The renin-angiotensin system plays an important role in the regulation of blood pressure and in body fluid homeostasis. There is increasing evidence for generation of endogenous angiotensin II in many organs and for its role in paracrine functions. Studies were designed to investigate whether hemorrhage produces rapid changes in the gene expression of angiotensinogen in peripheral and brain tissues. Wistar rats received saline drinking water for 7 days, were bled at a rate of $3\;ml\;kg^{-1}\;min^{-1}$ for 7 min, and then decapitated 0, 2, 4, 8, or 24 hr after hemorrhage. Hemorrhage produced a produced hypotension with tachycardia at $2{\pm}8\;hr$, but blood pressure and heart rate had not fully recovered to the basal level at 24 hr. Plasma renin concentration was significantly increased at 2, 4, and 8 hr (maximum sixfold increase at 4 hr) and had returned to the basal level at 24 hr. Renal renin content was significantly increased only at 4 hr after hemorrhage. Angiotensinogen mRNA in both the kidney and liver were stimulated at 2 to 8 hrs, but recovered to the basal level at 24 hr. On the other hand, angiotensinogen mRNA levels il the hypothalamus and brainstem were continuously increased from 2 to 24 hrs. The present study demonstrates the presence of angiotensinogen mRNA in both hepatic and extrahepatic tissues, and more importantly, their up-regulation after hemorrhage. These results suggest that the angiotensinogen-generating systems in the liver, kideny and brain are, at least in part, under independent control and play a local physiological role.
The ticks feed large amount of blood from their hosts and transmit pathogens to the victims. The salivary gland plays an important role in the blood feeding. When the female ticks are near engorgement, the salivary gland gradually loses its functions and begins to rapidly degenerate. In this study, data-independent acquisition quantitative proteomics was used to study changes in the phosphorylation modification of proteins during salivary gland degeneration in Haemaphysalis longicornis. In this quantitative study, 400 phosphorylated proteins and 850 phosphorylation modification sites were identified. Trough RNA interference experiments, we found that among the proteins with changes in phosphorylation, apoptosis-promoting Hippo protein played a role in salivary gland degeneration.
Jun, Jae-Yeoul;Yeum, Cheol-Ho;Goo, Yong-Sook;Kim, Jun
The Korean Journal of Physiology
/
v.25
no.2
/
pp.201-209
/
1991
The rostral ventrolateral medulla (RVLM) has been established recently as a sympathoexcitatory area. The present study was conducted to investigate whether the somatosympathetic pressor and/or depressor responses are mediated through RVLM in cats anesthetized with ${\alpha}-chloralose$. An occipital craniectomy was performed and ventrolateral medulla were stimulated either electrically or chemically to evoke changes in arterial blood pressure. And then the effect of lesions in the ventrolateral medulla on the changes in blood pressure elicited by the peripheral nerve stimulation was observed. Followings are the results obtained: 1) Pressor areas were found in the ventrolateral medulla, lateral reticular nucleus and rostral dorsal area. 2) Depressor areas were found mainly in the ventrolateral medulla rostral to the pressor areas. 3) Some areas showed biphasic responses: a depressor response to lower frequency and a pressor response to higher frequency stimulation. 4) After electrical lesion in pressor area in RVLM, the somatosympathetic pressor response was abolished or depressed markedly. The somatosympathetic depressor response, however, remained after the lesion. 5) Electrical lesion in the depressor area abolished somatosympathetic depressor response. From the above results it is concluded that somatosympathetic pressor response is mediated through RVLM, while somatosympathetic depressor response is not mediated through RVLM.
