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41 Cards in this Set

  • Front
  • Back
is arterial pressure lower or higher in infants?
How is renin released and activated?
It is released as pro-renin and is proteolytically processed
Renin antagonists like aliskiren can bind to the active site of renin
Where is renin released from?
The afferent arteriole of the kidney
What are the types of AT receptors?
Type 1 and 2 and only type 1's effect is known and this is the only receptor that angiotensin blockers affect
What are the primary roles of the RAA system?
To prevent hypotension and maintain renal perfusion
What do prostaglandins do to renin production? What does ANP do?
They increase it
ANP causes a decrease in renin production
What does 11 beta hydroxysteroid dehydrogenase do?
It is co-expressed with mineralcorticoid receptors
What does the angiotensin 2 receptor type 1 do exactly?
It is responsible for promoting aldosterone release and vasoconstriction
What percent of salt is reab. in the tubule?
What are the aldosterone sensitive nephron segments?
The CCTand ICT
What does aldosterone stimulate within the cel?
1. Na/K ATPase on the BL side
2. ENaC activity on the apical side
How does hyperaldosteronism look clinically?
Hypokalemia and Hypertensive
The ENaC channel is the product of three different components--mutation in any of these leads to what?
Liddle's Syndrome
Infants presenting with Hypotension and hypokalemia probably have what disorder?
Liddle Syndrome
A mutation in the ACE allele causing overproduction would cause what?
High BP
What is glucocorticoid remediable HTN?
Gene defect that allows a crossover of ACTH responsive promotor to aldosterone synthase = ALDOSTERONE OVERPRODUCTION

What is syndrome of apparent mineralcorticoid excess?
Gene defect in 11 beta-HSD that causes HTN because the enzyme doesn't readily cleave cortisol to cortisone
The built up cortisol can bind to mineralcorticoid receptors and cause HTN
Renal artery stenosis causes what?
Promotion of renin overproduction and RAAS facilitation
A patient presents with HTN and hypokalemia as well as a mass on one kidney..what is the diagnosis?
Aldosteronoma or Conn's Syndrome
What can overeating licorice cause?
Glycyrrhetic acid over-ingestion can lead to hypokalemia and hypertnesion due to 11-beta HSD inhibition
What does 11-Beta HSD do?
Converts cortisol to cortisone--there is far more cortisol in the body than aldosterone but both can bind mineralcorticoid receptors
If you convert cortisol to cortisone then it can't bind the mineralcorticoid receptors
Why do we put people with HTN on a low salt diet?
Because the RAAS system is relatively inactive at high salt levels...this means that it is not a critical determinant of BP
If you lower salt levels then RAAS is important and controlling it with an ACEi will lower BP
Lack of ETB receptors causes what?
Hypertension on a high salt diet
Lack of ETA receptors can cause what?
Where is ETA located and what are its affinities?
Located in vascular smooth muscle and has far more affinity for ET-1 than the other types
Where is ETB located and what are its affinities?
Located in the Collecting duct endothelium and has equal affinities for all ET's
How is ANP released?
Atrial stretch causes cleavage of Pro-ANP to active ANP with Corin which then binds to guanylyl cyclase receptors to convert GTP to cGMP which causes vasodilation and alters salt transport in the CD
How does ANP work?
It causes decrease in BP mediated by cGMP through...
1. Zona glomerulosa: DECREASE in release of aldosterone in response to angiotensin II and KCl
Vascular myocyte: Vasorelaxation
Endothelium:Increased vascular permeability
Glomerulus: INCREASE IN Glomerular filtration rate
Collecting tubule: DECREASE in Sodium reabsorption
Underproduction of ANP leads to what? Overproduction?
HTN due to gene knockout
If heterozygous then: will have circulating ANP but sensitive to high Na+
Overproduction = low BP
Increase in urinary sodium causes what?
Increase in urine cGMP
How is NO normally produced? How can that be screwed up?
Oxidation of L-arginine to NO
ADMA or Symmetric dimethyl ARG will bind NO synthase and inhibit NO production competitively
True/False: The end product of ANP and NO is the same.
TRUE--it is cGMP
What is the mechanism for NO production and action?
Arginine is brought into the endothelial cell and it binds the calmodulin and is converted to NO and citruline
NO then diffuses into the adjacent smooth muscle cell and increases cGMP production
Oral administration of NO syntthase inhibitors causes...
Increased BP
What can happen with regards to NO during sepsis?
Overproduction of NO synthase and fall in BP
Salt sensitive individuals do well with what?
thiazide diuretics!
True/False: There is no way to reverse increase in vascular stiffness that accompanies age.
FALSE--low salt diet can have an immediate effect and lower stiffness
High salt diets cause TGF-B levels to increase and this promotes vascular stiffness through matrix produection and smooth muscle hardening
How does TGF-B cause vascular hardening?
It downregulates Matrix Metalloproteinases
True/False: BP MUST be lowered to below normal in order to maintain health.
FALSE--just get it below 140/90
What is essential HTN?
Idiopathic HTN that is established between 30 and 50 years
What labs should be evaluated in order to assess an adult HTN patient?
Med history
Family history of kidney disease
Two BP readings prior to starting treatment
Thigh cuff pressure once on a young patient
Serum K+