Ridecamp: [RC] Re. B.C.A.A. Complex

Bob:

There's more to electrolytes than salt (NaCl). Which is actually the
cation Na+ with the anion Cl- attached to it. Electrolytes are broken
down into two groups. Cations and Anions. Here's a list of them.
Cations: Na+, K+, Ca++, and Mg++. The Anions are: Cl-, HCO3-,
HPO4-2/H2PO4-, SO4-2, Organic acids, and protein (as anion) average
plasma concentration is around 16 mEq/L. This is a portion of a group of
compounds referred to as major solutes.  Then there's the Hydrogen ion
H+, and pH. And the Non-electrolytes: Protein, with sub group Albumin,
and Globulins, Fibrinogen, and Glucose. And finally the blood gasses
pO2, and pCO2.

All of the above compounds are related to, and affected by the balance
of body water. There are three major fluid compartments in which fluids
containing these elements. Plasma,  Interstital fluid (fluid between
cellular structures), and Intracellular fluid (fluid within the cells).
Water balance is governed by by intake of fluids or food containing
water, as well as by the generation of water due to metabolism of
proteins, fats, and carbohydrates (which amounts to about 5mL/kg/day),
versus loss through the urine, feces, respiratory tract, and skin (up to
12L/hour for a working horse on a hot day).

Drinking is controlled by thirst, which in turn is induced mainly by
plasma hypertonicity or a contracted extracellular fluid volume,
although several other mechanisms may be involved. If plasma becomes
hypertonic because of water loss , osmoreceptors in the supraoptic
nucleus are stimulated to release antidiuretic hormone or vasopressin
from the neurohypophysis. ADH increases the permeability of the distal
renal tubules to water only, so that the water that is then reabsorbed
reduces ECF tonicity. ADH release also occurs via neural pathways when
ECF volume is markedly reduced due to dehydration or hemorrhage. Another
critical response to hypovolemia (reduction of blood volume) is
activation of the renin-angiotensin-aldosterone system. This response is
initiated by volume receptors in the renal juxtaglomerular apparatus,
through which renin is released. Renin (an enzyme) promotes the
formation of angiotensin I in the plasma, which in turn is converted to
angiotensin II in the lungs. Angiotensin II results in the release of
aldosterone from the adrenal cortex. Aldosterone promotes the
reabsorption of sodium (Na+) from the distal renal tubes in exchange for
potassium (K+) and hydrogen (H+) which are then excreted. As plasma
becomes hypertonic due to increasing sodium levels, ADH is released and
water retention is facilitated.

Angiotensin II is also an active vasoconstrictor, which is fine if your
horse is bleeding but not good if it's being made to travel at 22 KPH
with 20% of it's body weight upon it's back in a dehydrated condition.
Vasoconstriction results in the decrease of blood flow, which in turn
decreases nutrients being carried to working muscles, as well as a
decrease in the removal of some metabolic byproducts that are harmful to
muscle tissue. Feeding salt to an animal already experiencing excessive
hypotonic fluid loss can lead to hypernatremia which can manifest itself
as dry mucous membranes, constipation, (impaction colic) hyperpyrexia,
(Abnormally high fever) muscle tremors, and in advanced cases
convulsions.

The electrolytes that need to be replaced are the ones that are
excreted. Salt, or I should say the components of salt, Na+ and Cl- are
rarely found to be deficient. More often times Na+ and Cl- are found to
be too high. This is caused by people with your line of thinking that
salt is electrolytes. Salt contains some electrolytes and those it
contains aren't lost in the amounts that potassium (K+) is. Which is
vital for good pulse recovery times, and proper cardiac rhythms. And
magnesium (Mg++), and Calcium (Ca++) which are required for working
muscles.

The topic of electrolytes gets even more complex as you get into the
electrical aspect of it. Take for instance chloride balance. Chloride
(Cl-) is the major extracellular anion (103-110 mEq/L). It is ingested
with food and drinking water and is freely absorbed from the GI tract.
Although chloride readily follows the cationic Na+ in a passive fashion
when diffusion occurs across cellular membranes, in certain select sites
such as the ascending loop of Henle, a specialized carrier transport
system for Cl- is present and in these cases it is Na+ that follows
passively. Cl- is present in most secretions with Na+ except in gastric
juice in which Cl- and H+ are responsible for the acidity. In the ECF,
Cl- and bicarbonate (HCO3-) are inversely related to one another. For
example, with a constant plasma anion gap (made up of organic acids,
phosphates, sulfate and protein), if Cl- decreases, HCO3- will increase
proportionately, and vice versa. Depending on the body's need for HCO3-,
more or less Cl- is excreted in the urine as the ammonium salt. This
permits Na+ exchange for H+ since the tubule secretes ammonia and H+
into the lumen, and in exchange Na+ and HCO3- return to the plasma. The
regulation of Cl- concentration in the ECF is directly but passively
related to Na+ concentration (all body fluids are electrically neutral).

Rob





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