This study was carried out to investigate relationships between maximal running time (MRT) and glycogen supercompensation in fast twitch white fibers (white vastus, WV), fast twitch red fibers (red vastus, RV) and slow twitch red fibers (soleus muscle, SM) of endurance-trained rats. Male rats of a Sprague-Dawley strain were divided into the trained groups and untrained groups. Untrained groups were acquired to run on the treadmill 10 minutes for 3 days and remained rest and maintained with mixed diet for 4 weeks. For last 10 days of resting period, the untrained rats were divided into 3 groups i.e. mixed diet (untrained control), high and low carbohydrate (CHO) diet groups. And each group was subdivided into 2 groups, one group was tested for the MRT and the other was sacrificed to measure the blood glucose, blood lactate, glycogen contents of liver and muscles. The experimental groups were trained on treadmill by a modified method of Constable et al. (1984) maintained with mixed diet for 4 weeks. After measurement of MRT of this group, they were also divided into high and low CHO groups and fed with these diet for 2 days and MRT of each group was measured again to see the effect of high or low CHO feeding on the MRT. Each group was maintained with the same diet for next 2 days during which some of the rats were sacrificed at given time intervals for the measurements of blood glucose and lactate, liver and the muscles glycogen. The results were summarized as follows; 1) In the untrained group, there were no significant differences between subgroups in MRT, glycogen conent of SM, RV and WV. But blood glucose concentration and glycogen content of liver of low CHO group were significantly lower than those of mixed diet group. 2) The MRT and glycogen content of SM, RV and WV of trained mixed diet group were significantly increased compared to those of untrained mixed diet group, but there was no significant difference in glycogen content of liver. 3) MRT of trained mixed, high CHO and low CHO groups were $137{\pm}9.8,\;176{\pm}9.8\;and\;129{\pm}7.3\;min$ respectively with the significant difference between them. 4) There were no differences in blood lactate concentrations between the trained high and low CHO groups immediately after maximal running and during recovery period. 5) Glycogen contents in RV and SM of trained high CHO group were significantly increased, and glycogen contents in RV, WV and liver of trained low CHO group were significantly decreased compared to those of trained mixed diet group. 6) Immediately after maximal running, the blood glucose concentrations of trained high CHO and low CHO groups were $73{\pm}4.0\;and\;67{\pm}6.9mg%$ respecitively. The blood glucose of the trained high CHO group was fully recovered within one hour by feeding. But blood glucose concentration of low CHO group was slowly recovered up to $114{\pm}4.1mg%$ after two hours of feeding and maintained. Those values were still significantly lower than that of trained mixed diet group. The synthetic rates of glycogen in liver and muscles during the recovery period followed the similar time course of the blood glucose recoveries in each group. These results suggest that an increase in MRT of trained high CHO group was attributed to the glycogen supercompensation in slow twitch muscle fibers. And a decrease in MRT of trained low CHO may be due to decreased glycogen contents of liver and muscles. The results also suggest that glycogen supercompensation was more evident in slow twitch red fibers of endurance-trained rats and blood glucose is one of the limiting factors of glycogen synthesis.
To investigate whether the cervical sympathetics contains specific secretory fibers for the salivary glands, reflex salivation was evoked and the role of the sympathetics or the reflex was examined in ketamine-anesthetized cat. Stimulation of the central end of the glossopharyngeal nerve produced a copious secretion from the submaxillary gland and the response was not affected by the section of the cervical sympathetics or by the administration of phenoxybenzamine, whereas the response was abolished by severing the chorda tympani or by the administration of atropine. The salivary response was always associated with an increase in glandular blood flow. Both salivary and blood flow responses were decreased markedly by the superimposed stimulation of the cervical sympathetics or by the administration of norepinephrine. The decreased submaxillary blood flow always preceded the decrease in salivary flow on stimulation of the cervical sympathetics and the decreased blood flow recovered prior to the salivary flow upon cessation of the sympathetic stimulation. The inhibitory effects of the sympathetics and norepinephrine were completely abolished by the pretreatment with phenoxybenzamine. These results indicate that the glossopharyngeal nerve is one of the afferent limbs of the submaxillary salivary reflex and the chorda tympani is the only efferent limb of the reflex pathway. Thus, it is suggested that the cervical sympathetics does not contain the specific secretory fibers for the gland, but plays a role in inhibiting the reflex secretion by decreasing the blood flow to the gland.
