No abstract available.
Alprostadil ; Gastrointestinal Motility ; Lubiprostone

No abstract available.
Prostatectomy* ; Prostatic Intraepithelial Neoplasia*

No abstract available.
Prostatectomy* ; Prostatic Intraepithelial Neoplasia*

No abstract available.
Colon ; Interstitial Cells of Cajal ; Receptors, Cholinergic

No abstract available.
Cholecystokinin ; Colon

BACKGROUND: Prostaglandin system is known to participate in manifestation of the renin-angiotensin system. However, role of prostaglandins on the renin-angiotensin system in development of hypertension is not well established. This study was to examine whether the role of prostaglandins is altered in experimental hypertension. METHODS: Two-kidney, one-clip(2KIC) renal hypertension was made by clipping the left renal artery with a silver clip(internal gap of 0.2mm) and deoxycorticosterone acetate (DOCA)-salt hypertension by subcutaneous implantation of DOCA(200mg/kg) strip plus saline(1%) drinking. They were used 3 weeks later. Age-matched normal rats served as a control. Femoral artery was cannulated and arterial blood pressure and heart rate were monitored continuously. RESULTS: 1) In normotensive rats, saralasin infusion(20 microg/kg/min, IV) caused a decrease in mean arterial pressure without significant alterations in heart rate. Indomethacin-pretreatment(10mg/kg, IP) abolished the depressor response to saralasin. 2) The depressor response to saralasin was more marked in renal hypertensive rats than in normotensive rats. The magnitude of maximum decrease in blood pressure, however, was comparable between the hypertensive and normotensive rats. Indomethacin-pretreatment did not affect the depressor response to saralasin in renal hypertensive rats. 3) In DOCA-salt hypertensive rats, saralasin infusion rather caused an increase in mean arterial pressure without significant alterations in heart rate. The pressor response to saralasin was not affected by indomethacin-pretreatment. CONCLUSION: These results indicate that prostaglandin system may modify renin-angiotensin system in normotensive rats. It is suggested that mechanisms other than prostaglandin system participate in the full-blown manifestation of renin-angiotensin system in 2KIC renal hypertensive rats.
Animals ; Arterial Pressure ; Blood Pressure ; Desoxycorticosterone ; Drinking ; Femoral Artery ; Heart Rate ; Hypertension ; Hypertension, Renal ; Prostaglandins I ; Prostaglandins* ; Rats* ; Renal Artery ; Renin-Angiotensin System* ; Saralasin ; Silver

BACKGROUND: Aside from its well known peripheral antihypertensive effects, calcium also lowers blood pressure, when administered into the cerebral ventricle. The present study was aimed to determine whether the central depressor response to calcium is mediated by a stimulation of endogenous L-arginine-nitric oxide (NO) pathway. METHODA: Mean arterial pressure (MAP) and heart rate (HR) were continuously recorded from the femoral artery in anesthetized rats. Administration of calcium was performed into the right lateral cerebral ventricle. The effects of N G-nitro-L-arginine methyl ester (L-NAME) on the cardiovascular response to calcium were examined. RESULTS: Intracerebroventricular (ICV) injection of calcium consistently produced a decrease in MAP and HR. The depressor and bradycardiac responses to calcium showed a dose-dependent fashion. Pretreatment with a calcium channel blocker, diltiazem (1 micromol, ICV), attenuated cardiovascular responses to calcium. ICV infusion (1 microl/min) of L-NAME (200 microgram/kg and 20 microgram/kg/min for 60 min) increased MAP without significant changes in HR. Chronic ingestion of L-NAME (5 mg/100 ml in drinking water, 4 weeks) also increased the systolic blood pressure as compared with control. The depressor effect of ICV calcium was significantly diminished in acute or chronic L-NAME treated rats. CONCLUSION: These findings suggest that the central depressor response to calcium, at least in part, is NO-dependent.
Animals ; Arterial Pressure ; Blood Pressure ; Calcium Channels ; Calcium* ; Cerebral Ventricles ; Diltiazem ; Drinking Water ; Eating ; Femoral Artery ; Heart Rate ; NG-Nitroarginine Methyl Ester ; Nitric Oxide* ; Rats

