Upregulation of type 1 IP 3 receptors in mesenteric arteries of hypertensive rats

Hypertension is associated with profound alterations of calcium (Ca 2+ ) homeostasis in vascular smooth muscle cells (VSMCs). The upregulation of Ca 2+ influx channels including the long‐lasting (L‐type) Ca 2+ channel and transient receptor potential (TRP) channels suggests their contribution to altered Ca 2+ signaling and increased vascular tone. The inositol 1,4,5‐trisphosphate receptor (IP 3 R), a Ca 2+ release channel located on the sarcoplasmic reticulum (SR), also mediates agonist‐ induced contraction and may couple to Ca 2+ influx channels to synchronize vasoconstrictor responses. We investigated whether expression of the IP 3 R1 is altered in VSMCs in rat models of hypertension. Western blots revealed that the IP 3 R1 protein was upregulated in mesenteric arteries of spontaneously hypertensive rats (SHR) and angiotensin II ‐induced hypertensive rats compared to arteries from age‐matched normotensive rats. We also observed increased IP 3 R1 transcript in the arteries of SHR. These findings add to emerging evidence that Ca 2+ ‐permeable ion channels that mediate rises in cytosolic Ca 2+ are coordinately upregulated in VSMCs during hypertension. Additional studies are designed to identify the mechanisms that dysregulate the expression of vascular Ca 2+ handling proteins during hypertension. Supported by Grant NPRP 08‐392‐3‐087 from the Qatar National Research Foundation.