The difference in genetic makeup and family history has a significant impact on salt sensitivity, and is being studied more with improvement on the efficiencies and techniques of genetic testing.  In both hypertensive and non-hypertensive individuals, those with haptoglobin 1-1 phenotype are more likely to have sodium sensitivity than people with haptoglobin 2-1 or 2-2 phenotypes. More specifically, haptoglobin 2-2 phenotypes contribute to the characteristic of sodium-resistance in humans.  Moreover, prevalence of a family history of hypertension is strongly linked with the occurrence of sodium sensitivity.
Hemostasis, or the clotting of blood and formation of scabs, is managed by the platelets of the blood. Platelets normally remain inactive in the blood until they reach damaged tissue or leak out of the blood vessels through a wound. Once active, platelets change into a spiny ball shape and become very sticky in order to latch on to damaged tissues. Platelets next release chemical clotting factors and begin to produce the protein fibrin to act as structure for the blood clot. Platelets also begin sticking together to form a platelet plug. The platelet plug will serve as a temporary seal to keep blood in the vessel and foreign material out of the vessel until the cells of the blood vessel can repair the damage to the vessel wall.