BACKGROUND: Pemphigus is an autoimmune bullous disease with circulating desmosomal autoantibodies of IgG. In direct IF studies with perilesional tissue, IgA or IgM antibodies can be seen in addition to IgG. OBJECTIVE: We examined sera of patients with pemphigus for the presence/frequency of IgA autoantibodies as well as IgG by indirect IF and immunoblot assay. Patients: Twenty patients of pemphigus (PV 10, PF 10) who showed positive findings in indirect IF examinations. METHODS: Indirect IF study with normal human skin substrates and immunoblot analysis using A431 cell extracts (with multi-step immunostaining) were performed with patients sera. RESULTS: In indirect IF, IgA autoantibodies that bind to the epidermal keratinocyte antigens were detected in 4 cases among the 20 patients (PV 2 and PF 2). In immunoblot analysis IgA bands reacting to PV/PF antigens were observed in 7 cases from the 20 patients with pemphigus (PV 3, PF 4). The serum titers of IgA autoantibodies were lower than those of IgG in every single case. CONCLUSION: In patients with pemphigus (PV/PF), 35% of cases have serum IgA autoantibodies as well as IgG autoantibodies specific to the pemphigus antigens (Dsg 1/Dsg 3). However, pathogenic roles of the associated IgA autoantibody are not clear.
Antibodies ; Autoantibodies ; Cell Extracts ; Humans ; Immunoglobulin A* ; Immunoglobulin G ; Immunoglobulin M ; Keratinocytes ; Pemphigus* ; Skin

The vanilloid receptor type-1 (VR1) is a nonselective cation channel activated by capsaicin and can be act as mediator of chemical and physical stimuli that elicit pain. The presence of VR1 in the dorsal root, trigeminal and nodose ganglia has been firmly established, but it unclear in the mouse intestinal wall. The distribution of VR1 receptors in mouse afferent neurons innervating the intestinal tract was investigated by immunohistochemistry. Also small and large intestines were dual-labelled with antibody for VR1 and marker for interstitial cells of Cajal (c-kit). VR1-immunopositive cells were localized on fine fibers in myenteric plexus and expressed weakly myenteric ganglia. The majority of VR1-immunopositive fibers are not colocalized with or apposed to c-kit positive interstitial cells of Cajal. Also electrophysiologically capsaicin had no effect on cultured interstitial cells of Cajal. It is concluded that VR1-immunoreactive intestinal nerves are mainly distributed in myenteric plexus of murine intestinal wall, and vanillod may be not directly related to interstitial cells of Cajal in regulation of intestinal motility.
Animals ; Capsaicin ; Ganglia ; Gastrointestinal Motility ; Immunohistochemistry ; Interstitial Cells of Cajal ; Intestines ; Mice* ; Myenteric Plexus* ; Neurons, Afferent ; Nodose Ganglion ; Spinal Nerve Roots

The vanilloid receptor type-1 (VR1) is a nonselective cation channel activated by capsaicin and can be act as mediator of chemical and physical stimuli that elicit pain. The presence of VR1 in the dorsal root, trigeminal and nodose ganglia has been firmly established, but it unclear in the mouse intestinal wall. The distribution of VR1 receptors in mouse afferent neurons innervating the intestinal tract was investigated by immunohistochemistry. Also small and large intestines were dual-labelled with antibody for VR1 and marker for interstitial cells of Cajal (c-kit). VR1-immunopositive cells were localized on fine fibers in myenteric plexus and expressed weakly myenteric ganglia. The majority of VR1-immunopositive fibers are not colocalized with or apposed to c-kit positive interstitial cells of Cajal. Also electrophysiologically capsaicin had no effect on cultured interstitial cells of Cajal. It is concluded that VR1-immunoreactive intestinal nerves are mainly distributed in myenteric plexus of murine intestinal wall, and vanillod may be not directly related to interstitial cells of Cajal in regulation of intestinal motility.
Animals ; Capsaicin ; Ganglia ; Gastrointestinal Motility ; Immunohistochemistry ; Interstitial Cells of Cajal ; Intestines ; Mice* ; Myenteric Plexus* ; Neurons, Afferent ; Nodose Ganglion ; Spinal Nerve Roots