Long term regulation of blood pressure is primarily accomplished by altering ❌ via the ❌ mechanism.

❌ cells in the kidney monitor alterations in blood pressure. If blood pressure falls to low, these specialised cells release the enzyme ❌ into the bloodstream.
Renin travels through the bloodstream and binds to inactive plasma protein, ❌ activating it to Angiotensin I. As ❌ passes through the ❌ capillaries and enzyme in the lungs called ❌, converts Angiotensin I to Angiotensin II.

Angiotensin II continues through the blood stream until it reaches the ❌ where it stimulates cells in the ❌ to release the hormone ❌.
When aldosterone reaches the kidneys it promotes ❌ reabsorption of sodium from the kidney tubules. As water follows sodium movement, water is also reabsorbed from the tubule lumen into the blood stream, thus increasing blood volume and therefore blood pressure.

Angiotensin II also acts as a ❌ and therefore raises blood pressure in the body's arterioles.

Regulation of ❌ is another way to regulate blood pressure with both long and short term effects.

As increased osmolarity and thus ❌ in blood volume is detected in the ❌, it sends signals to the ❌ to release ❌.

ADH ❌ water reabsorption in the kidney by stimulating an increase in the number of water channels in the ❌ and walls of the collecting ducts. These channels aid the movement of water ❌ the capillaries, ❌ the osmolarity of the blood volume and therefore decreasing blood pressure.

In the short term, increased osmolarity excites the ❌ of the hypothalamus and stimulates the individual to drink more water.