Key result
Healthy Greyhounds show no difference in basal RAAS activation compared to non-Greyhounds.
Why the study?
Alterations in the renin-angiotensin-aldosterone system in Greyhounds may be associated with their unique hemodynamic and clinicopathologic differences compared to non-Greyhounds.
Are alterations in the RAAS in Greyhounds associated with hemodynamic and clinicopathologic differences observed in the breed?
Observational (n=40)
Are alterations in the RAAS in Greyhounds associated with hemodynamic and clinicopathologic differences observed in the breed?
Absolute Event Rate: 0.69% vs 0.65%
p-value: p=0.60
Basal RAAS activation does not differ between healthy Greyhounds and non-Greyhounds, but lower aldosterone in Greyhounds suggests an appropriate physiologic response to higher serum sodium and blood pressure.
Basal RAAS similarity does not support breed-specific targeting in healthy Greyhounds; leaves open aldosterone or alternative pathways for further study.
BACKGROUND: The renin-angiotensin-aldosterone system (RAAS) regulates blood pressure, electrolyte homeostasis, and renal function. Blood pressure, serum sodium concentrations, and urinary albumin excretion are higher in Greyhounds than other purebred and mixed-breed dogs. HYPOTHESIS: Alterations in the RAAS in Greyhounds are associated with hemodynamic and clinicopathologic differences observed in the breed. ANIMALS: Clinically healthy Greyhound and non-Greyhound dogs consecutively enrolled as blood donors (n = 20/group). METHODS: Prospective study. Standard chemical analysis was performed on serum and urine. Serum angiotensin-converting enzyme (ACE) activity was determined by fluorometric assay. All other RAAS hormones were determined by radioimmunoassay. Symmetric dimethylarginine (SDMA) was measured by immunoassay. Measurements were compared to blood pressure and urine albumin concentration. Data are presented as mean ± SD or median, range. RESULTS: Serum creatinine (1.5 ± 0.2 vs 1.0 ± 0.1 mg/dL, P < .001), sodium (149, 147-152 vs 148, 146-150 mEq/L, P = .017), and SDMA (16.1 ± 2.9 vs 12.2 ± 1.8 μg/dL, P < .001) were significantly higher in Greyhounds versus non-Greyhounds, respectively. Plasma renin activity (0.69, 0.10-1.93 vs 0.65, 0.27-2.93 ng/mL/h, P = .60) and ACE activity (4.5, 2.1-8.5 vs 4.6, 2.1-11.4 activity/mL; P = .77) were similar between groups and did not correlate with higher systolic pressures and albuminuria in Greyhounds. Plasma aldosterone concentration was significantly lower in Greyhounds versus non-Greyhounds (11, 11-52 vs 15, 11-56 pg/mL, respectively, P = .002). CONCLUSIONS AND CLINICAL IMPORTANCE: Basal RAAS activation did not differ between healthy Greyhounds and non-Greyhounds. Lower aldosterone concentration in Greyhounds is an appropriate physiologic response to higher serum sodium concentration and blood pressure, suggesting that angiotensin II effects in the renal tubule predominate over those of aldosterone.
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Martinez et al. (2017) conducted an observational in Clinically healthy dogs (n=40). Greyhound breed vs. Non-Greyhound dogs was evaluated on Plasma renin activity (ng/mL/h) (p=0.60). Basal RAAS activation did not differ between healthy Greyhounds and non-Greyhounds, with similar median plasma renin activity (0.69 vs 0.65 ng/mL/h; P=0.60).
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