Cardio - CHF, RAAS Flashcards
In the short-term, RAAS is _____. Why?
great; BP is maintained in the face of low CO
In the long-term, RAAS is _____. Why?
Terrible;
Cardiac fibrosis, renal damage, cytokine activation
What are the RAAS activation events?
- Juxtaglomerular apparatus releases renin
- Renin converts angiotensinogen to angiotensin I
- Angiotensin converting enzyme (ACE) converts ATI to ATII in the lungs
What do the jusxtaglomerular cells detect?
Low BP, renal blood flow, or sodium
High SNS tone
Where is angiotensinogen produced?
liver
Where is ACE produced?
endothelial cells in the lungs
What can you do if there is low BP?
Increase CO or VR (more volume or more vasoconstriction)
What are the actions of ATII?
- Increase volume
- Increase vascular resistance
- Negative effects on the heart
Where does ATII act?
PCT to cause Na and water retention
What does ATII stimulate?
Aldosterone release from the adrenals and ADH release from the posterior pituitary
Where does aldosterone act?
DCT to retain Na and water (K loss)
What does ADH do?
Inserts aquaporins into the DCT to allow for free water retention (without Na)
What effect does ADH have on thirst?
Increases it by stimulating the thirst center in the hypothalamus
What receptors does ATII bind and where?
AT receptors on the vessels leading to vasoconstriction
ATII binds to the _____ arterial in the glomerulus, causing ____ and increasing intraglomerular pressure to maintin the _____.
efferent, vasconstriction, GFR
