I posted this info back in a blog back in July 2007 but from some of the questions recently, think it's time to post it again.........


Here's a lot of the info put more generally:

The main thing is the PVN (Paraventricular Nucleus of the Hypothalamus) is responsible for putting out the hormone Arginine Vasopressin. It is also responsible for the regulation of circulating Angiotensin. Both of these are important in regulating blood pressure. And Arginine Vasopressin --- if you don't have enough of it--- you may have diabetes insipidus symptoms. This may explain all the over urinating yet constant dehydration many of us experience.

And actually, in my further researching apparently diabetes insipidus (which is either inherited or caused my trauma, inflammation, etc) is responsible for progressively destroying Arginine Vasopressin-producing cells in the Hypothalamus/ PVN.

It is also notable that the creation of Angiotensin comes from two things combined: Renin and Angiotensinogen.

Renin is kidney related. In very general terms if the kidney area senses a lot of salt, it just won't create much Renin. Obviously, that would cause less Angiotensin. [One might then wonder just how good of an idea that we should all "salt up" is--- Haven't gotten to research on that thought but that's my current "hmmmm".]

Also note that Angiotensin comes in 4 different forms; Angiotensin I, Angiotensin II, Angiotensin III, and Angiotensin IV. Angiotensin I eventually turns into Angiotensin II, II turns into III.

"Angiotensin II acts on the adrenal cortex, causing it to release aldosterone, a hormone that causes the kidneys to retain sodium and lose potassium. Elevated plasma angiotensin II levels are responsible for the elevated aldosterone levels present during the luteal phase of the menstrual cycle."

The Paraventricular Nucleus of the Hypothalamus (PVN)
http://en.wikipedia.org/wiki/Paraventricular_nucleus
The PVN receives afferent inputs from many brain regions.

Amongst these, inputs from neurons in structures adjacent to the anterior wall of the third ventricle ("AV3V region") carry information about the electrolyte composition of the blood, and about circulating concentrations of hormones such as angiotensin and relaxin to regulate the magnocellular neurons.

Inputs from the brainstem nucleus of the solitary tract and the ventrolateral medulla carry information from the heart and stomach. Inputs from the hippocampus to the CRH neurones are important regulators of stress responses.

Inputs from neuropeptide Y-containing neurons in the arcuate nucleus co-ordinate metabolic regulation via TRH secretion with regulation of energy intake.


So the PVN not only effects the hormone output Arginine Vasopression, but also regulates the circulating amount of Angiotensin. http://en.wikipedia.org/wiki/Angiotensin

**Angiotensin 1 is formed by Renin and Angiotensinogen.** Also, note that Angiotensin 1 eventually creates Angiotensin 2 which then creates Angiotensin 3.

Plasma angiotensinogen levels are increased by plasma corticosteroid, estrogen, thyroid hormone, and angiotensin II levels. FLORINEF is a corticosteroid by the way.

Renin is produced in the kidneys in response to both decreased intra-renal blood pressure at the juxtaglomerular cells, or decreased delivery of Na+ and Cl- to the macula densa. If more Na+ is sensed, renin release is decreased.

**In other words, the more circulating salt level, the less Renin will be released, thus less Angiotensin will be created.**


Effects of angiotensin
See also Renin-angiotensin_system#Effects
Angiotensins II, III & IV have a number of effects throughout the body:

Cardiovascular effects
It is a potent direct vasoconstrictor, constricting arteries and veins and increasing blood pressure.

Angiotensin II has prothrombotic potential through adhesion and aggregation of platelets and production of PAI-1 and PAI-2.[2][3]

It has been proposed that angiotensin II could be a cause of vascular and cardiac muscle hypertrophy (enlargement of the heart).

Neural effects
Angiotensin II increases thirst sensation (dipsogen) through the subfornical organ (SFO) of the brain, decreases the response of the baroreceptor reflex, and increases the desire for salt. It increases secretion of ADH in the posterior pituitary and secretion of ACTH in the anterior pituitary. It also potentiates the release of norepinephrine by direct action on postganglionic sympathetic fibers.

