Mechanosensitive modulation of peristaltic contractions in the mouse renal pelvis.

The renal pelvis develops spontaneous phasic contractions (SPCs) that underlie pyeloureteric peristalsis. Increased urine flow into the renal pelvis mechanically stimulates the contractile machinery within the renal pelvis to facilitate the propagation of peristalsis. Here, the effects of mechanostimulation of the pelvicalyceal junction (PCJ), where SPCs originate from, on the properties of SPCs were investigated.

Neural regulation of the contractility of nutrient artery in the guinea pig tibia.

Nutrient arteries provide the endosteal blood supply to maintain bone remodelling and energy metabolism. Here, we investigated the distribution and function of perivascular nerves in regulating the contractility of the tibial nutrient artery. Changes in artery diameter were measured using a video tracking system, while the perivascular innervation was investigated using fluorescence immunohistochemistry.

Exercise-induced sympathetic dilatation in arterioles of the guinea pig tibial periosteum.

Strength training induces not only muscle growth but also increased bone strength, a change that is expected to be associated with increased bone blood flow. However, the effects of exercise on contractile properties of bone microvascultaure have not been investigated. Once-a-week strength training with electrical muscle stimulation was applied unilaterally to tibialis anterior muscle of guinea pigs, while muscle force was measured from both legs to compare their muscle strength and endurance.

Contractile properties of periosteal arterioles in the guinea-pig tibia.

The periosteal arterioles of the compact bone may play a critical role in bone growth. To explore the contractile properties of tibial arterioles, spontaneous and nerve-evoked constrictions were compared in preparations from 3-week-old and 1-year-old guinea-pigs. Changes in arteriole diameters were measured using video microscopy.

Synthesis and Structure-Activity Relationships of 2-Aminoacetamide Derivatives as Peroxisome Proliferator-Activated Receptor α/γ Dual Agonists.

We describe the design, syntheses, and structure-activity relationships of novel zwitterionic compounds as nonthiazolidinedion-based peroxisome proliferator-activated receptor (PPAR) α/γ dual agonists. In our previous report, we obtained compound 1 showing potent PPARα/γ dual agonistic activities, together with a sufficient glucose-lowering effect in db/db mice. However, this compound possessed an issue, i.

Voltage-operated Ca(2) (+) currents and Ca(2) (+) -activated Cl(-) currents in single interstitial cells of the guinea-pig prostate.

Objective: To investigate the expression of 'T-type' and 'L-type' voltage-operated Ca(2) (+) channels in single interstitial cells of the guinea-pig prostate.

Material And Methods: Whole-cell and perforated patch-clamp techniques were applied to prostatic interstitial cells (PICs) dispersed using collagenase.

Results: In contrast to prostatic myocytes, PICs under voltage clamp and filled with K(+) (130 mm) were distinguished by the absence of a voltage-operated transient outward K(+) current or spike discharge upon membrane depolarisation when under current clamp.

Synthesis and structure-activity relationships of novel zwitterionic compounds as peroxisome proliferator activated receptor α/γ dual agonists with improved physicochemical properties.

We describe herein the design, syntheses and structure-activity relationships (SAR) of novel zwitterionic compounds as non-thiazolidinedion (TZD) based peroxisome proliferator activated receptor (PPAR) α/γ dual agonists. In the previous report, we obtained compound 1 showing potent PPARα/γ dual agonistic activities, together with a great glucose lowering effect in the db/db mice. However, this compound possessed fatal issues such as potent cytochrome P450 (CYP)3A4 direct inhibitory activity.

Properties of submucosal venules in the rat distal colon.

Background And Purpose: Venules within the gut wall may have intrinsic mechanisms for maintaining the circulation even upon the intestinal wall distension. We aimed to explore spontaneous and nerve-mediated contractile activity of colonic venules.

Experimental Approach: Changes in the diameter of submucosal venules of the rat distal colon were measured using video microscopy.

Enhanced K(+)-channel-mediated endothelium-dependent local and conducted dilation of small mesenteric arteries from ApoE(-/-) mice.

