Final answer:
Administration of a selective alpha 1 receptor agonist intravenously is expected to cause vasoconstriction, decreased gastrointestinal motility, piloerection, and potentially a rise in blood pressure and reflex bradycardia due to its effects on Gq protein-coupled adrenergic receptors.
Step-by-step explanation:
When a drug that is a selective alpha 1 receptor agonist is administered intravenously, several direct effects would be anticipated due to its action on different organs. As alpha 1 adrenergic receptors are coupled with Gq proteins, their activation leads to an increase in intracellular IP3 and calcium, resulting in smooth muscle contraction. Thus, this can cause vasoconstriction in numerous blood vessels, including those of the skin, gastrointestinal system, renal artery, and brain.
Additionally, this receptor agonism can lead to a decrease in gastrointestinal tract motility, along with contraction of other smooth muscles like the ureter, vas deferens, arrector pili muscles (resulting in piloerection or 'goosebumps'), and the uterine when pregnant. Other effects include an increase in glycogenolysis and gluconeogenesis in adipose tissue and liver, enhanced secretion from sweat glands, and increased sodium reabsorption from the kidneys.
The clinical manifestations of an alpha 1 agonist can be a rise in blood pressure due to vasoconstriction, reduction in gastrointestinal motility, and potentially reflex bradycardia as a response to increased blood pressure.