In order to determine the extent of the placental transfer of Lithium ion, pregnant rabbits at $27{\sim}29$ days of gestation, which has hemochorial placenta similar to the human placenta, received 2 mM/Kg of $Li^+$ in the form of LiCl intravenously. Maternal arterial blood, placental sinus blood, fetal blood, amniotic fluid and maternal urine were drawn two hours after the single dose of LiCl. Concentrations of $Li^+$, $Na^+$, $K^+$ and osmolarity were measured in plasma of collected bloods, amniotic fluid and urine. Followings are the results obtained. 1) Evident level of $Li^+$ was detected in fetal blood, although fetal plasma concentration of $Li^+$ found to be almost one third of maternal plasma. 2) Plasma concentration of $Li^+$ in placental sinus blood was higher than that in fetal plasma but lower than that in maternal plasma. It means that downward concentration gradient of $Li^+$ from mother to fetus was still remarkable two hours after the injection. 3) Significant level of $Li^+$ was also detected in amniotic fluid. It seemed likely that $Li^+$, at least in part, excreted by the fetal urinary tract. 4) There were no differences in $Na^+$ and osmolar concentration between fetal and maternal blood. 5) From above results, it was concluded that $Li^+$ may transfer across the placenta but limited passage capacity through placental barrier for $Li^+$ is significant, beacause net transfer assumed to be going on even at two hours, at which time maternal equlibrium has been reached.
Journal of Physiology & Pathology in Korean Medicine
/
v.17
no.1
/
pp.151-156
/
2003
This study was carried out to investigate the optimal mixed extract with Bambusae Caulis in Liquamen in order to strengthen anti-diabetic effects on the hyperglycemia induced by streptozotocin in mice. The original Bambusae Caulis in Liquamen filtered and refined. The effects of Bambusae Caulis in Liquamen and Mixed extracts(Bamboo Juice) with Bambusae Caulis in Liquamen were administered to mice for 4weeks and its anti-diabetic effect examined. Mice used in this experiment were divided into three groups and saline(control), Bamboo Juice mixed with refined Bambusae Caulis in Liquamen(BJ+BCL.D) and distrilled water mixed with refined Bambusae Caulis in Liquamen(DW+BCL.D) were given orally for 28days respectively. And then, experemental groups were observed in terms of blood sugar, creatinine, BUN and GPT. The amount of glucose was significantly decreased in the Bambusae Caulis in Liquamen and Mixed extracts(Bamboo Juice) with Bambusae Caulis in Liquamen-treated groups compared with the control group(P<0.01). The amount of creatinine, BUN and GPT did not show any differences among Control, BJ+BCL.D and DW+BCL.D groups. In conclusion. it was found that Bambusae Caulis in Liquamen and Mixed extracts(Bamboo Juice) with Bambusae Caulis in Liquamen were nontoxic to kidney and liver and also effective on murine hyperglycemia induced with STZ. Mixed extracts(Bamboo Juice) were more effective for decreasing blood glucose than Bambusae Caulis in Liquamen D. BJ+BCL.D can be used as optimal mix material with Bambusae Caulis in Liquamen D for control Diabetes.
The present study was designed to investigate whether endogenous nitric oxide(EDNO) is involved in submandibular vasodilation and salivation induced by parasympathetic nerve stimulation. Effects of $N^w$-nitro-L-arginine-methyl ester (L-NAME) which blocks the synthesis of EDNO from L-arginine on the submandibular vasodilation and salivation induced by chords stimulation or administration of various vasodilators were examined in anesthetized cats. Effect of L-NAME on $K^+$ efflux induced by carbachol was also examined using the excised submandibular slice in vitro. In the submandibular slices, acetylcholine$(10^{-5}\;mol/L)$ or vasoactive intestinal polypeptide$(VIP,\;10^{-5}\;mol/L)$ increased $NO_2$ contents, which was Prevented by pretreatment with L-NAME. Salivary secretion in response to the chords stimulation$(3\;V,\;1\;msec,\;10{\sim}20\;Hz)$ was completely blocked by treatment with atropine(1 mg/kg). Increased blood flow response to the low frequency(1, 2, 5 Hz) stimulation was significantly reduced, whereas the blood flow induced by the higher frequency(10,20 Hz) stimulation was not affected. Lingual-arterial infusion of L-NAME(100 mg/kg) significantly diminished the vasodilatory and salivary responses to the chorda stimulation at all stimuli frequencies used. Intra-arterial infusion of L-NAME(100 mg/kg markedly diminished the vasodilatory responses to acetylcholine$(5\;{\mu}g/kg)$, VIP$(5\;{\mu}g/kg)$ or bradykinin$(5\;{\mu}g/kg)$. In the excised submandibular slice, $K^+$ efflux in response to carbachol$(10^{-5}\;mol/L)$ was significantly decrease by pretreatment with L-NAME$(10^{-5}\;mol/L)$. In the isolated submandibular artery precontracted with phenylephrine$(10^{-5}\;mol/L)$, the vasorelaxation induced by ACh$(10^{-7}\;mol/L)$ was reversed into a contraction by methylene blue$(10^{-4}\;mol/L)$. These results suggest that EDNO may play an important role in vasodilation and secretion of the submandibular gland.