Adrenal effects
Angiotensin II acts on the adrenal cortex, causing it to release aldosterone, a hormone that causes the kidneys to retain sodium and lose potassium. Elevated plasma angiotensin II levels are responsible for the elevated aldosterone levels present during the luteal phase of the menstrual cycle.

Renal effects
Angiotensin II has a direct effect on the proximal tubules [of the kidneys] to increase Na+ resorption. Although it slightly inhibits glomerular filtration by indirectly (through sympathetic effects) and directly stimulating mesangial cell constriction, its overall effect is to increase the glomerular filtration rate by increasing the renal perfusion pressure via efferent renal arteriole constriction. Angiotensin II causes the release of prostaglandins from the kidneys.

http://ndrf.org/eve/forums/a/tpc/f/2621035343/m/2391062974/p/1

This is where the original blog is by the way

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1588596&blobtype=pdf

http://www.pubmedcentral.nih.gov/pagerender.fcgi?artid=...596&pageindex=2#page

"The opposite clinical syndrome-primary lack of renin or hyporeninism-has also been recognized recently. In this disease primary lack of renin (and hence of its active product angiotension II) apparently leads to selective deficiency of aldosterone associated with normal cortisol production. The literature contains reference to some 20 cases of isolated analdosteronism, the first a report by J. B. Hudson and his colleagues15 in 1957. Only recently however has the primary deficiency been recognized as renin lack in at least some of these patients. At page 650 of this issue of the B.M.7. we publ.sh what appears to be the first report of a case in
Britain.

Isolated hypoaldosteronism usually occurs in elderly patients and is characterized by attacks of loss of consciousness, cardiac arrhythmias, muscle weakness, and weight loss."

My question is---
Perhaps salt loading is a good treatment for emergency low blood pressure situations, however, does it cause more problems as a long term treatment plan?

Salt-loading elevates blood pressure and aggravates insulin resistance in Wistar fatty rats: a possible role for enhanced Na+ -H+ exchanger activity.

http://www.ncbi.nlm.nih.gov/pubmed/11564985

Hayashida T, Ohno Y, Otsuka K, Suzawa T, Shibagaki K, Suzuki H, Ikeda H, Saruta T.
Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.

OBJECTIVE : Increased Na+-H+ exchanger activity (NHE) has been reported as an intermediate phenotype in hypertensive subjects, particularly those with insulin resistance. To investigate whether NHE abnormality plays a role in hypertension, Wistar fatty rat (WFR) with overt obesity, hyperglycemia and marked hyperinsulinemia was examined. METHODS : WFR and Wistar lean rats (WLR) as a control (n = 12, each) were fed either with normal (0.38%) or high sodium (4% NaCl) diet for 12 weeks and then sacrificed to examine platelets NHE activity. RESULTS : Mean arterial pressure (MAP) was higher in WFR than in WLR (113 +/- 4 versus 96 +/- 7 mmHg, P < 0.05) under a normal chow. Vmax values of NHE activity were significantly higher in WFR than in WLR. WFR fed with a high sodium diet showed higher MAP than those with a normal chow (128 +/- 3 versus 113 +/- 4 mmHg, P < 0.05). Though Km values were not different between WFR and WLR under a normal chow, both maximal transport rate (Vmax) and half maximal transport (Km) values were significantly higher in WFR with a high salt diet than those with a control diet. Vmax showed significant correlation with MAP, whereas Km values correlated with immunoreactive insulin (IRI) levels. Significant interaction between dietary sodium intake and the strain differences was observed both on blood pressure and on IRI levels by two-way analysis of variance (ANOVA). CONCLUSION : WFR presented salt-sensitive blood pressure elevation. NHE activity was enhanced in WFR in correlation with the blood pressure. These results suggest that augmented NHE activity contributes to the development of salt-sensitive blood pressure elevation in WFR.