Systemic and regional hemodynamic effects of 1, 25-dihydroxyvitamin d₃ administration

Objective: To evaluate the cardiovascular effects of 1, 25-dihydroxyvitamin D₃ (1, 25-D). Design: Recent studies suggest that Ca-regulating hormones may contribute to the genesis of hypertension. We determined systemic and regional hemodynamics 24 h after administration of 1, 25-D or vehicle to normal conscious Sprague-Dawley rats. In addition, to dissociate the vascular effects of 1, 25-D from changes in serum ionized Ca²⁺, 1, 25-D and vehicle were administered to rats maintained for 3 days on a low-Ca diet. To evaluate the effect of the slight rise in serum ionized Ca²⁺ with 1, 25-D administration, we infused CaCI or vehicle over 1 h into normal rats to raise the serum Ca²⁺ to near that of rats treated with 1, 25-D. Methods: The radioactive microsphere technique was used. Results: Systemic hemodynamics (blood pressure, heart rate, cardiac output, total peripheral resistance and stroke volume) did not differ between the two groups receiving a normal-Ca diet. In these rats 1, 25-D significantly decreased renal blood flow (RBF), increased renal vascular resistance (RVR) and slightly increased serum ionized Ca²⁺. Similarly, in rats receiving a low-Ca diet, 1, 25-D administration decreased renal blood flow, increased renal vascular resistance and caused only a minimal increase in serum ionized Ca²⁺ . A low-Ca diet also increased heart rate, cardiac blood flow and renal blood flow. Although CaCI infusion raised serum ionized Ca²⁺, blood pressure, renal blood flow and renal vascular resistance did not change significantly.Conclusion: 1, 25-D may constrict the renal vasculature directly or indirectly by enhancing the vascular sensitivity to circulating vasoconstrictors.