摘要:

The arginine vasopressin (AVP) producing hypothalamo‐neurohypophysial system also has high activities of NO‐synthase. Vasopressin production and secretion is drastically upregulated during salt intake and the NO‐producing enzyme may be involved. We have studied the influence of the NO‐synthase inhibitorNG‐nitro‐l‐arginine (l‐NNA on neurohypophysial and hypothalamic AVP and its amidating enzymes in salt‐loaded and control rats as well as on stimulated AVP releasein vitroin such rats. Rats were given 2% NaCl solution as the only fluid for 4 days and then returned to tap water. The specific amount of AVP (μg (mg protein)‐1) and the activities of peptidylglycine α‐ hydroxylating monooxygenase (PHM) and peptidyl‐α‐hydroxyglycine α‐amidating lyase (PAL), components of its amidating processing enzyme in the supraoptic (SON) and paraventricular nuclear (PVN) regions, did not change during the salt‐loading or the following recovery period. In contrast, the AVP and PHM and PAL in the neurohypophysis fell drastically during the salt loading. After that, PHM and PAL increased even more rapidly than AVP, the latter reaching control levels in about 10 days. Salt loading did not change the protein content of the neurohypophysis. When salt loading was performed after administration ofl‐NNA, the neurohypophysial AVP at the end of the salt loading and 3 days later was lower than in rats not receivingl‐NNA, whereas PHM and PAL were not affected. Fractional AVP release from isolated neurohypophyses of salt loaded rats treated withl‐NNA and stimulated with K+was similar to that found in non‐treated rats. It is suggested thatl‐NNA may affect

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09970.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

The aim of the present study was to evaluate the role of the endothelium in low pH‐, capsaicin‐, and prostacyclin (PGI2,)‐evoked release of calcitonin gene‐related peptide (CGRP)‐like immunoreactivity (‐LI) from C‐fibre afferents in the isolated, perfused guinea‐pig heart. CGRP‐LI release, and formation of the stable PGI2‐metabolite 6‐keto‐PGF1α,in response to moderate acidosis (pH 7, 6, but not 5) were significantly reduced after removal of the endothelium using saponin (50 μg mL‐1) perfusion. In contrast, the release of CGRP‐LI evoked by capsaicin (10‐7M) or PGI2, (10‐5M) remained unchanged after removal of the endothelium. Saponin treatment did not influence the vasodilator action of CGRP, whereas the vasodilation evoked by substance P (SP) was abolished. It is concluded that CGRP release evoked by low pH, but not that evoked by capsaicin or exogenous PGI2, is partly endothelium dependent. Our data suggest that endothelially produced PGI2, is involved in low pH‐evoked release of CGRP from caps

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09971.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Relaxant effects of acetylcholine (ACh), histamine, calcitonin gene‐related peptide (CGRP) and the calcium ionophore A23187 were examined in rat femoral (Ø ≅ 0.2 mm), mesenteric (0.2 mm), intrarenal (0.2 mm) and hepatic (0.3 mm) arteries, and aorta (2 mm). Acetylcholine elicited an endothelium‐dependent relaxation in all arteries. Histamine induced an endothelium‐dependent relaxation in aorta, and mesenteric and intrarenal arteries, whereas a partly endothelium‐dependent and mainly endothelium‐independent relaxation was observed in hepatic and femoral arteries, respectively. In hepatic, mesenteric and intrarenal arteries, CGRP induced an endothelium‐independent relaxation, whereas either small or no relaxation was obtained in aorta and femoral arteries respectively. A23187 induced an endothelium‐dependent relaxation in the aorta and hepatic artery, whereas A23187 had no relaxant effect in femoral, mesenteric and intrarenal arteries. Nω‐nitro‐l‐arginine (l‐NOARG, 0.3 mM) reduced the maximum ACh‐induced relaxation (in the presence of 10 μM indomethacin) by 66% in the aorta, and abolished the relaxation in femoral and intrarenal arteries. A markedl‐NOARG/indomethacin‐resistant relaxation was obtained in mesenteric and hepatic arteries. Levcromakalim induced a concentration‐dependent and almost complete relaxation in all arteries. When contracted by a 60 mM K+solution, all arteries responded to ACh with a relaxation that was abolished byl‐NOARG. These results demonstrate marked regional differences with regard to the vascular effects of ACh, histamine, CGRP and A23187. Whereas nitric oxide appears to mediate endothelium‐ dependent relaxation regardless of the vascular region, anl‐NOARG/indomethacin‐resistant relaxation, presumably mediated by an endothelium‐derived hyperpolarizing factor, was observed only i

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09972.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

This study was designed to evaluate the effect of modulating cardiac parasympathetic input on the high frequency component of heart rate variability. We stimulated the right vagus nerve with three different stimulation patterns in anaesthetized, vagotomized and spinal anaesthetized dogs. We kept the mean stimulation frequency constant; controlled the amplitude of modulation with programmed stimulation patterns, and analysed the resulting heart rate variability by power spectral analysis. Constant frequency vagal stimulation increased the cardiac interval, but did not change heart rate variability markedly. There was a slight increase, from 11 pL 2 to 27 pL 11 ms2, in the high frequency component. However, when the instantaneous stimulation frequency oscillated between 4 and 17 Hz during 5 s period, we could produce a marked heart rate variation, with 91 pL 9% of the variation corresponding to the frequency of the modulation (0.20 Hz). The high frequency component was 12932 pL 7701 ms2. With an increased magnitude of modulation, i.e. the difference between minimum and maximum instantaneous frequency, the high frequency component increased to 32711 pL 17943 ms2. Thus, the high frequency component of heart rate variability reflects the magnitude of fluctuation in the cardiac parasympathetic input rather than parasympathetic ‘tone