Aims: Agonists that evoke smooth muscle cell hyperpolarization have the potential to stimulate both local and conducted dilation. We investigated whether the endothelium-dependent vasodilators acetylcholine (ACh) and SLIGRL stimulated conducted dilation and whether this was altered by deficiency in apolipoprotein E (ApoE(-/-)).

Methods And Results: Isolated mesenteric arteries were cannulated, pressurized, and precontracted with phenylephrine.

Liver volume, as assessed by four ultrasonic crystals arranged to form a tetrahedron, decreases during anaphylactic shock in anesthetized rats.

We determined the hepatic volume change in anaphylactic hypotension by using four ultrasonic crystals in anesthetized rats. The hepatic volume was measured with four ultrasonic crystals arranged to form a tetrahedron on the liver surface. Before in vivo experiments, using isolated perfused rat liver preparations, we compared the measured liver volume changes with the whole-liver weight changes during hepatic blood flow rate changes and venoconstriction induced by norepinephrine.

Mouse hepatic portal venoconstrictive response to vasoconstrictors is much weaker than that in rat.

We previously reported that the portal venous pressure (PPV) response of perfused mouse livers to various vasoactive agents was much weaker than that of other mammals such as rat, rabbit, and guinea pigs. The purpose of this study was to determine the responsiveness of PPV in in vivo BALB/c mouse to intraportal injections of the 3 major vasoconstrictors of angiotensin II, norepinephrine, and endothelin-1 in comparison with that in Sprague-Dawley rats. In anesthetized spontaneously breathing animals, PPV, systemic arterial pressure, and central venous pressure were directly and continuously measured.

Hepatic microvascular pressure during anaphylactic shock in anesthetized rats.

Objective: Hepatic venoconstriction plays a significant role in anaphylactic hypotension in anesthetized rats. The purpose of this study is to determine whether the primary site of anaphylactic venoconstriction in the liver venous circulation occurs prior to or distal to the sinusoidal capillaries. We also determined whether the hepatic blood volume is increased during anaphylactic hypotension.

PAF, rather than histamine, participates in mouse anaphylactic hypotension.

We determined the roles of platelet-activating factor (PAF) and histamine in anaphylactic hypotension in ovalbumin-sensitized anesthetized BALB/c mice. The effects of PAF and histamine on hemodynamic variables were studied by measuring the systemic arterial (Psa), portal venous (Ppv) and central venous (Pcv) pressures. Intravenous PAF evoked a biphasic Psa response, an initial rapid and transient drop followed by marked hypotension, accompanied by a decrease in Pcv.

7-nitroindazole, but not L-NAME or aminoguanidine, attenuates anaphylactic hypotension in conscious rats.

The roles of NO and isozymes of NO synthase (NOS) are not known in anaphylactic hypotension of unanesthetized rats. Effects of inhibition of NOS, iNOS, and nNOS by N-nitro-L-arginine methyl ester (L-NAME), aminoguanidine, and 7-nitroindazole, respectively, were determined on the antigen-induced systemic hypotension and portal hypertension in conscious Sprague-Dawley rats sensitized with the ovalbumin antigen. The MAP and portal venous pressure were directly and simultaneously measured.

Venous resistance increases during rat anaphylactic shock.

Anaphylactic shock is a sudden, life-threatening allergic reaction associated with severe hypotension. The increased venous resistance accounts for the anaphylactic hypotension in anesthetized dogs. However, the change in peripheral vascular resistances during anaphylactic hypotension in other animals such as rats is not known.

The roles of mast cells and Kupffer cells in rat systemic anaphylaxis.

Mast cells and other cells such as macrophages have been shown to mediate systemic anaphylaxis. We determined the roles of mast cells and Kupffer cells in hepatic and systemic anaphylaxis of rats. Roles of mast cells were examined by using the mast cell-deficient white spotting (Ws/Ws) rat; the Ws/Ws and wild type (+/+) rats were sensitized with ovalbumin (1 mg).

Head-down tilt posture attenuates anaphylactic hypotension in mice and rats.

