Lecture 1

Question 1

How does angiotensin II effect blood pressure

Answer 1

• it is more potent than norepinephrine
• it has little to no effect on bradycardia due to the fact that it effects the brain and not the heart

ANS:
Stimulates autonomic ganglia increases release of epinephrine and norepinephrine from the adrenal medulla

Question 2

How does angiotensin effect the adrenal cortex and kidneys

Answer 2

Aldosterone synthesis acts on zone glomerulosa
Glucocorticoid synthesis so ag II is higher
Can contribute the cardiovascular hyper trophy
Can caused hypertensive disease
Due to overactivity of renin

Question 3

Angiotensin II on the CNS

Answer 3

• Central effects on blood pressure
• Stimulates drinking
• Increase secretion of vasopressin and adrenocorticotropic hormone

Question 4

How is the renin angiotensin system inhibited

Answer 4

Some drugs:
block renin release,
but most:
inhibit the conversion of ANG I to ANG II,
block angiotensin AT 1 receptors, or
inhibit the enzymatic action of renin.

Question 5

What are some anginotensin converting enzyme inhibitors

Answer 5

Captopril, enalapril, lisinopril, ramipril

Question 6

How do the anginotensin converting enzyme inhibitors work

Answer 6

Inhibits ACE by constricting the efferent arterioles, so increase renin due to loss of negative feedback and prevents inactivation of bradykinin
Can be used for hypertension
But could cause hypotension, coughing and hyperklalcemia

Question 7

What causes hereditary angioedema

Answer 7

C1 esterase inhibitor deficiency due to unregulated activation of kallokrenin characfised by low CD4 levels

Question 8

When are angiotensin II receptor blockers used and what are they

Answer 8

They have a diff mechanism to ACE inhibitors, it is used as a treatment to hypertension to people that can not tolerate ACE inhibitors due to cough or angioedema which is supposed to be mediated by elevated bradykinin levels

They DO NOT INCREASE BRADYKININ

Question 9

Patients with HF have what

Answer 9

Elevated levels of aldosterone due to angiotensin II stinulation and reduced hepatic clearance of the hormone

Question 10

What enzyme catalyzes the conversion of angiotensinogen to angiotensin I?

Answer 10

Renin

Question 11

What is the function of the renin-angiotensin system?
A

Answer 11

A: It regulates fluid and electrolyte balance and arterial blood pressure.

Question 12

Q: What factors affect renin secretion?

Answer 12

Macula densa, renal baroreceptor, and the sympathetic nervous system.

Question 13

How does the macula densa regulate renin release?

Answer 13

It signals changes in renin release, with an inverse relationship between NaCl concentration and renin release.

Question 14

What is the role of angiotensin II in blood pressure regulation?

Answer 14

It is a potent vasoconstrictor that increases blood pressure and promotes aldosterone release.

Question 15

What are the effects of angiotensin II on the kidney?

Answer 15

A: It causes renal vasoconstriction, increases sodium reabsorption, and inhibits renin release.

Question 16

Q: What are the primary intracellular messengers controlling renin release?

Answer 16

A: cAMP, cGMP, and intracellular Ca2+ concentration

Question 17

Name three drugs that stimulate renin releas

Answer 17

Vasodilators (hydralazine), β-adrenoceptor agonists, and phosphodiesterase inhibitors.

Question 18

Q: What drugs inhibit renin release?

Answer 18

A: Clonidine, propranolol, and other β-blockers.

Question 19

What is the function of ACE2?

Answer 19

: It converts angiotensin II to angiotensin 1-7, which acts as a vasodilator.

Question 20

What is the primary function of aldosterone?

Answer 20

A: It promotes sodium retention and potassium excretion in the kidney.

Question 21

How do ACE inhibitors lower blood pressure?

Answer 21

A: They block the conversion of angiotensin I to angiotensin II and inhibit bradykinin degradation.

Question 22

Q: What is the mechanism of angiotensin receptor blockers (ARBs)?

Answer 22

A: They block angiotensin II type 1 receptors to reduce vasoconstriction and aldosterone secretion.

Question 23

What are spironolactatw and epleeenone

Answer 23

Spironolactone and eplerenone are antagonists of aldosterone at the mineralocorticoid receptor, thereby preventing salt retention, myocardial hypertrophy, and hypokalemia.
• Spironolactone also has affinity for androgen and progesterone receptors, and is associated with endocrine-related adverse effects such as gynecomastia and dysmenorrhea.
• Aldosterone antagonists are indicated in patients with symptomatic HFrEF or HFrEF and recent myocardial infarction.

Question 24

What are natriuretic peptides, and what do they do?

Answer 24

A: They are hormones that promote natriuresis (salt excretion), diuresis, and vasodilation.

Question 25

What enzyme metabolizes natriuretic peptides?

Answer 25

Neutral endopeptidase.

