the protocol is that waves are stored on the service provider's servers instead of being sent between users. Waves are federated; copies of waves and wavelets are distributed by the wave provider of the originating user to the providers of all other participants in a particular wave or wavelet so all participants have immediate access to up-to-date content. The originating wave server is responsible for hosting, processing, and concurrency control of waves.   The protocol allows private reply wavelets within parent waves, where other participants have no access or knowledge of them.  
Masteron will significantly suppress natural testosterone production making exogenous testosterone therapy important when using this steroid. Failure to include exogenous testosterone will lead most men to a low testosterone condition, which not only comes with numerous possible symptoms but is also extremely unhealthy.
As most will use Masteron in a cutting cycle, it’s very common not to want to use a lot of testosterone due to the high levels of estrogenic activity it can provide. If this is the case, you will find a low dose of 100-200mg per week of testosterone to be enough to combat suppression and give you the needed testosterone.
Once Masteron is discontinued and all exogenous steroidal hormones have cleared your system, natural testosterone production will begin again. Prior levels will not return to normal over night, this will take several months. Due to the slow recovery, Post Cycle Therapy (PCT) plans are often recommended. This will speed up the recovery greatly; however, it won’t bring your levels back to their peak, this will still take time. A PCT plan will ensure you have enough testosterone for proper bodily function while your levels continue to naturally rise and significantly cut down on the total recovery time. This natural recovery does assume no prior low testosterone condition existed. It also assumes no damage was done to the Hypothalamic-Pituitary-Testicular-Axis (HPTA) through improper supplementation practices.