A head-down tilt posture, the Trendelenburg position, which could facilitate venous return from the splanchnic organs and lower extremities, is recommended for the treatment of anaphylactic shock. However, few data of animal studies support its effectiveness. We examined the effects of a head-down tilt maneuver on anaphylactic hypotension in BALB/c mice and Sprague-Dawley rats.

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice.

Using in vivo and isolated perfused liver preparations of BALB/c mice, we determined the roles of the liver and splanchnic vascular bed in anaphylactic hypotension. Intravenous injection of ovalbumin antigen into intact-sensitized mice decreased systemic arterial pressure (P(sa)) from 92 +/- 2 to 39 +/- 3 (SE) mmHg but only slightly increased portal venous pressure (P(pv)) from 6.4 +/- 0.

Leukotrienes and cyclooxygenase products mediate anaphylactic venoconstriction in ovalbumin sensitized rat livers.

Hepatic anaphylactic venoconstriction is partly involved in anaphylactic hypotension. We determined the chemical mediators responsible for anaphylaxis-induced segmental venoconstriction in perfused livers isolated from ovalbumin-sensitized rats. Livers were perfused portally and recirculatingly at constant flow with diluted blood.

Effects of L-NAME on thromboxane A2-induced venoconstriction in isolated perfused livers from rat, guinea pig and mouse.

Effects of L-NAME on U-46619 (a thromboxane A(2), analogue) -induced hepatic segmental venoconstriction were examined in mouse, rat and guinea pig isolated perfused livers. All livers were perfused portally and recirculatingly at a constant flow with diluted blood. U-46619 was administrated into the reservoir in a cumulative manner to gain the concentrations of 0.

N(G)-nitro-L-arginine methyl ester, but not methylene blue, attenuates anaphylactic hypotension in anesthetized mice.

To clarify the role of NO in mouse anaphylactic hypotension, effects of a nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), on antigen-induced hypotension and portal hypertension were determined in anesthetized BALB/c mice. Systemic arterial pressure (Psa), central venous pressure (Pcv), and portal venous pressure (Ppv) were directly and simultaneously measured. Mice were first sensitized with ovalbumin, and then the injection of antigen was used to decrease Psa and increase Ppv.

L-NAME augments PAF-induced venoconstriction in isolated perfused livers of rat and guinea pig, but not mouse.

Platelet-activating factor (PAF), one of vasoconstrictive lipid mediators, is involved in systemic anaphylaxis. On the other hand, nitric oxide (NO) is known to attenuate anaphylactic venoconstriction of the pre-sinusoids in isolated guinea pig and rat livers. However, it is not known whether NO attenuates PAF-induced hepatic venoconstriction.

The sinusoidal pressure during ischemia-reperfusion injury in perfused mouse liver pretreated with or without L-NAME.

Background: Hepatic ischemia-reperfusion (I/R) is accompanied by liver weight gain and ascites formation possibly caused by an increase in the sinusoidal pressure, a determinant of hepatic transvascular fluid movement. However, changes in the sinusoidal pressure during hepatic I/R in mice are not known. It is also controversial whether nitric oxide (NO) exerts a beneficial or detrimental effect on hepatic I/R injury.

N(G)-nitro-L-arginine methyl ester potentiates anaphylactic venoconstriction in rat perfused livers.

1. The effects of the nitric oxide (NO) synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) on anaphylaxis-induced venoconstriction were examined in rat isolated livers perfused with blood-free solutions in order to clarify the role of NO in anaphylactic venoconstriction. 2.

Effects of Hct on L-NAME-induced potentiation of anaphylactic presinusoidal constriction in perfused rat livers.

Effects of hematocrit (Hct) on N-nitro-L-arginine methyl ester (L-NAME)-induced modulation of anaphylactic venoconstriction were determined in isolated perfused rat livers. The rats were sensitized with ovalbumin (1 mg), and the livers were excised 2 weeks later and perfused portally and recirculatingly under constant flow at Hct of 0%, 5%, 16%, and 22%. The hepatic sinusoidal pressure was estimated via the double occlusion pressure (Pdo), and the presinusoidal resistance (Rpre) and the postsinusoidal resistance (Rhv) were calculated.