Question 26

What is the function of neprilysin inhibitors

Answer 26

? A: They increase circulating vasoactive peptides by inhibiting neprilysin. It breaks down vasoactive peptides

Question 27

Why is ARB rather than ACE inhibitors combined with Neprilysin

Answer 27

To reduce incidence of angioedema

Question 28

Q: What is Sacubitril-Valsartan used for?

Answer 28

A: It treats heart failure by combining an ARB with neprilysin inhibition.

Question 29

What drugs block the endothelin system?

Answer 29

A: Bosentan, ambrisentan, and sitaxsentan.

Question 30

Where are some drugs that block the release of renin and how?

Answer 30

Clonidine- by causing a centrally mediated reduction in renal sympathetic nerve activity, and it may also exert a direct intrarenal action. • Propranolol and other B-blockers- by blocking the intrarenal and extrarenal B receptors involved in the neural control of renin release.

Question 31

What is the role of ACE inhibitors

Answer 31

ACE inhibitors not only block the conversion of ANG I to ANG Il but also • inhibit the degradation of bradykinin, substance P, and enkephalins. We can have adverse side effects like engioedema and cough These drugs are contraindicated in pregnancy because they cause fetal kidney damage.

Question 32

What is the kallikrein kinkn system

Answer 32

Factor XII -> prekalikrein-> Kallikrein-> 1) plasminogen to plasmin 2) bradykinin

Question 33

What is the Kim effect on the cardiovascular system

Answer 33

Kinins produce marked arteriolar dilation in several vascular beds, including the heart, skeletal muscle, kidney, liver, and intestine

Question 34

What is the kinkn effect on the endocrine and exocrine glands

Answer 34

Prekallikreins and kallikreins are present in several glands, including the pancreas, kidney, intestine, salivary glands, and sweat glands, and they can be released into the secretory fluids of these glands.

Question 35

Kinkn role in inflammation and pain

Answer 35

Bradykinin produces the four classic symptoms of inflammation-redness, local heat, swelling, and pain. Kinins are rapidly generated after tissue injury and play a pivotal role in the development and maintenance of these inflammatory processes. Kinins are potent pain-producing substances when applied to a blister base or injected intradermally. They elicit pain by stimulating nociceptive afferents in the skin and viscera.

Question 36

What 2 plasma kinase have been well characterised

Answer 36

Two plasma kininases have been well characterized. • Kininase I, synthesized in the liver. • Kininase Il is present in plasma and vascular endothelial cells throughout the body.

Question 37

What is the role of vasopressin

Answer 37

Vasopressin (AVP/ADH) helps regulate blood pressure in two ways: 1. Long-term regulation – It increases water reabsorption in the kidneys, helping maintain blood volume and pressure. 2. Short-term regulation – It acts as a vasoconstrictor, increasing total peripheral resistance and raising arterial pressure, even at low doses.

Question 38

What drug is used to treat diabetes inspindus

Answer 38

Desmopressin

Question 39

ET1

Answer 39

ET-1 is the predominant endothelin secreted by the vascular endothelium. It is also produced by neurons and astrocytes in the central nervous system and in endometrial, renal mesangial, Sertoli, breast epithelial, and other cells. VIV administration of ET-1 causes a rapid and transient decrease in arterial blood pressure followed by a sustained increase.

Question 40

ET2

Answer 40

ET-2 is produced predominantly in the kidneys and intestine; ET-3 is found in highest concentration in the brain but is also present in the gi tract, lungs, and kidneys. Endothelin-1 structure in humans • Endothelins are present in the blood but in low concentration;

Question 41

Systemic administration of endothelin receptor antagonists or endothelin-converting enzyme inhibitors causes what

Answer 41

• vasodilation and • decreases arterial pressure in humans and experimental animals.

Question 42

What is substance P

Answer 42

Belongs to the tachykinin family (along with neurokinin A & B). • Functions: Involved in pain perception and chemotherapy-induced nausea & vomiting. • Vascular effects: • Potent arteriolar vasodilator, causing hypotension. • Mediated by nitric oxide (NO) release from endothelium. • Conversely, causes venous, intestinal, and bronchial smooth muscle contraction. • Other effects: • Stimulates salivary gland secretion. • Causes diuresis and natriuresis in the kidneys.

Question 43

Vasoactive intestinal peptide

Answer 43

28-amino-acid peptide from the glucagon-secretin family. • Neurotransmitter in the central and peripheral nervous systems. • Cardiovascular effects: • Potent vasodilator (stronger than acetylcholine). • Coronary vasodilation. • Positive inotropic & chronotropic effects (enhances heart contraction & rate). • Regulates coronary blood flow, cardiac contraction, and heart rate.

Question 44

what are some vasoconstrictors

Answer 44

vasopressin angiotensin II Neuropeptride Y urotensin endothelials

Question 45

what are some vasodilators

Answer 45

bradykinin natriuitic peptides substance P neurotensin cGRP