Kilfer
Bluelighter
Are you actually measuring your blood pressure or is this all based upon percieved effects? 15mg of temazepam isn't a super low dose. If you don't use benzos on a regular basis that's more than enough to give you a little buzz... probably quite a bit more than just vasodilation.
I have been using a prescribed dose of 45mg temazepam fairly regularly over the last decade as a hypnotic although I have toned it down a bit over the last few months. Availability rather than optimal suitability is the reason why it was used in this early experiment. I intend to procure a pediatrics-potency benzo for further experiments, most likely diazepam 2mg since few others appear to be available. The immediate objective is to determine if satisfactory effects of coronary vasodilation can be achieved with a dosage that will not trigger perceivable benzodiazepine central effects on a subject familiar with therapeutic doses of a strong benzo.
My advice is to not take doses of stimulants that jack your blood pressure and/or cause anxiety to the point where it's an issue... benzodiazepines should be drugs used in emergency freakouts, not as part of a cocktail to make your stimulant tolerable.
Like many otherwise beneficial drugs, several if not most amphetamine-like substances -including methylphenidate and several of its derivatives- cause certain untoward effects and it is my opinion that cessation of use is not always the only solution if an acceptable adjunct can be found to mitigate adverse effects. This project is only one of many that have been or are being casually investigated on an empirical basis by otherwise satisfied users. The primary objective is the reducing of the discomfort caused by coronary vasoconstriction, with the ultimate but optional benefit of reducing systemic vasoconstriction. Whether or not a benzo is the most appropriate agent for these purposes has not yet been even tentatively established at this early stage.
It doesn't help that it's very easy to cause a self-perpetuating loop of anxiety and panic for some people.
If the stimulant itself was causing me an unacceptable level of anxiety and panic I wouldn't be using it. My objective concerns a specific user profile, those who are concerned about issues pertaining specifically to the discomfort of coronary vasoconstriction (tightness of chest and associated pains) but otherwise tolerant of annoying but manageable (to them) stimulant side effects.
there's no real long term 'harm reduction' in telling them to practice polypharmacy so they can use a drug their body doesn't agree with.
The harm reduction aspect is not meant to be of universal appeal. Instead it concerns users who are determined to continue their usage because they find productivity benefits in it. Being part of this marginal fringe should not automatically obligate one to have to deal with an untoward side effect if it can be mitigated through the use of an acceptable agent.
Have you tried using lorazepam sublingually rather than orally? I've never heard of it taking 2 hours to kick in.
I have a slow metabolism rate, in fact that's the reason why I was prescribed a fast-acting -and thus more addictive- benzo hypnotic by the neurologist I had ben referred to treat intractable insomnia, a condition I have lived with for nearly 35 years. Unfortunately neither temazepam nor lorazepam are best suited for the project.
The idea is to use the lowest potency, least centrally active benzo you can find at the lowest dose.
Exactly. But for now I have to settle for diazepam 2mg, it's the lowest-potency benzo I could find on the US market so far.
There are a lot of subtypes of GABAa receptors, not all agonists/allosteric modulators will lower bp.
Indeed, but for now benzos' affinity for GABA-a receptors appears to have evolved into a secondary concern since their direct vasodilator activity at the coronary level is being achieved through their property as adenosine re-uptake inhibitors which is independent from central activity. Peripheral vasodilator effects, on the other hand, appear to be the result of anxiolytic activity which is why these are no more part of my main focus.
I also question how direct the effect of benzodiazepines on vasodilation is. I was under the impression it was related to their effects as muscle relaxants.
See above

I don't see how encouraging the use of dependency forming drugs to mask the bad effects intrinsic to certain poorly designed RC stimulants is 'harm reduction', but to each his own I guess.
I hope I have answered, or at least properly addressed some of your concerns in this regard. Perhaps my initial use of an overpowered benzo that was not ideally suited with regards to the stated and constantly evolving objective gave the false impression that I am promoting double-dependency but that is not the case. I used what I had on hand and extrapolated certain results using personal experience, known benzodiazepine pharmacology, and common sense.