Long Term Control of Blood Pressure

Question 1

<p>Which organ is responsible forlong term control of blood pressure?</p>

Answer 1

<p>•Revolves around the control of plasma volume by the kidney</p>

Question 2

<p>What are the functions of the kidney?</p>

Answer 2

<p>–Excretion of waste products</p>

<p>–Maintenance of ion balance</p>

<p>–Regulation of pH</p>

<p>–Regulation of osmolarity</p>

<p>–Regulation of plasma volume</p>

Question 3

<p>What is the effect f the renal counter current system?</p>

Answer 3

<p>Creates a very high osmolarity outside the collecting duct</p>

Question 4

<p>How is control over how much water is lost with urine acheived?</p>

Answer 4

<p>Osmotic gradient exists between the collecting duct and outside the collecting duct.</p>

<p></p>

<p>Na+ transport determines this gradient</p>

<p></p>

<p>•Control over the permeability of the collecting duct to water determines if water follows that osmotic gradient or not</p>

Question 5

<p>Where is sodium pumped?</p>

Answer 5

<p>Pumped outside of the distal tube -concentration of the solute therefore decreases significantly before it reaches the collecting duct</p>

Question 6

<p>What is the affect of varying the permeability of the collecting duct?</p>

Answer 6

<p>•Making the collecting duct very permeable to water will result in lots of water reabsorption, little urine, and conserve plasma volume</p>

<p>•Making the collecting duct very impermeable to water will result in little reabsorption, lots of urine (= diuresis), and a reduction in plasma volume</p>

Question 7

<p>What are the three main hormones that regulate water reabsorption?</p>

Answer 7

<p>Renin - angiotensin - aldosterone system</p>

<p>Antidiuretic factor (ADH, vasopressin)</p>

<p>Atrial natriuretic peptide</p>

Question 8

<p>Where is the renin produced?</p>

Answer 8

<p>–From the juxtaglomerular (= granule cells) of the kidney</p>

Question 9

<p>What triggers renin production?</p>

Answer 9

<p>–Activation of sympathetic nerves to the juxtaglomerular apparatus</p>

<p>–Decreased distension of afferent arterioles (the “renal baroreflex”)</p>

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

Question 10

<p>What is responsible for detecting a reduced delivery of sodium and chlorine ions?</p>

Answer 10

<p>Macula densa</p>

Question 11

<p>Where do you find the macula densa?</p>

Answer 11

<p>The ascending loop of henle</p>

<p></p>

<p>(distal convulated tubule)</p>

Question 12

<p>Where is renin produced?</p>

Answer 12

<p>In the juxtaglomerular of the kidneys - granule cells</p>

Question 13

<p>What triggers renin production?</p>

Answer 13

<p>Signs of low mean arterial pressure:</p>

<ul> <li>Activation of sympathetic nerves to the juxtaglomerular apparatus</li> <li>Decreased distension of afferent arterioles (renal baroreflex)</li> <li>Decreased delivery of sodium and chlorine through the tubule</li></ul>

Question 14

<p>What does renin do?</p>

Answer 14

<p>Converts angiotensinogen to angiotensin 1</p>

<p>Angiotensin converting enzyme</p>

<p>Angiotensin 2</p>

<p></p>

Question 15

<p>How does angiotensin increase MAP?</p>

Answer 15

<p><strong>Stimulates release of aldosterone from the adrenal cortex.</strong></p>

<p>(this increases the amount of sodium reabsorption in the loop of henle - less diuresis and increased plasma volume)</p>

<p><strong>Increases the release of ADH from the pituitary</strong></p>

<p>(increases the permeability of the collecting duct, reduces diuresis. Increases sense of thirst)</p>

<p><strong>Is a vasoconstrictor</strong></p>

<p>(increases total peripheral resistance)</p>

Question 16

<p>How is the formation of angiotensin 2 a form of negative feedback?</p>

Answer 16

<p>•Multiple mechanism detect any decrease in MAP</p>

<p>•Stimulates release of renin</p>

<p>•This evokes multiple mechanisms which increase MAP</p>

Question 17

<p>Where is ADH produced?</p>

Answer 17

<p>–Synthesised in the hypothalamus</p>

<p>–Released from the posterior pituitary</p>

Question 18

<p>What triggers ADH release?</p>

Answer 18

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

<p>An increase in osmolarity in interstitial fluid (osmoreceptors in the hypothalamus)</p>

<p>Circulating angiotensin 2 (triggered by the renin-angiotensin-aldosterone system)</p>

Question 19

<p>What is the effect of ADH?</p>

Answer 19

<p>Increases the permability of the collecting duct to H2O</p>

<p>Causes vasoconstriction (hence why it is sometimes known as vasopressin)</p>

Question 20

<p>Why is the release of ADH classed as a negative feedback mechanism?</p>

Answer 20

<p>–Multiple mechanism detect any decrease in MAP</p>

<p>–Stimulates release of ADH</p>

<p>–This evokes multiple mechanisms which increase MAP</p>

Question 21

<p>What does ANP stand for?</p>

Answer 21

<p>Atrial natriuretic peptide</p>

Question 22

<p>Where is atrial natriuretic peptide formed?</p>

Answer 22

<p>Produced in and released from the myocardial cells in the atria</p>

Question 23

<p>What triggers release of ANP?</p>

Answer 23

<p>Increased distension of the atrium ( a sign of increased MAP)</p>

Question 24

<p>What does ANP do?</p>

Answer 24

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

<p><strong>Inhibits the release of renin</strong></p>

<p><strong>Acts on the medullary CV centres to reduce MAP</strong></p>

<p></p>

Question 25

<p>Why is the release of ANP described as a negative feedback mechanism?</p>

Answer 25

<p>–A mechanism that detects any increase in MAP</p>

<p>–Stimulates release of ANP</p>

<p>–This evokes multiple mechanisms which reduce MAP</p>

Question 26

<p>What percentage of hypertension cases are as a result of secondary (knoown) causes?</p>

Answer 26

<p>Only 5% to 10%</p>

Question 27

<p>What are the rational drug treatments for hypertension?</p>

Answer 27

<p><strong>–Ca2+ channel antagonists</strong></p>

<p><strong>–b-adrenoceptor antagonists</strong> – specifically beta 1 receptor antagonist – reduces cardiac output and blood pressure</p>

<p>–<strong>Thiazide diuretics</strong> – work in sodium transporter in kidney – stops build up of sodium gradient – makes you excrete more water</p>

<p>–<strong>Angiotensin converting enzyme inhibitors</strong></p>

<p>–<strong>Angiotensin 2 antagonist</strong></p>