Altered expression of V1a receptors mRNA in the brain and kidney after myocardial infarction and chronic stress.

Vasopressin released during myocardial infarction and in response to stress regulates blood pressure through multiple actions exerted in the brain, cardiovascular system and kidney. The aim of the present study was to determine whether myocardial infarction influences expression of vasopressin V1a receptor (V1aR) mRNA and protein in the brain and kidney and whether stress has an impact on expression of these parameters during the post-infarct state. Male, adult Sprague Dawley rats were subjected to myocardial infarction or sham surgery. Seven days later some rats were exposed to mild stress for 4weeks whereas other stayed at rest. Tissue fragments were harvested from four groups of rats (control, infarct, stress, infarct+stress). Expression of V1aR mRNA (Real time PCR) was determined in the preoptic, diencephalic, mesencephalopontine and medullary regions of the brain and in the renal cortex and medulla. Protein V1aR expression (Western blotting) was determined in the brain mesencephalopontine region and in the kidney medulla. In the preoptic, diencephalic, and mesencephalopontine regions, V1aR mRNA expression was significantly lower in the infarcted rats than in the sham-operated unstressed controls. The infarcted rats manifested also lower expression of V1aR protein in the mesencephalopontine region than the other groups. The stressed group demonstrated significantly higher V1aR mRNA expression in the brain medulla and in the renal cortex and renal medulla than the control group. In all brain regions and in the kidney, V1aR mRNA expression was significantly higher in the stressed rats than in the infarcted rats. The stressed rats showed also higher expression of V1aR protein in the renal medulla than the other groups. It is concluded that myocardial infarction and chronic stress cause significant but differential changes in the regulation of V1a receptors expression in the brain and the kidney.