blood pressure

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the kidney maintains correct blood volume/plasma volume which allows for correct blood pressure

blood pressure also controlled by cardiac output and peripheral resistance
cardiac output regulated by stroke volume and heart rate
stroke volume regulated by end-diastolic volume
heart rate and stroke volume regulated by norepinephrine
heart rate also regulated by epinephrine

peripheral resistance regulated by vasodilation/vasoconstriction

there's more, this is just a sample of control mechanisms
 
wait, isn't heart rate also regulated by the vagus nerve of the parasympathetic division. Thus, acetalcholine is also involved in heart rate. Right?
 
wait, isn't heart rate also regulated by the vagus nerve of the parasympathetic division. Thus, acetalcholine is also involved in heart rate. Right?

The natural rhythm of the pacemaker cells of the heart (SA node) is actually much faster than the rate at which your heart normally beats. To ensure that the SA node doesn't beat too fast, the pacemaker cells are constitutively inhibited by firing from the parasympathetic nervous system (vagus nerve). Thus, when your heart rate increases, say during exercise, the parasympathetic system is actually reducing it's effect on the heart, allowing the SA node to beat closer to its natural rhythm.

Does that make it clearer?
 
There's a ton of hormones involved in BP - the renin/angiotensin system, aldosterone, ADH, ANP, etc..
 
I want to make sure I have this straight, please tell me if I got anything wrong or missing anything. Thanks 😀

Low blood pressure, (triggered by something like high Na concentration, dehydration or blood loss). The NS responds by RAAS, which reabsorbs Na and water. Low bp so, the blood osmolarity is high, it triggers the release of ADH. Water is then absorbed, the blood pressure and volume is now high.

High blood pressure, ANF is triggered and opposes RAAS, which lowers the blood pressure and volume.
 
don't forget about renin (enzyme converting angiotensinogen to ang I) and ACE (enzyme converting ang I to ang II)

ang II is a strong vasoconstrictor causing systemic vasoconstriction and increases aldosterone levels (increases Na+ reabsorption which triggers ADH and thus H20 retention)--all this results in increased blood volume
 
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