armygas

Also painful stimuli travel up the spinomesecephalic tract which can cause increased dopamine release in the nucleus accumbens so I would argue some people do find pain pleasurable (however I am not one of them....) Also, painful stimuli will traverse the spinoreticular tract to activate the RAS and increase awareness. Lastly, noxious (painful) stimuli travel to the dorsal horn via A-delta (fast pain) and C fibers (slow pain) so there is a fast component to pain. I don't know about you but I just cracked my toe going to the bathroom and it hurt immediately. A-delta and C fibers synapse in the Rexed Lamina onto second order neurons (the spinothalamic, spinoreticular, and spinomesecenphalic tracts) and ascend rostrally to the thalamus onto a third order neuron.

That depends on the agent you are using through the nasal passage, the steroidal compounds don't have that profile.

Don't forget the calcium channel blockers, also for the OP there are two types of hypertension essential and secondary. If you use the keyphrase "causes of hypertension" in google it will lead you to several peer reviewed sites on the topic.

Dopamine levels rise with excitement and dopamine-induced nausea/vomiting is quite common. In fact we use dopamine-blocking agents in anesthesia to treat N/V.

Understood, but according to factor 1 of the fair use act that small quotation used for and educational, not-for-profit use is "fair use"... Just FYI

Actually glucagon will agonize a GPCR (Gs type) and eventually activate phosphorylase. Now phosphorylase is a rate limiting step in the whole glycogenolysis process so glycogenolysis is enhanced thus breaking down glycogen into glucose. Glucagon itself is not made into glucose, it only activates a Gs protein coupled receptor. If you want a good pharm book get Goodman and Gilman...it is a great but expensive book

PCP blocks the NMDA receptor at the phencyclidine binding site to induce analgesia. Its relative is ketamine, a widely used anesthetic in humans.

Glucagon's actions actually oppose those of insulin..... "Exogenous administration of glucagon produces the same pharmacologic effects as endogenous glucagon. These effects include increases in blood glucose, relaxation of smooth muscle of the GI tract, and a positive inotropic and chronotropic effect on the heart. Increases in blood glucose are secondary to stimulation of glycogenolysis. In liver and adipose tissue, glucagon increases the production of adenylate cyclase, which catalyzes the conversion of ATP to cAMP. Cyclic AMP then initiates a series of enzymatic reactions that include activation of phosphorylase, which promotes the breakdown of glycogen to glucose. As a result, blood glucose levels are increased within minutes of glucagon administration. The degree to which glucagon increases blood glucose is dependent on the liver glycogen reserves and the presence of phosphorylases. The increase in blood glucose is not as great in patients with type I diabetes mellitus as compared to those with type II diabetes mellitus. The exact mechanism by which glucagon exerts its effects on GI smooth muscle and cardiac muscle are unknown."

If you look up epidural or spinal anesthesia you will find your video to present.