Cornerstones Final Exam Questions with resources Essay

I listed the resources I used by question. I hope that is okay.
Cornerstones Final Exam Questions
Physiology
Dr. Kath Curtis
Select a hormone from the list below and briefly answer the following questions. Each answer should be 1-2 paragraphs together, the answers should be no more than 1.5 single-spaced pages.
Vasopressin
Oxytocin
Corticosterone
Estrogen
Angiotensin
Insulin
1) How is this hormone regulated (include signals for release/inhibition of release, as well as feedback control, if applicable)? [Sorry for the length of this first answer]
Angiotensin is released at a basal rate primarily from the liver but can also be produced from other tissues, most notably by the tissues of the vascular system itself. Animal models have shown that angiotensin release from the vascular tissue is upregulated by the presence of renin, a major player in the renin-angiotensin aldosterone system (RAAS). However, the presence of angiotensin II, a downstream biologically active hormone of RAAS, does not inhibit the release of angiotensin from the tissues(1). Instead, the regulation of the angiotensin comes for the enzymatic modifications of angiotensin's prohormone, angiotensinogen, and its largely biologically inactive upstream hormone, angiotensin I. These enzymatic modifications are made by renin and by angiotensin-converting enzyme (ACE). Renin is the rate limiting step of RAAS, and because of this largely dictates the activity of angiotensin(2).
Renin is released by the juxtaglomerular cells of the kidney in response to decreases in blood pressure, decreases in blood flow to the kidneys, and sympathetic activity. Renin release is inhibited by a negative feedback mechanism by the biologically active angiotensin II hormone(2).
References
Kato H, Iwai N, Inui H, Kimoto K, Uchiyama Y, Inagami T. Regulation of vascular angiotensin release. Hypertension. 1993 Apr21(4)446-54. PubMed PMID8458646.
The renin-angiotensin aldosterone system pathophysiological role and pharmacologic inhibition. Atlas SA. J Manag Care Pharm. 2007 Oct13(8 Suppl B)9-20. Review. http//www.amcp.org/data/jmcp/pages%209-20.pdf
2) What are the physiological consequences of insufficiency and excess of this hormone?
I could not really find much about angiotensin excess alone. I imagine that because of the downstream regulation of its biologically active produce, angiotensin excess alone would not have much physiological effect.
Insufficient amounts of angiotensin release, as in the case of severe liver disease, causes hypotension and possibly hypoperfusion, such as reversible renal insufficiency and shock(1).
References
Kato H, Iwai N, Inui H, Kimoto K, Uchiyama Y, Inagami T. Regulation of vascular angiotensin release. Hypertension. 1993 Apr21(4)446-54. PubMed PMID8458646.
3) What class of hormone is the hormone you selected and how might that influence its function?
As we learned in class, Angiotensin is a peptide hormone. As was also discussed, a peptide hormone is a hydrophilic protein that has biological effects. Because peptide hormones are hydrophilic, they can be easily stored in the cell in vesicles for later release. This means that the release of the hormone is not solely dependent on the manufacture of that hormone by the cell. The hydrophilic nature of the hormone also means that the hormone's receptors are located primarily on the external surface of the cell's membrane.