Hypertension Flashcards
What are the 2 mechanisms of getting hypertension?
Excessive vasoconstrictoin
Increased extracellular fluid volume (ECFV)
What is the affect of changing amount of NaCl in diet?
Low NaCl –> activation of sympathetic n system, renin/angiotensin system, and ADH
Deactivation of atrial natriuretic peptide
- net effect = sodium retention
High NaCl –> decrease in SNS, Renin/Angio systsem and ADH
Activation of ANP
net effect = sodium excretion
What contributes to arterial blood pressure?
Arterial pressure = CO * Vascular resistance
CO = myocardial work x cardiac return
Vascular resistance = vascular tone = regulated by most of the same mechanisms that regulate ECFV
How do we know that people on a low salt diet more “dependent” on angiotensin II?
Both maintain a similar pressure before but when we give them ACEI’s, their BP drops way more than those on a high-salt diet
To maintain the same pressure, their body uses more angiotensin II so blocking it has a larger effect
How do we know that vasopressin is critical to maintain normal pressure during extracellular volume depletion?
Vasopressin blockers have no effect in normal mice
If you withhold food and water, vasopressin levels are much higher than normal, so when you give these mice vasopressin blockers there’s a huge effect on arterial pressure
What is the effect of NE, Angio II, ADH, ANF, and NO on the vasculature?
NE, Ang II, = vasoconstrictors
ADH, ANF, NO = vasodilators
Hypertension due to excessive vasoconstriction v. due to increased ECFV
Excessive vasoconstriction:
Pheochromocytoma
Acute renal artery stenosis
Increased ECFV:
Chronic renal a. stenosis
High salt diet
Impaired global kidney function
Excessive aldosterone
Hyperactive Na+ channel in collecting duct
Pheochromocytoma
Tumor of adrenal medulla –> high NE
Surgical removal normalizes BP
Acute renal artery stenosis
Acute renal artery stenosis –> kidney perceives low arterial presure –> generation of excess renin-angiotensin II –> hypertension
Angiotensin II –> systemic vasoconstriction =major acute effect
in the long run, ang II also constricts the efferent & leads to aldosterone release
Chronic renal artery stenosis
Ang II goes up –> lots of salt retention –> expansion of ECFV
Can be so extensive that it counteracts that angiotensin II which means that you might have no idea that the initial event was even an increase in renin bc ang II goes down in second stage of the dz after the volume goes up
Impaired global kidney function
i.e. renal failure –> very low GFR
Dialysis acutely leads to huge drop in weight which shows that this type of htn is due to ECFV increase
Hyperactive Na+ channel in collecting duct
This is where aldosterone acts
Several mutations result in constant activation of the channel –> reabsorption of sodium, volume expansion
Excessive aldosterone
Tumor of the adrenal cortex; equivalent to pheochromocytoma but it’s in the adrenal cortex, not the medulla
Lots of aldosterone –> increase in Na reabsorption –> ECFV expansion
High salt diet
Salt intake alone is capable of inducing hypertension
Why deso high ECFV cause hypertension?
Mechanism is unclear
Acutely, CO increases, after increase in SVR due to vasoconstriction probably
Most patients with htn have no measureable anomaly
