In my post on The Complex Relationship Between Salt, Sodium, and Blood Pressure: Myths, Facts, and Scientific Debates, I looked at sodium and hypertension and what we have been thought about it with respect to blood pressure. In continuation, even if we are going to accept this, how does it happen?
The pathophysiologic mechanism leading to increase in blood pressure value in association with sodium has been debated for the longest of time, so the connection between the two is intricate with no 100% certainty that intake of salt causes increase of BP. There are a few theories about salt in the body with one being the water retention theory.
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Sodium is an electrolyte and we know that electrolytes causes a retention of water so is it possible that an increase in sodium leads to an increase in water retention in the body? The kidney only let go of excess water leaving us with a maintained state of water so we don't become dehydrated, and more water in the body means increase blood volume which also mean increased blood pressure but is this theory correct seeing that salt is in the picture?
A group of researchers wrote a paper titled "High dietary sodium chloride consumption may not induce body fluid retention in humans" after carrying out a research in the lab on six healthy men that were nn-hyperthensive and gave them salt increasingly over a 24 day period with the intention getting result and at the end, they found that an increase in sodium didn't lead to increased water retention in the body rather it led to a shift in body water. After this finding, they had to perform another one with 32 healthy men who were not hypertensive, splitting them into 4 groups and feeding them different amount of salt (0.6g, 2.4g, 4.8g, and 6.6g)for a period of 7 days and there was no water retention effect in the entire group.
Fluid can be both intracellular and Extracellular and water outside the cell can be found in different areas of the body including in the vessels (intravascular fluid), and interstitial fluid which is the water that is found within everything in the body. After loading with salt, the intravascular fluid increased while extracellular fluid volume was not affected as there was a shift in fluid from the interstitial fluid into the intravascular fluid. In all, the participants blood pressure was not affected so there was no increase in blood pressure. Blood volume should increase blood pressure but according to the research, it looks like this change is transient as the increase in intravascular volume only stayed for about 1 to 2 hours. According to the study, the blood pressure throughout the study was not affected but this doesn't account for the blood pressure immediately after ingesting the salt.
Another theory is the Guyton theory which says that the kidney is responsible for determining if we undergo high blood pressure or not from excess salt. The kidney is made up of hormones that are responsible for fluid balance, vessel tightening and relaxing, and blood pressure. The theory looks at increased salt to lead to increased water which would balance it out. This will increase the blood volume in the body which will increase blood pressure but from Guyton theory, provided the kidneys are working well consuming either extremely small amount of salt or large amount up to 50 times would not have any alteration in arterial pressure. So the theory says that salt sensitive is determined by how effective or ineffective the kidneys are as the kidney would pee out salt.
While traditional views link high salt intake to increased blood pressure via water retention, recent research challenges this notion. The role of the kidneys and individual physiological responses are critical factors in this complex relationship. Understanding these dynamics helps clarify the ongoing scientific debates and offers a more nuanced perspective on managing sodium intake for blood pressure control.
Reference
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6770596/
https://pubmed.ncbi.nlm.nih.gov/2063193/
https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.113.01831#R1R
https://journals.physiology.org/doi/full/10.1152/ajprenal.2000.278.4.F585
https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.116.024446
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7318881/
https://nap.nationalacademies.org/read/25353/chapter/13