Chapter 19 - guyton renal compensation cardiac events

Role of Kidneys in Long-Term Arterial Pressure Control

• Long-term arterial pressure regulation intertwines with body fluid volume homeostasis.
• Nervous, hormonal, and local kidney systems work together to balance fluid intake and output.

Renal-Body Fluid System for Arterial Pressure Control

• Acting slowly but powerfully, the system increases arterial pressure with increasing blood volume if vascular capacitance remains unchanged.
• Elevated pressure prompts kidneys to excrete excess volume, restoring normal pressure.
• This pressure control mechanism is primitive, fully functional in hagfish, a low vertebrate.
• Hagfish arterial pressure (8-14 mm Hg) directly responds to blood volume, rising as it drinks seawater.
• Kidneys excrete excess volume when pressure is too high, and less fluid when low.
• This ancient control method persists in higher species, refined by nervous, hormonal, and local kidney controls.
• Human kidneys are as sensitive as hagfish kidneys to pressure changes; a slight pressure increase can double water excretion (pressure diuresis) and salt excretion (pressure natriuresis).

Quantitation of Pressure Diuresis

• Pressure diuresis serves as a foundation for controlling arterial pressure.
• Isolated kidneys show greatly increased urine output with rising arterial pressure.
• In humans, at 50 mm Hg, urine output is essentially zero; at 100 mm Hg, it is normal; and at 200 mm Hg, it's 4-6 times normal.
• Increased arterial pressure leads to an almost equal increase in sodium output (pressure natriuresis).

Experiment with the Renal-Body Fluid System

• Dogs with blocked nervous reflex mechanisms elevated arterial pressure through intravenous blood infusion of 400ml
• Cardiac output doubled, increasing mean arterial pressure to 205 mm Hg (115 mm Hg above normal.).
• Markedly increased urine output reduces arterial pressure and cardiac output, which then return to normal within an hour.
• Kidneys are extremely capable of removing excess fluid volume, lowering arterial pressure.

Renal-Body Fluid Mechanism with Near-Infinite Feedback Gain

• The near-infinite feedback gain principle demonstrates how the renal-body fluid mechanism works
• Renal output rises with arterial pressure
• Net water and salt intake: long term water and salt output balances with intake
• The equilibrium point describes where output balances intake, and mean arterial pressure
• Any variance from equilibrium is self-corrected and has near infinite feedback gain.

Key Determinants of Long-Term Arterial Pressure

• Two primary factors decide long-term arterial pressure
• Renal output curve for water and salt: the first primary
• Level of water and salt intake: the second primary
• Only two factors can change the equilibrium point's pressure
• Shift in the renal output curve for salt and water is the first
• Change in water and salt intake the second
• Arterial pressure depends on:
• Renal output curve for water and salt
• Level of water and salt intake

Chronic vs Acute Curves

• Hypertension can be caused with a shift in renal output curve, or change the intake level

• Renal output curve shifts 50 mm Hg to the right: equilibrium point shifts 50 mm Hg, pressure increases by that amount.

• Fourfold increase in salt/water intake increases equilibrium point to 160 mm Hg, 60 mm Hg above normal.

• Renal function curve is much steeper than in figures, salt intake has only a modest effect.

• Chronic arterial pressure changes affect urine output more than acute ones.

• Chronic changes invoke nervous, hormonal adjustments.

• Increased pressure lowers sympathetic nervous system activity and some hormone production.

• Reduced activity in antinatriuretic systems enhances pressure natriuresis and diuresis.

• Decreased blood pressure activates sympathetic nervous and antinatriuretic hormones.

• A combination of effects on kidneys with the autonomic nervous system results in powerful long term blood pressure/fluid volume control.

Factors impacting salt and water

• Normal kidney function and low salt intake has little effect on blood pressure
• Injury, or excessive antinatriuretic hormones, will impact blood pressure

If Fluid Intake and Renal Function Do Not Change

• Peripheral resistance acutely increases arterial pressure, which returns normal within days if kidneys normal.
• Vasoconstriction outside kidneys doesn't change equilibrium point, because kidneys initiate pressure diuresis and natriuresis.
• Fluid loss ceases when blood pressure returns to equilibrium and blood volume drops below normal.

