Chapter 19 ( role of kidneys in long term arterial pressure) Flashcards
elevated arterial pressure does what to the kidneys?
causes them to excrete more fluid and return the pressure back to normal
pressure diuresis-
increase of only a few mm Hg can cause the renal output to more than double the output of water
Pressure natriuresis-
same as diuresis but with salt
equilibrium point
intake =output
2 determinants of long term arterial pressure
- degree of pressure shift of renal output curve for water and salt
- level of water and salt intake
what does reduced blood pressure do?
activates the sympathetic nervous system and formation of antinatriuretic hormones are increased. The decrease in renal output increases the arterial pressure back to normal
salt insensitive people
large amounts of salt changes blood pressure by a little
salt sensative people
moderate increases in salt cause significant changes in pressure
arterial pressure
cardiac output times peripheral resistance
mechanism by which increased fluid volume can elevate arterial pressure by increasing cardiat output or total peripheral resistance
- increased extracellular fluid volume
- increases blood volume
- which increases mean circulatory filling pressure
- which increases venous return of blood to the heart
- which increases cardiac output
- which increases arterial pressure
2 ways in which cardiac output can increase arterial pressure
- ( direct) increased cardiac output increases pressure. 2. ( indirect) effect to raise total peripheral vascular resistance.
how does salt incread extracellular fluid volume?
excess salt in the extracellular fluid stimulates the brain for thirst. This causes someone to drink water to return the extracellular salt concentration back to normal.
increased salt levels also stimulates the hypothalamic-posterior pituitary gland to secrete antidiuretic hormone ( ADH). ADH causes the nephron to re-absorb large amounts of water which increases the bodys temperature.
chronic hypertension
mean arterial pressure is greater than a upper range of a normal measure ( greater than 110 mmHg)
effects of hypertension
excess work load on the heart which leads to coronary disease and heart attacks. Damaging of blood vessels in the brain followed by cerebral infarct ( stroke)., Paralysis, dementia, blindness, kidney problems.
reduced kidney mass effects
basically when part of your kidney doesn’t work you retain more salt and increases your blood pressure
aldosterone
causes hypertension because it causes the kidneys to reabsorb more water
Renin
protein enzyme released by the kidneys when arterial pressure falls too low. It helps correct the pressure level in many ways
Prorenin
inactive form of renin and is made in the JG cells
JG cells
juxtaglomerular cells. They are modified smooth muslce cells located in afferent arteriole walls
Is renin a vasoactive substance?
no its just an enzyme
what does renin act on?
angiotensinogen which releases angiotensinogen 1
angiotensin 1
mild vasoconstrictor properties but not enough to cause significant changes in circulatory function. Renin persists in blood for 30 minutes to 1 hour and continues to cause formation of still more angiotensin 1 during this entire time
angiotensin 2-
powerful vasoconstrictor. It persists in the blood only for 1 to 2 minutes because it is rapidly inactivated by multiple blood and tissue enzymes called antiotensinases
effects of angiotensin 2
vasoconstriction , decreases excretion of salt and water from kidneys
how long does the renin-angiotensin process take to be fully active?
20 min.
retaining salt by angiotensin
acts on kidneys to retain salt and water. Causes adrenal glands to secrete aldosterone
mechanism of retention by angiotensin 2
restricts the renal arterioles, which diminishes blood flow through kidneys, acts on tubular cells to increase reabsorption of sodium and water, it stimulates aldosterone from adrenal glands.
neurogenic hypertension
caused by strong stimulation of sympathetic nervous system which causes vasoconstriction to occur
genetic causes of hypertenstion
in humans is caused by a single gene mutation
primary hypertenstion
in 90-95 % of hypertension cases. ITs an unknown origin but lifestyle plays a major role.
charecteristics of primary hypertension
cardiac output is increased to additional blood flow required for adipose tissue. Sympathetic nerve activity iis increased. Angiotensin 2 and aldosterone levels are increased twofold to threefold in obese folks. Renal pressure natriuresis mechanism is impaired