The effect of salinity on the survival, oxygen consumption and blood physiology of Korean rockfish Sebastes schlegelii (body weight $97.4{\pm}1.7g$, $mean{\pm}SD$) was investigated at nine different salinities of 33.4 (control), 33.1, 32.8, 32.2, 31.0, 28.7, 23.9, 14.5 and 3.8 psu, respectively. Survival and blood physiology were measured at each salinity in two separate trials of 96 and 24 hr duration, respectively. Oxygen consumption rate (OCR) was determined at stepwise salinity exposure ($33.4{\rightarrow}33.1{\rightarrow}32.8{\rightarrow}32.2{\rightarrow}31.0{\rightarrow}28.7{\rightarrow}23.9{\rightarrow}14.5{\rightarrow}3.8$ psu) with an interval of 24 hr for each salinity. No death of fishes were observed in the range of 33.4 to 14.5 psu, but the survival rate was reduced to 26.7% at 3.8 psu after 96 hr. The OCRs were not significantly different in the range 33.4 to 28.7 psu (p > 0.05), but significantly increased until 14.5 psu and then drastically decreased at 3.8 psu compared to the control (p < 0.05). The concentrations of plasma $Na^+$ and $Cl^-$ were significantly lower in fish exposed at 3.8 psu compared to the control (p < 0.05). The results of this study provide evidence that S. schlegelii exposed to concentrations below 23.9 psu show significant physiological responses to tolerate salinity changes under the experimental conditions we established.
The role of neurohumoral mechanisms in the regulation of cardiovascular functions and the effects of ethanol (EOH) on these mechanisms were examined in hemorrhaged conscious Wistar rats. The rats were bled at a constant rate (2 ml/kg/min) through the femoral artery until mean arterial pressure (MAP) was reduced by 30 mmHg. We studied the responses to hemorrhage 1) under normal conditions (Normal), and after pretreatments with 2) neural blockade (NB), pentolinium, 3) arginine vasopressin V1-receptor antagonist (AVPX) + NB, 4) angiotensin II ATI-receptor antagonist (AngIIX) + NB, 5) combined humoral blockade (HB), and 6) neurohumoral blockade. Intravenous administration of 30% EOH (6.3 ml/kg) attenuated the baroreceptor reflex sensitivity, and enhanced the depressor action of AngIIX. During hemorrhage, NB produced a faster fall ill MAP than Normal both in the saline and EOH groups. However, HB accelerated the rate of fall in MAP only in the EOH group. The recovery from hemorrhagic hypotension was not different between NB and Normal rats, but was attenuated in HB rats in the saline group. Under NB, AngIIX, but not AVPX, retarded the recovery rate compared with NB alone. EOH attenuated the recovery of MAP after hemorrhage in Normal rats, but completely abolished the recovery in HB rats. We conclude that 1) the maintenance of MAP during hemorrhage is mediated almost entirely by the autonomic functions, 2) angiotensin II plays an important role in the recovery from hemorrhagic hypotension, but AVP assumes little importance, 3) AVP release largely depends on the changes in blood volume, whereas renin release depends on the changes in blood pressure rather than blood volume, and 4) EOH increases the dependence of cardiovascular regulation on angiotensin II and impairs the recovery from hemorrhagic hypotension through the attenuation of autonomic functions.
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