Renal Control of BP

MCT

Hemorrhage Venous return blood volume

SV and CO

Atrial volume

MAP HP Baroreceptors Central Chemoreceptors Peripheral Chemoreceptors

LP Baroreceptors

Medullary Cardiovascular Control Center SYMPATHETIC RESPONSE

Hormonal response -Angiotensin/Renin -ADH release -ANP (decreased)

Heart rate Contractility

Vasoconstriction (arteriole/venous)

Long-term and short-term control of ABP

Short-term heart resistence & compliance Baroreflex Blood Volume

Long-term

hypertrophy

Angiotensin II Vasopressin NO ANP Endothelin Sympathetic nervous system

Drinking Renal excretion Na-intake EPO

Ackermann

Blood pressure regulation

vasodilatation
stimulation of cGMP stimulation of cAMP

vasoconstriction
inhibition of cAMP Stimulation of IP3

In smooth muscle, cGMP and cAMP stimulates Ca2+ pump of the sarcoplasmic reticulum Decrease of Ca2+ concentration in smooth muscle cell

Slower decrease IP3 releases Ca2+ of Ca2+ from the sarcoplasmic reticulum

NO ANP

adenosine A2 histamine H2 adrenaline b2 VIP

serotonin
adrenaline a2 angiotensin II

serotonin
adrenaline a1 vasopressin

Regulation of blood flow

myogenic metabolic shear dependent stretch-activated cation channels cause vasoconstriction metabolic products cause vasodilatation vasodilatation by NO, which is produced in vascular endothelium

neural

humoral

sympathetic constrictor nerves in most tissues parasympathetic dilator nerves in some secretory and spongiform tissues constriction by angiotensin II, epinephrine, vasopressin, serotonin dilatation by ANP, histamine, inflammatory mediators

circulation

local metabolic control hypoxia adenosine CO2 H+

sympathetic control least important least important

mechanical effects compression during systola increased intracranial pressure decreases CBF

coronary cerebral

skeletal muscle

during exercise lactate K+ adenosine

at rest muscular a vasoconstriction activity compresses b vasodilatation blood vessels a vasoconstriction least important lung inflation

skin pulmonary

hypoxia vasoconstricts

renal

myogenic

least important

Juxtaglomerular Apparatus

raglomerular sangial cells = ration, structural pport, and agocytosis

raglomerular /Lacis sangial cells = EPO

Renal circulation
25 % of cardiac output (1.3 L/min) Renal blood flow is autoregulated
Constant blood flow even when renal perfusion pressure changes (80-200 mmHg)
Renal autoregulation is independent of sympathetic innervation (transplanted kidney) Angiotensin II vasoconstrictor for both afferent and efferent arterioles, but Efferent arteriole is more sEnsitive Prostaglandins (E2, I2 produced locally) vasodilatation of both arterioles

Glomerular Filtration of Blood

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 muscle cells that comprise the juxtaglomerular apparatus and they detect changes in this pressure. NB These cells are regulating GFR, not BP.

Glomerular Filtration of Blood

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

Renin Angiotensin Aldosterone System (RAAS)

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)

Unilateral Stenosis of Renal Artery (2-Kidney Goldblatt HTN)

One renal artery is occluded in a patient with two kidneys Constricted kidney:
Decreased renal arteriolar pressure Renin secretion Angiotensin II effects

Normal kidney:

Increased GFR Increased Na and H2O absorption

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