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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. histamine. vasopressin. epinephrine. inflammatory mediators . serotonin •dilatation by ANP. 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.
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. and agocytosis raglomerular /Lacis sangial cells = EPO . structural pport.
I2 – produced locally) – vasodilatation of both arterioles .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.
NB These cells are regulating GFR.Glomerular Filtration of Blood • The filtration relies on a net differential pressure comprised of three components: • Capillary hydrostatic pressure (45 mmHg) • Bowman’s 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. not BP. . and therefore there are a group of smooth muscle cells that comprise the juxtaglomerular apparatus and they detect changes in this pressure.
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 . granular smooth muscle cells on afferent and efferent glomerular arterioles.Glomerular Filtration of Blood Juxtaglomerular cells • Modified.
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” .