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Plasma Renin Activity and Aldosterone Concentrations in Hypertensive Cats…

- - - - other study showed that only approximately 20% of cats diagnosed with systemic hypertension are nonazotemic and do not have an identifiable cause for their hypertension. Cats were said to have ‘mild CKD’. This means that hypertension is more often attributed to renal failure.
    - - often considered "the link renal disease, sodium retention, volume expansion, PVR and systemic hypertension"
      - Tissue RAAS Vs Systemic RAAS:
        The demonstration of local angiotensin II (Ang II) synthesis in numerous tissues and organs has led to the concept of local or tissue-based RAASs that are independent of but can interact with the traditional circulating RAAS [1]. These local RAASs appear to act in a paracrine/autocrine manner to regulate organ function and are involved in pathologic events associated with end-organ damage. The kidney contains all the elements of the RAAS, and intrarenal formation of Ang II independent of the circulating RAAS
  - - - causes
        
        "Low renin levels are seen in essential hypertension as there is a higher perfusion pressure at the juxta glomerular cells which suppresses renin release." (internet)
        
        Decrease in PRA may be the result of a combination of decreased renal mass, appropriate response to increased blood pressure or could be the consequence of age
  - - - " not all of cats with hyperaldrenocorticism will have
        systemic hypertension" so aldosterone PAC not the only factor in hypertension
      - A recent study suggests that bilateral adrenocortical hyperplasia is an almost ubiquitous finding in cats >9 years (97%), but there was no significant difference in histopathologic grading between hypertensive (n = 37) and normotensive cats (n = 30), supporting that adrenocortical hyperplasia is unlikely to be a primary factor in feline hypertension
      - aldosterone is under the influence of many factors
        
        aldosterone production apart from angiotensin II
        
        including extracellular potassium concentration,
        
        adrenocorticotropic hormone, adrenomedullin, atrial
        
        natriuretic peptide, dopamine, endogenous digitalis-like
        
        factors (eg, ouabain) and endothelin-1, but the effect
        
        these play in regulating aldosterone production in the
        
        cat has not been investigated
    - - This observation may reflect a relative increase in PAC
      - This study showed no association to be identified between plasma potassium concentration and
        PAC.
      - failure of this study to find a link between systemic hypertension and hypokalemia may be due to sample size.
- - - - So they think that increase in plasma renin--> increase in aldosterone
  - - - showed increased PAC but variable renin activity.
      - limitations:
        
        limited by small group sizes
        
        prior introduction of low sodium renal diets
        
        lack of appropriate age-matched control groups
      - have shown low potassium= hypertension
  - - - WHY??
        
        autonomous aldosterone
        production ?
        
        do cat represents a potential model for low-renin hypertension identified in hypertensive as seen in black humans?