07: Blood Pressure Regulation Flashcards
Outline the sequelae of hypertension.
What is blood pressure and what are its factors?
Blood pressure is the outward pressure of blood against vessel walls.
Product of blood flow from the heart and inward resistance of blood vessel walls.
How do you calculate blood pressure?
BP = CO x TPR
CO = SV x HR
What factors regulate cardiac output?
- Filling pressure (volume)
- Sodium retention
- Heart rate
- Sympathetic = ↑
- Parasympathetic (vagus) = ↓
- Force of contraction
- Sympathetic = ↑
What factors regulate vascular resistance?
- Vasoconstriction
- Norepinephrine ↑
- Angiotensin ↑
- Nitric oxide ↓
- Structural changes
- Vascular remodeling/hypertrophy
What two major systems regulate blood pressure, and how?
-
Autonomic Nervous System (ANS)
- Via brain, sympathetic nerves, adrenal glands
- ↑CO & TPR
- ↑renin release from kidneys (promotes angiotensin –> ↑BP)
- Feedback loop via baroreceptors
-
Renin-Angiotensin-Aldosterone System (RAAS)
- Via kidney, blood stream, adrenal glands
- ↑Na+ and H2O retention and TPR
- Feedback loop in kidneys
Outline the baroreceptor reflex to increased arterial pressure.
How are catecholamines synthesized, where are they released from, and what is their role in blood pressure regulation?
- Dopa (in sympathetic nerve terminal) –> dopamine –> **norepinephrine **(released by sympathetic nerves) –> epinephrine (released by adrenal glands)
- ↑sympathetic response (vasoconstriction, ↑HR)
Describe the synthesis of angiotensin II.
- **Prorenin **(from juxtaglomerular cells) converted into renin and secreted from kidney into blood.
- Renin converts angiotensinogen (secreted by liver) into angiotensin I.
- Angiotensin-converting enzyme (ACE) (found in lungs, kidney) converts angiotensin I into angiotensin II.
Describe the role of angiotensin II
-
Adrenal cortex:
- Stimulate synthesis/secretion of aldosterone
- Aldosterone acts on **renal distal tubule **and collecting duct
- ↑Na+reabsorption into blood (↑ECF volume and blood volume –> ↑CO)
- Arterioles: vasoconstriction (↑TPR)
- Kidney: stimulates Na+-H+ exchange in renal proximal tubule and ↑Na+ & HCO3- reabsorption (↑CO)
-
Hypothalamus:
- ↑Thirst, water intake
- Stimulates antidiuretic hormone (ADH) (increase water reabsorption in collecting ducts –> ↑CO; causes vasoconstriction –> ↑TPR)
-
Heart:
- ↑contractility, ventricular hypertrophy
NB: To fulfill actions, must acto on AT1 subtype receptors.
What stimulates renin secretion?
- Decreased renal perfusion (sensed by mechanoreceptors)
- Decreased sodium
- Sympathetic activation
Outline the RAAS response to a decrease in arterial pressure.
Other than the ANS and RAAS pathways, what mechanisms regulate blood pressure?
- Chemoreceptors in carotid and aortic bodies
- Sense ↓ PO2, ↑CO2
- Sense ↓pH
- Affect sympathetic vascoconstrictor centers
- Central (medullary) chemoreceptors
- Sense changes in PCO2 or pH
- Affect outflow of medullary brain centers
- Antidiuretic hormone
- Stimulated by angiotensin II, increases in serum osmolarity
- From posterior lobe of pituitary gland
- **V1 receptors **(vascular smooth muscle)
- Vasoconstriction (↑TPR)
-
V2 receptors (renal collecting ducts)
- ↑water reabsorption
- Cardiopulmonary (low-pressure) baroreceptors
- Respondd to increased pressure in veins, atria, and pulmonary artery
- ↑blood volume –> ↑venous/atrial pressure –> baroreceptor activation
- ↑atrial natriuretic peptide (ANP) secretion –> relax smooth muscle –> vasodilation and ↓TPR; vasodilation of kidney –> ↑Na & H2O excretion
- ↓ADHB
- Renal vasodilation (via inhibition of sympathetic vasoconstriction in renal arterioles)
- Increased heart rate
- Info from atrial receptors –> vagus nerve –> nucleus tractus solitarius
- Bainbridge reflex: ↑CO –> increased renal perfusion –> ↑Na+ & H2O excretion
What pathologies cause hypertension?
-
CNS
- ↑basal sympathetic tone
- Abnormal stress response
- Abnormal response to signals from baroreceptors
-
Pressure/volume receptors
- Desensitization
-
Kidney
- RAA dysfunction
- Ion channel defects
-
Adrenal
- Catecholamine leak or malregulation
-
Blood vessel
-
Functional
- ↑Endothelin production (vasoconstrictors)
- ↓NO secretion
- Channel defects
- Hyperresponsiveness to catecholamines
-
Structural
- Exaggerated medial hypertrophy
-
Functional