Increased Fluid Volume

• Extracellular fluid volume causes increased arterial pressure if vascular capacity isn't simultaneously increased:
• Increase extracellular fluid volume
• Increase blood volume
• Increase mean circulatory filling pressure
• Increase venous return to the heart
• Increase cardiac output
• Autoregulation- increased arterial pressure- increased urine output
• Autoregulation raises total peripheral resistance due to blood vessel constriction and increases blood flow

Importance of Salt Sodium Chloride

• Salt is more impactful than water, because the body holds onto it more
• Pure water is excreted often right away, but salt is kept
• High salt concentrates in the body, increases fluid volume, because water tries to even itself out

Chronic Hypertension & Impaired Renal Function

• Chronic hypertension means their mean arterial pressure is beyond the accepted range
• Normal is about 90 mm Hg, and hypertensive is over 110 mm Hg.
• Lethal effects of hypertension
• Heart workload increases
• Brain blood vessels are often damaged, causing major issues
• Kidneys get injured, and eventually fail

Experimental Volume-Loading Hypertension

• Dogs with reduced kidney mass and salt intake were tested
• At 70% kidney mass removed, arterial pressure rose slightly
• Giving salt solution further increased pressure, as fluid volume increased
• Volume loading causes hypertension, due to salt and water retention
• Reduction in kidney mass impacts excretion and high arterial pressure
• High pressure causes excess salt and water excretion

Development of Volume-Loading Hypertension

• Decreased Kidney caused high intake of salt and water, with the effects, extracellular fluid volume

• Arterial pressure increases slower than above, and peripheral resistance decreased due to baroreceptors

• Baroreceptors adapted after a few days

• Arterial pressure rose, but total peripheral resistence was normal

• Prolonged secondary changes happened in the next few weeks.

• Increase in peripheral resistence

• Blood volume also decreased

• Cardiac output also normal

• Peripheral resistance led to decresed capillary pressure

• Elevated arterial ressure meant kidneys volume loss

• Effects after a few weeks

• Hypertension

• Marked increase peripherial resistance

• Comple return blood voluem etc

• Two stages of volume loading

• Increase fluid volume and cardiac output

• High blood pressure plus return of cardiac, now at normal levels

Volume-Loading and Artificial Kidneys

• Important to make sure body fluid is good in people with artificial heart
• Hypertension occurs if the above does not happen

Hypertension caused by Excess Aldosterone

• Increase in salt, water, blood volume, extracelluar fluid volume, and all other results from above

Renin-Angiotensin System

• Another mechanism to keep arterial pressure good
• Renin released with arterial pressure is low, raises pressure
• Synthesized, stored in kidneys JG
• Multiple factors affect the systems
• JG cells release with decrease

Rapid response

• Rapidly, high intensity response with severe hemorrhage
• Returns more to normal
• slower effect in 20 mins
• causes kidneys and adernal glands to raise normal level

Angiotensin II Effect

• Cause retention or loss of salt, water
• Decreases urine output
• Decreases capilaries which decreases reabsorbtion

Angiotensin II graph graph

• High angiotensin cause kidney retention and increased chronic elevation
• Helps balance arterial pressure with high or low salt
• Will rise no more then 4-6mm hg in increased salt
• Prevented with ACE inhibitor, will rise 40

Renin-Secreting Tumor

• Causes large amounts of angiotensin.
• This can lead to long term hyptertension

One-Kidney Goldblatt Hypertension

• Putting a clamp on kidney after removing the the other kidney
• Greatly reduces pressure
• Increase the systemic pressure
• Causes constricter to increase
• Early hypertension is caused by with system
• After which volume load increases

Two-Kidney

• Causes of constricter and stenois
• Kidneys keep in and cause high pressure

Decreased Kidney

• High tissue secretes high renin

Combinion Effects

• High in coarctation
• Very rare to find

High Pressure

• Will develop almost 100%
• High presure returns to normal

Aortic Contraction

• Blood flow becomes normal
• Low is almost normal
• Presure goes out in the top body

Preeclamp

Preeclampsia/Tox

• High BP cause high salt intake
• Sympathetic causes high BP
• Angiotension caused high salt
• Kidneys wont keep in enough

Hypertensitivity

• Low sodium reduces salt
• Can be managed

Three Groups

• Acting presssure
• Nervous is powerful and acute

The Middle Group

• Angotentsin
• Stress release
• Capilaries

Long Term

• In long term control