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What is the equation for blood pressure?
BP= CO x SVR

Cardiac output times systemic vascular resistance

CO = HR x SV
How is BP maintained?
Rgulation of HR, SV and vascular resistance.
What happens to organs in hypotension?
Hypotension reduced organ perfusion
How is hypoperfusion sensed?
Where do the afferent loops of the baroreceptor reflex end?
Nucleus tractus solitarius (NTS) and rostral ventrolateral medulla.
What doe the baroreceptor reflex augment?
Augments vagal tone; reduces HR (β receptors), reduces SV (β receptors) and vasodilation (α receptors).
What are α1 receptors responsible for?
Vasoconstriction increasing SVR
What are β1 receptors responsible for?
Myocardial contractility- increase CO. HR- increase CO. Renal stimulation. Adrenal stimulation- glucocorticoid release leads to vasoconstriction)
How does the kidney regulate BP?
Plasma volume and [Na+] homeostasis occurs at juxtaglomerular apparatus. Regulate function of the nephrons. Found between the vascular pole of the renal corpuscle and returning distal convoluted tubule.
Location of the glomerular apparatus
Describe the juxtaglomerular apparatus.
Senses renal perfusion pressure at level of the glomerulus. Sodium concentration sensed in fluid surrounding distal convoluted tubule. If either reduced, renin is released.
What are the roles of angiotensin II?
Vasoconstriction increasing SVR. Induce release of catecholamines and aldosterone- increasing CO & SVR and plasma volume.
Describe aldosterone.
Mineralocorticoid from adrenal medulla in response to neural stimulation (ANS) and angiotensin II. Has renal tubular effects, increases Ang II receptors (as do glucocorticoids). Acts on DCT and collecting duct. Internalised and binds to intracellular aldosterone receptor. Increased transcription of gene for epithelial Na+ channels (eNaCs). Induces reabsorption of Na+ and H2O, excretes K+.
What are the endothelial mechanisms for maintaining normotension in BP increases?
Arterial shear stress activates nitric oxide synthase (NOS) leads to vasodilatation. L-arginine--> L-citrulline + NO. This system is counterbalanced by endothelin-1.
What atrial mechanisms help maintain normotension when BP rises?
Atrial strech induces release of atrial natriuretic peptide (ANP) and excrete sodium and water.
What are the dangers associated with hypertension?
For every 2mm rise in systolic BP; 7% rise in mortality from IHD/MI, 10% rise in mortality from stroke. £1billion in drug costs in primary care (2006).
What percentage of hypertensive cases have a defined cause?
5%. Due to neurohormonal overactivation (Cushing's), coarctation of the aorta, genetic defects (Liddle's syndrome).
What is essential hypertension defined as?
Overactivation of physiological mechanisms- due to maladaption. Age-related vascular and endocrine degeneration. Polygenic influence with environmental overlap.
What happens to baroreceptor sensitivy as we age?
It reduces. Age also associated with weight gain, chronically stimulating SNS- leading to raised HR, myocardial contractility and SVR.
What happens to the renin-angiotensin system in hypertension?
Vasoactive functions become chronically activated. Ongoing renin production releases prorenin. Chronic exposure to Ang II leads to VSMC hyperplasia and vascular remodelling.
What does prorenin do in the body?
Trophic factor for vascular smooth muscle cells, induces myocardial and renal fibrosis and release occurs despite ACEi and ARB use.
What is a also a trophic stimulant for vascular smooth muscle cells (VSMC)?
Aldosterone.
What factors induce vascular remodelling?
Hypertension, hyperlipidaemia, insulin resistance and weight gain- which commonly co-exist. Have complex interactions at molecular level. Lead to endothelial dysfunction and disturbance of endothelin-nitric oxide balance.
What causes vascular remodelling?
Chronic favouring of vasoconstrictive elements.
What occurs in vascular remodelling?
Age-related changes in vessel elasticity: generalised fibrosis, raised collagen: elastin ratio, trophic stimulation by prorenin, AngII and aldosterone. Different between artery vs. arteriole. Affects systolic and diastolic BP.
What occurs in small vessel eutrophic remodelling?
Rearrangement of VSMC layer with encrouchment onto lumen.
What happens in large vessel hypertrophic remodelling?
Stiffer tunica media with no change in lumen size.
What is often the first step of hypertension?
Raised SVR by chronic overstimulation of arteriolar VSMCs- leading to eutrophic remodelling and smaller lumen. This causes chronic pressure rises.
What happens in large vessel degeneration?
Chronically 'activated' large vessels (aorta, carotids) undergo hypertrophy- doesn't affect luminal diameter so diastolic BP stays same. Vessels stiffen due to raised collagen:elastin ratio means less distensible. Delays normal diastolic pulse-wave reflection such that it falls into systole.
What does chronic increase in afterload induced LVH lead to?
Reduced compliance, leading to diastolic dysfunction, raised LA pressure and dilatation, increased diastolic LV volume. LA/LV stretch leads to systolic dysfunction. LA pressure can track back through pulmonary circulation ro right heart, resulting in congestive cardiac failure.
What is Virchow's triad?
Change in blood constituents, change in vessel wall and change in blood flow.
What occurs in a pro-thrombotic state?
Vessel wall- VSMC hypertrophy/medial fibrosis and increase atheroma. Blood flow- atheroma/turbulence effects. Blood constituents- increased circulating vasoactive substances, growth factors and platelet activation.
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