ABSTRACT
The aim of the present study was to investigate whether protein kinase C (PKC) was involved in the effect of mesenteric lymph duct ligation or mesenteric lymph drainage on vascular calcium sensitivity in hemorrhagic shock rats. Male Wistar rats were randomly divided into Sham, Shock (hemorrhagic shock), Shock+Ligation (mesenteric lymph duct ligation plus shock) and Shock+Drainage (mesenteric lymph drainage plus shock) groups. After being in shock (hypotension 40 mmHg) for 3 h, the tissue of superior mesenteric artery (SMA) was taken out for detecting the PKC expression and phospho-PKC (p-PKC) activity, and the vascular rings of SMA were prepared and used to measure the response to gradient calcium concentration for assaying the calcium sensitivity, the parameters of which including tension, maximum tension (E(max)) and negative logarithm of EC(50), called the pD(2). Other vascular rings from Shock+Ligation and Shock+Drainage groups were incubated with PKC regulator PMA or Staurosporine before the measurement of calcium sensitivity. The results showed that, PKC expression, p-PKC activity and calcium sensitivity of SMA in Shock group was significantly lower than that of Sham group, whereas the above-mentioned indexes were significantly elevated in Shock+Ligation and Shock+Drainage groups compared with those in Shock group. PKC agonist PMA enhanced the contractile activity of vascular rings to gradient calcium ions, and increased E(max) of SMA in Shock+Ligation and Shock+Drainage groups. On the contrary, PKC inhibitor Staurosporine significantly decreased the response to gradient calcium ions and E(max) of SMA in Shock+Ligation and Shock+Drainage groups. These results suggest that PKC plays a role in the improvement of vascular calcium sensitivity by blockade of mesenteric lymph return in hemorrhagic shock rats.
Subject(s)
Animals , Male , Rats , Calcium , Pharmacology , Drainage , Ligation , Lymph , Physiology , Lymphatic Vessels , Physiology , Mesenteric Artery, Superior , Physiology , Mesentery , Muscle, Smooth, Vascular , Metabolism , Protein Kinase C , Metabolism , Physiology , Rats, Wistar , Shock, Hemorrhagic , Vasoconstriction , PhysiologyABSTRACT
<p><b>OBJECTIVE</b>To explore the impact of prenatal exposure to lipopolysaccharide on renin-angiotensin system of offspring rats.</p><p><b>METHODS</b>Six pregnant SD rats were randomly divided into 2 groups. The rats in the lipopolysaccharide (LPS) group were treated with LPS 0.79 mg/kg (i.p.) on the 8th, 10th and 12th day of gestation, and rats in the control group were treated with saline at the same time points. The blood pressure of offspring rats was measured by the tail cuff method. Protein expression of Angiotensin II (AngII) in thoracic aorta vessel was determined by immunohistochemistry. Protein expressions of AngII type 1 and type 2 receptor in thoracic aorta vessel were detected by Western blot.</p><p><b>RESULTS</b>Blood pressure of 12-week-old offspring rats of LPS group was significantly higher than that of 12-week-old offspring rats of control group (P < 0.01). The protein expression of AngII and AngII type 1 receptor in thoracic aorta vessel were significantly higher while protein expression of AngII type 2 receptor was lower in 15-week-old offspring rats of LPS group than in control group, resulting in a significant increase in the ratio of AngII type 1 receptor/AngII type 2 receptor in the aorta at 15-week-old of offspring rats than in 15-week-old offspring rats of control group (P < 0.01).</p><p><b>CONCLUSION</b>Prenatal lipopolysaccharide exposure results vascular renin-angiotensin system dysfunction, which may play an important role on the pathogenesis of hypertension development in offspring rats.</p>