The objective of the paper is to determine the influence of IGF-1
deletion on renal sympathetic nerve activity (RSNA), left
ventricular dysfunction, and renal function in deoxycorticosterone
acetate (DOCA)-salt hypertensive mice. The DOCA-salt
hypertensive mice models were constructed and the experiment
was classified into WT (Wild-type mice) +sham, LID (Liverspecific IGF-1 deficient mice) + sham, WT + DOCA, and LID +
DOCA groups. Enzyme-linked immunosorbent assay (ELISA) was
used to detect the serum IGF-1 levels in mice. The plasma
norepinephrine (NE), urine protein, urea nitrogen and creatinine,
as well as RSNA were measured. Echocardiography was
performed to assess left ventricular dysfunction, and HE staining
to observe the pathological changes in renal tissue of mice.
DOCA-salt induction time-dependently increased the systolic
blood pressure (SBP) of mice, especially in DOCA-salt LID mice.
Besides, the serum IGF-1 levels in WT mice were decreased after
DOCA-salt induction. In addition, the plasma NE concentration
and NE spillover, urinary protein, urea nitrogen, creatinine and
RSNA were remarkably elevated with severe left ventricular
dysfunction, but the creatinine clearance was reduced
in DOCA-salt mice, and these similar changes were obvious in
DOCA-salt mice with IGF-1 deletion. Moreover, the DOCA-salt
mice had tubular ectasia, glomerular fibrosis, interstitial cell
infiltration, and increased arterial wall thickness, and the
DOCA-salt LID mice were more serious in those aspects.
Deletion of IGF-1 may lead to enhanced RSNA in DOCA-salt
hypertensive mice, thereby further aggravating left ventricular
dysfunction and renal damage.
The purpose of the present study was to define the indirect central effect of hydrogen sulfide (H2S) on baroreflex control of sympathetic outflow. Perfusing the isolated carotid sinus with sodium hydrosulfide (NaHS), a H2S donor, the effect of H2S was measured by recording changes of renal sympathetic nerve activity (RSNA) in anesthetized male rats. Perfusion of isolated carotid sinus with NaHS (25, 50, 100 μmol/l) dose and timedependently inhibited sympathetic outflow. Preconditioning of glibenclamide (20 μmol/l), a ATP-sensitive K+ channels (KATP) blocker, the above effect of NaHS was removed. With 1, 4-dihydro-2, 6-dimethyl-5-nitro-4-(2-[trifluoromethyl] phenyl) pyridine-3-carboxylic acid methyl ester (Bay K8644, 500 nmol/l) pretreatment, which is an agonist of L-calcium channels, the effect of NaHS was eliminated. Perfusion of cystathionine γ-lyase (CSE) inhibitor, DL-propargylglycine (PPG, 200 μmol/l), increased sympathetic outflow. The results show that exogenous H2S in the carotid sinus inhibits sympathetic outflow. The effect of H2S is attributed to opening KATP channels and closing the L-calcium channels., Qi Guo, Yuming Wu, Hongmei Xue, Lin Xiao, Shneg Jin, Ru Wang., and Obsahuje bibliografii