Long Term Control of Blood Pressure Flashcards

1
Q

What controls blood pressure in the long term?

A

Renin-Angiotensin-Aldosterone System (RAAS)

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2
Q

What is renin?

A

A peptide hormone released by the granular cells of the juxtaglomerular apparatus in the kidney.

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3
Q

What is renin released in response to?

A

Sympathetic stimulation
Reduced sodium-chloride delivery to the distal convoluted tubule
Decreased blood flow to the kidney

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4
Q

What kidney function is important when discussing the long term control of blood pressure?

A

Regulation of plasma volume as controlling plasma volume is used to regulate MAP

Big plasma volume = high MAP vice versa

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5
Q

What is Bowman’s Capsule?

A

A part of the nephron which is a part of your kidney. The nephron is the filtering unit of your kidney.

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6
Q

What creates a very high osmolarity outside collecting duct of kidney?

A

Renal counter current system

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7
Q

Control over what determines size of the osmotic gradient?

A

Na+ (sodium) transport

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8
Q

Osmolarity of filtrate coming out of Bowman’s Capsule?

A

300 mOsm - same as blood

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9
Q

What happens as Na+ goes down the Bowman’s capsule?

A

Na+ transported out and builds big osmotic gradient w/ increased sodium in ECF

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10
Q

What happens to MAP when the collecting duct of the kidney is made very permeable to water?

A

Lots of water moves out of collecting duct
Lots of water reabsorption
Little urine and plasma volume = very small vol. of concentrated urine
Retaining water results in increased MAP due to increased plasma volume

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11
Q

What happens to MAP when the collecting duct of the kidney is made impermeable to water?

A

Little water reabsorption
Decreased plasma volume
Decreased MAP

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12
Q

What are the three main hormones that regulate water reabsorption?

A

Renin - angiotensin - aldosterone system (RAAS)

Antidiuretic factor (ADH, vasopressin)

Atrial natriuretic peptide

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13
Q

What triggers renin production?

A

–Activation of sympathetic nerves to the juxtaglomerular apparatus

–Decreased distension of afferent arterioles (the “renal baroreflex”)

–Decreased delivery of Na+/Cl- through the tubule

ALL SIGNS OF LOW MAP

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14
Q

What does renin do?

A

Converts inactive angiotensinogen to angiotensinogen I
Which is in turn converted by angiotensin converting enzyme to angiotensinogen II

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15
Q

What is the active hormone in the RAAS system?

A

Angiotensinogen II

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16
Q

What does angiotensinogen II do?

A

Stimulates release of aldosterone form the adrenal cortex
- Increases Na+ absorption in loop of Henle, reducing diuresis and increases PV

Increases release of ADH from the pituitary
- Increases water permeability of the collecting duct, reducing diuresis and increases PV and thirst

Vasoconstrictor therefore increases total peripheral resistance

ALL INCREASE MAP

17
Q

What type of feedback is the RAAS system?

A

Negative feedback

18
Q

What is diuresis?

A

Increased or excessive production of urine.

19
Q

Where is ADH synthesised and where is it released from?

A

S: hypothalamus
R: posterior pituitary

20
Q

What is responsible for detecting a reduced delivery of sodium and chlorine ions?

A

Macula densa

Found in the ascending loop of henle

21
Q

What triggers ADH release?

A

A decrease in blood volume - (Baroreceptors from CVS relayed by medullary cardiovascular centres)

An increase in osmolarity in interstitial fluid (osmoreceptors in the hypothalamus)

Circulating angiotensin 2 (triggered by the renin-angiotensin-aldosterone system)

ALL SIGNS OF LOW PV OR MAP

22
Q

What is the effect of ADH?

A

Increases the permability of the collecting duct to H2O

Causes vasoconstriction (hence why it is sometimes known as vasopressin)

Both tend to increase MAP

23
Q

Why is the release of ADH classed as a negative feedback mechanism?

A

–Multiple mechanism detect any decrease in MAP

–Stimulates release of ADH

–This evokes multiple mechanisms which increase MAP

24
Q

Where is ANP and BNP produced?

A

In and released from myocardial cells in the atria and the ventricles respectively

25
Q

What triggers ANP and BNP release?

A

Increased distention of the atria and ventricles

A SIGN OF INCREASED MAP

26
Q

What do ANP and BNP do?

A

Increases the excretion of sodium (natriuresis) - (opposes the act of angiotensin 2 which causes lots of sodium to be reabsorbed by the loop of henle)

Inhibits the release of renin

Acts on the medullary CV centres to reduce MAP

ALL DECREASE MAP

27
Q

Why is the release of ANP described as a negative feedback mechanism?

A

–A mechanism that detects any increase in MAP

–Stimulates release of ANP

–This evokes multiple mechanisms which reduce MAP

28
Q

What does ANP stand for?

A

Atrial natriuretic peptide

29
Q

What percentage of hypertension cases are as a result of secondary (knoown) causes?

A

Only 5% to 10%

30
Q

What are the rational drug treatments for hypertension?

A

–Ca2+ channel antagonists

–b-adrenoceptor antagonists – specifically beta 1 receptor antagonist – reduces cardiac output and blood pressure

–Thiazide diuretics – work in sodium transporter in kidney – stops build up of sodium gradient – makes you excrete more water

–Angiotensin converting enzyme inhibitors

–Angiotensin 2 antagonist