Which two hemodynamic properties affect htn?
HTN = ^Cardiac output x ^Peripheral Resistance
CO: [na] (SV) and catecholamines (contractility)
PR: raa and catecholamines
- *kidneys are involved in both [na] and raa/pvr
- *most pathology is caused by changes in vascular resistance!
How is SVR regulated?
Hormonal:
- angio II
- norepi > renin secretion
Local factors: autoregulation of kidneys
- endothelin [constriction]
- EDRF: vasodilation
SNS: tonic vasocontriction due to adrenergic activation
- increase na retention
- increase in cardiac ionotrophy
What are the three functions of angio II?
- release aldo > results in increase Na reabsorption in CD*
- vasoconstriction
- increase Na retention in PCT: increase BP*
*main issues that lead to HTN
Describe salt sensitivity
some pts have marked increases in BP with increased salt intake.
curve on Na:arterial P, shifts to the right and becomes less narrow = larger increases in BP
normal pts: have ways to deal with increased [na] in the body leading to normalization of BP
Describe pressure naturesis
- increase in pressure leads to increased urine output of the kidneys
- this innate property of the kidney may be suppressed in patients with HTN and lead to dysregulation of BP**
- *instigator of HTN
- *guyton’s hypothesis
Describe primary HTN
main cause of htn with no known etiology: 90-95% of all HTN
often idiopathic: 90%
*monogenic cause does exist but is extremely rare (linked to Na sensitive pts)
Describe secondary HTN
htn can be linked to a specific cause
common causes:
- kidney disease **most common
- renal artery stenosis
- hyperaldosteronism
- pheochromcytoma
- Cushings
- MR producing tumor
List the “volume related” causes of htn
renal: instigator!
- renal failure
- acute glomerulonephritis
nonrenal:
- hyperaldosteronism
- MR tumor
- Cushing tumor: excess cortisol increases epi release and vasoconstriction
List the “vasoconstriction related” causes of htn
- phenochromocytoma: excess release of catecholamines
- renal artery stenosis
- hypercalcemia: causes contraction of the tubule
Name the three types of renal artery stenosis (RAS)
- bilateral stenosis
- solitary kidney
- unilateral/classic
What is most common cause of RAS
atherosclerotic disease
Uncontrollable htn with meds and lifesytle change + kidney failure + pulm edema are symptoms of?
Renal artery stenosis
Describe unilateral/classic stenosis
stenotic kidney: decreased pressure due to decrease RBF > leads to activation of RAAS
> increased vasoconstriction
>Na reabs = increased BP
normal kidney: senses increase in BP from stenotic kidney
>pressure naturesis
>increase Na and urine excretion
> normalization of fluid status but still htn (due to RAAS w/o meds)
Treat: ARB or ACEi
Describe bilateral/classic stenosis AND bilateral stenosis
stenotic kidney: decreased pressure due to decrease RBF > leads to activation of RAAS
> increased vasoconstriction
>Na reabs = increased BP
BUT
no normal kidney to perform pressure naturesis
>volume overload
treat:
- ACEi/ARB + diuretics (solitary)
- transplant (bilateral)
Treatment of htn
- diuretics to decrease volume overload
- lower bP: ARB and ACEi
- perserve renal autoregulation
What are some instances in which htn damages the kidney?
malignant htn:
- fibrin deposits
- normal kidney size
- associated with neuroretinopathy and papilledema
essential htn: benign nephrosclerosis/hyaline arterioloscl
- contracted kidney and decreases size
- ischemic atrophy
