Renal Control of BP

8/2/2019 Renal Control of BP

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Renal Control of BP

MCT


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Hemorrhage

Venous return blood volume

MAP

SV and CO Atrial volume

LP Baroreceptors

HP BaroreceptorsCentral

Chemoreceptors

Peripheral

Chemoreceptors

Medullary

Cardiovascular

Control Center

SYMPATHETIC RESPONSE

Heart rate

Contractility

Vasoconstriction

(arteriole/venous)

Hormonal response

-Angiotensin/Renin

-ADH release

-ANP (decreased)


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Long-term and short-term control of ABP

resistence &

compliance

Short-termBaroreflex

Long-term

hypertrophy Angiotensin II

Vasopressin

NO

ANP

Endothelin

Sympathetic nervous

system

heart Blood Volume

Drinking

Renal excretion

Na-intake

EPO

Ackermann


4/12

Blood pressure regulation

vasodilatation vasoconstriction

stimulation ofcGMP

stimulation ofcAMP

inhibition ofcAMP

Stimulation ofIP

3

In smooth muscle, cGMP and cAMPstimulates Ca2+ pump of thesarcoplasmic reticulum

Decrease of Ca2+ concentration in

smooth muscle cell

Slower decreaseof Ca2+

IP3releases Ca2+from thesarcoplasmicreticulum

NO

ANP

adenosine A2histamine H2adrenaline b2

VIP

serotonin

adrenaline a2

angiotensin II

serotonin

adrenaline a1

vasopressin


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Regulation of blood flow

myogenic stretch-activated cation channels causevasoconstriction

metabolic metabolic products cause vasodilatation

sheardependent

vasodilatation by NO, which is produced invascular endothelium

neural sympathetic constrictor nerves in mosttissues

parasympathetic dilator nerves in somesecretory and spongiform tissues

humoral constriction by angiotensin II, epinephrine,vasopressin, serotonin

dilatation by ANP, histamine, inflammatory

mediators


6/12

circulation local metabolic

control

sympathetic

control

mechanical

effects

coronary hypoxia

adenosine

least important compression

during systolacerebral CO2

H+

least important increasedintracranialpressuredecreases CBF

skeletalmuscle

during exercise

lactate

K+

adenosine

at rest

a vasoconstriction

b vasodilatation

muscularactivitycompressesblood vessels

skin - a vasoconstriction -

pulmonary hypoxiavasoconstricts

least important lung inflation

renal myogenic least important


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Juxtaglomerular Apparatus

aglomerular

angial cells =

ation, structuralport, and

gocytosis

aglomerular /Lacis

angial cells = EPO


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Renal circulation

25 % of cardiac output (1.3 L/min)

Renal blood flow is autoregulated

Constant blood flow even when renal perfusion pressurechanges (80-200 mmHg)

Renal autoregulation is independent of sympatheticinnervation (transplanted kidney)

Angiotensin II vasoconstrictor for both afferent and

efferent arterioles, but Efferent arteriole is more sEnsitive

Prostaglandins (E2, I2 produced locally) vasodilatation ofboth arterioles


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The filtration relies on a net differential pressure

comprised of three components: Capillary hydrostatic pressure (45 mmHg)

Bowmans hydrostatic pressure (10 mmHg)

Plasma protein oncotic pressure (25mHg)

Net pressure = PHyd + POnc = (45-10) 25 = 10 mmHg

The GFR is dependent on perfusion pressure to the

kidney, and therefore there are a group of smooth musclecells that comprise thejuxtaglomerular apparatus andthey detect changes in this pressure. NB These cells areregulating GFR, not BP.

Glomerular Filtration of Blood


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Juxtaglomerular cells

Modified, granular smooth muscle cells on

afferent and efferent glomerular arterioles,

responsible for synthesizing and releasing renin

Release renin in response to:

Decreased afferent arteriolar pressure

(detected directly)

Increased sympathetic tone

Decreased [NaCl] as detected in the Macula

densa cells

Prostaglandin and NO release

Macula densa cells

Tubular cells that detect [NaCl] in the distal

tubule

When [NaCl] is low MD cells:

Release vasodilator in to afferent arterioles

Increase renin release in to afferent and

efferent arterioles by stimulating JG cells

Net effect of activation within this system is to

increase arteriolar pressure to restore GFR

Glomerular Filtration of Blood


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Renin (an enzyme) released in to blood due to:

Decreased renal arteriolar pressure b1 receptor activation from SNS

Decreased [NaCl] at MD cells

Renin cleaves angiotensin I from angiotensinogen Angiotensinogen is made in the liver

Angiotensin I has no activity

Angiotensin II is cleaved from angiotensin I by ACE Angiotensin II effects:

Systemic vasoconstriction (AT-I receptor)

Increased Na+ and H20 retention Direct action on renal cells

Aldosterone release from adrenal cortex

ADH release from pituitary

Thirst

Cardiac and vascular growth (AT-II receptor)

Renin Angiotensin Aldosterone System (RAAS)


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One renal artery is occluded in a patient with two kidneys

Constricted kidney:

Decreased renal arteriolar pressure

Renin secretion

Angiotensin II effects Increased GFR

Increased Na and H2O absorption

Normal kidney: Also increases Na and H2O absorption due to ischemic kidney renin production

Hypertension

Markers of renal insufficiency such as plasma creatinine are often masked

due to the hyperfiltrationin the functional kidney.

2 Major causes of renal artery stenosis:

Atherosclerotic disease

Fibromuscular dysplasia = Autosomal dominant disorder resulting in an

abnormal thickening of the intima, media or adventitia of the renal artery

Unilateral Stenosis of Renal Artery (2-KidneyGoldblatt HTN)

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Renal Control of BP