Satoshi Maruyama

A power-law distribution of inter-spike intervals in renal sympathetic nerve activity in salt-sensitive hypertension-induced chronic heart failure.

To assess sympathetic variability in chronic heart failure (CHF), we evaluated a distribution of inter-spike intervals (ISIs) in renal sympathetic nerve activity (RSNA) in salt-sensitive hypertension-induced CHF (DSSH-CHF) rats. Dahl salt-sensitive rats were fed an 8% NaCl diet for 9 weeks to induce salt-sensitive hypertension-induced CHF. ISIs in RSNA were obtained from chronically instrumented conscious rats, and counts (frequency) and ranks of ISIs in RSNA were plotted with a histogram. We found that ISIs in RSNA followed a power-law distribution in rats, and the power-law distribution of ISIs for RSNA in DSSH-CHF rats was significantly different from that in normal rats. These results indicated that sympathetic variability may be significantly different between salt-sensitive hypertension-induced CHF and healthy individuals, which suggests that sympathetic variability may be used to predict abnormality of the sympathetic regulatory system.

Central Endogenous Vasopressin Induced by Central Salt‐Loading Participates in Body Fluid Homeostasis through Modulatory Effects on Neurones of the Paraventricular Nucleus in Conscious Rats

Peripherally secreted arginine vasopressin (AVP) plays a role in controlling body fluid homeostasis, and central endogenous AVP acts as a neurotransmitter or neuromodulator. The limbic system, which appears to exert an inhibitory effect on the endocrine hypothalamus, is also innervated by fibres that contain AVP. We examined whether central endogenous AVP is also involved in the control of body fluid homeostasis. To explore this possibility, we examined neuronal activity in the paraventricular nucleus of the hypothalamus (PVN), periventricular parts of the PVN and limbic brain areas, as well as AVP mRNA expression in the PVN and the peripheral secretion of AVP after central salt‐loading in rats that had been pretreated i.c.v. with the AVP V1 receptor antagonist OPC‐21268. Neuronal activity in the PVN evaluated in terms of Fos‐like immunoreactivity (FLI), especially in the parvocellular subdivisions, was suppressed. On the other hand, FLI was enhanced in the lateral septum, the bed nucleus of the stria terminalis and the anterior hypothalamic area. Similarly, AVP mRNA expression was enhanced in the magnocellular subnucleus of the PVN, despite the lack of a significant difference in the peripheral AVP level between OPC‐21268‐ and vehicle‐pretreated groups. We recorded renal sympathetic nerve activity (RSNA) as sympathetic nerve outflow during central salt‐loading. The suppression of RSNA was significantly attenuated by i.c.v. pretreatment with OPC‐21268. These results suggest that the suppression of RSNA during central salt‐loading might be the result of a decrease in neuronal activity in the parvocellular subdivisions of the PVN via the inhibitory action of central endogenous AVP. The parvocellular and magnocellular neurones in the PVN might show different responses to central salt‐loading to maintain body fluid homeostasis as a result of the modulatory role of central endogenous AVP.

Teeth clenching and positive acceleration-induced cerebral arterial hypotension in rats.

INTRODUCTION High positive acceleration (+Gz) stress is known to cause cerebral hypoperfusion, resulting in brain insults. Muscular contraction is reported to induce a pressor response. The effects of teeth clenching on cerebral hypoperfusion were examined. METHODS The masseter muscle of anesthetized Sprague-Dawley rats was electrically stimulated to cause maximum clenching of the teeth. Arterial pressure at the level of the brain (APBr), heart rate, and central venous pressure were measured when rats were exposed to +1.5 Gz by using a centrifuge without an anti-C system. RESULTS Acceleration of +1.5 Gz decreased APBr by 18.3 +/- 2.0 mmHg, which was reduced to 1.9 +/- 2.0 mmHg by masseter muscle contraction, but was not reduced by femoral muscle contraction. Stimulation of the masseter muscle but not the femoral muscle induced a pressor response of 11.8 +/- 2.1 mmHg, which was eliminated by dantrolene, a postsynaptic skeletal muscle relaxant. When masseter contraction was blocked by dantrolene, masseter stimulation did not reduce cerebral hypotension in the presence of +1.5-Gz acceleration (delta 18.9 +/- 2.6 mmHg). CONCLUSION Our results suggest that teeth clenching induced a pressor response that prevented +Gz-induced cerebral hypotension, which suggests the possible development of a new anti-G method.

Severe hypotension during the decreasing phase of Gz stress in anesthetized rats wearing an anti-G suit.

INTRODUCTION Physiological responses to +Gz stress have been reported in several studies. However, no reports exist on differences in arterial pressure responses between increasing and decreasing G phases. We hypothesized that +Gz stress and/or an anti-G support might disturb the circulation system and cause potential brain hypoperfusion, even if the anti-G support protects against G-induced loss of consciousness. METHODS Dependency of +Gz magnitude, hemodynamic changes, renal sympathetic nerve activity (RSNA), and aortic blood flow (AoBF) were estimated in anesthetized rats to analyze the effects of +Gz stress and/or an anti-G support on arterial pressure at a level of the brain (APLB). The rats were exposed to +Gz using a centrifuge for small animals while wearing an anti-G suit. RESULTS APLB remained at the control level while the anti-G suit was inflated. However, a decrease in APLB was observed twice during increasing and decreasing G phases using the anti-G suit. Hypotension in the decreasing C phase at +5 Gz was significantly deeper than that in the increasing G phase (47.5 +/- 7.7 vs. 29.6 +/- 3.0 mmHg). RSNA responses to Gz loads were greater in the decreasing G than in the increasing G phase (129.7 +/- 8.6 vs. 147.3 +/- 10.4%). Both AoBF and calculated vascular resistance were suppressed more significantly in the decreasing G than in the increasing G phase (38.3 +/- 4.4 vs. 34.4 +/- 3.4 ml x min(-1), 1.44 +/- 0.22 vs. 1.09 +/- 0.14 mmHg x min(-1) x ml(-1)). DISCUSSION We conclude that transient excessive decreasing G hypotension may occur during the decreasing G phase, which may be due to anti-G suit functioning.