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09973.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

The rates of oxygen consumption, colonic and interscapular brown adipose tissue temperature, and discharge of sympathetic nerves innervating the same tissue were recorded before and after orbital frontal cortex stimulation in three groups of rats. These groups consisted of animals with electrolytic lesions of the nucleus medialis septi, with lesions of nucleus lateralis septi or with sham lesions. The values of all the variables considered were similar during the pre‐stimulation time in the three groups of rats. There was an increase in all the parameters in sham‐lesioned animals after electrical stimulation, while no changes were found in the two groups of injured rats. The results showed that the frontal cortex is involved in the control of thermogenesis through the activation of the sympathetic nervous system. Medial and lateral septal nuclei, in spite of their neurochemical and pharmacological differences, share a common role in the pathway from the frontal cortex to the hypothalamic area and the amygdala, which in turn drive the sympathetic nervous sys

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09974.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

The objective of this study was to investigate renal phosphate excretion during 24 h of hypoxia in conscious rats fed by total parenteral nutrition. Wistar rats weighing 190 g were exposed to hypoxia (inspired oxygen fraction = 0.10) or normoxia (inspired oxygen fraction = 0.21) for 24 h in a normobaric chamber. Renal clearance and hormonal studies were performed. The results showed a greater fractional excretion of phosphate (5.37 pL 0.07%, P<0.05) and hypophosphataemia (7.40 pL 0.12 mg dL‐1, P<0.01) in hypoxic rats (n= 10) than in normoxic rats (n= 13; 3.50 pL 0.37% and 8.02 pL 0.16 mg dL‐1, respectively). In addition, during hypoxia there was a significant decrease in the excretion of urinary adenosine 3′,5′‐cyclic monophosphate per glomerular filtrate (2.97 pL 1.27 nmol dL‐1, P<0.005), a parameter of the renal action of parathyroid hormone, and a stable level of serum parathyroid hormone (10.2 pL 2.6 ng mL‐1) (cf. normoxia: 8.57 pL 0.70 nmol dL‐1and 8.0 pL 1.7 ng mL‐1, respectively). However, creatinine clearance and the renal adenosine triphosphate level, both of which affect adenosine 3′,5′‐cyclic monophosphate excretion, were not different between the two groups. These data suggest that exposure of conscious rats to 24 h of hypoxia causes renal hyporesponsiveness to physiological levels of parathyroid hormone, which is manifested as a decrease in adenosine 3′,5′‐cyclic monophosphate excretion. Phosphaturia is not a direct net effect of hypoxia and secondary hypocapnia on renal phosphate transport, which is known to be regulated by parathyroid hormone through adenosi

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09975.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

The present study was undertaken to determine whether exercise‐training for 6 weeks would inhibit pulmonary vasoconstriction induced by hypoxia in isolated, blood‐perfused rat lungs. Hypoxic pulmonary vasoconstriction (HPV) and angiotensin II (AH)‐induced pulmonary vasoconstriction were significantly less in the exercise‐trained (ET) group than in the control (cont) group with all challenges. Normoxic pulmonary arterial and capillary pressures in the ET group were significantly lower than those in the cont group and capillary pressor response to hypoxia was less in the ET group than in the cont group. In conclusion, it appears that HPV and AII‐induced vasoconstrictions can be reduced by exercise‐training, because it would seem that exercise‐training repeated responses to increased shear‐stress resulting from elevated blood flow in pu

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09976.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

We examined the responses of slowly adapting pulmonary stretch receptors (PSRs), total lung resistance (RL) and dynamic lung compliance (Cdyn) to administered veratridine before and after pretreatment with atropine or flecainide in anaesthetized, artificially ventilated rabbits with bilateral vagotomy. Administration of veratridine (10 and 30 μg kg‐1) caused vigorous stimulation of PSRs, resulting in a tonic discharge of receptors during both inflation and deflation, but did not significantly alter either RLor Cdyn. The veratridine‐induced PSR stimulation became more prominent, as the dose of this alkaloid was increased. Pretreatment with atropine (1 or 2 mg kg‐1) had no significant effect on the excitatory response of PSRs to veratridine. The veratridine induced PSR stimulation was inhibited by treatment with flecainide (1, 2 and 3 mg kg‐1), a sodium channel blocker, and this inhibition was dose‐dependent. These results suggest that activation of PSRs following veratridine administration probably related to the increased influx of sodium ions into the receptive terminals but does not depend upon bronchoco

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09977.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

To elucidate the role of adenosine in coronary vasoregulation, we studied the effects of adenosine antagonism (by theophylline) on coronary blood flow at different levels of adenosine formation (stimulated by hypoxia and exercise). Six healthy subjects were studied. Coronary sinus (CS) blood flow (thermodilution) and cardiac oxygen extraction {(A‐CS)O2D} were determined while breathing room air at rest, and 12% oxygen, both at rest and during light exercise, on two occasions. One of the experiments was performed during infusion of theophylline. The basal CS flow was 118 (67–168) mL min‐1(mean and 95% confidence interval), and the (A‐CS)O2D was 125 (111–142) mL L‐1.Inhalation of 12% 02decreased the arterial haemoglobin oxygen saturation to 83 (80–86)% at rest and to 77 (73–81)% during exercise. CS flow increased to 167 (93–214) and 261 (179–343) mL min‐1, respectively, and (A‐CS)O2D decreased to 102 (85–119) and 94 (77–111) mL L‐l, respectively. Theophylline, at a dose lacking effects on myocardial work, markedly attenuated the coronary flow response to exogenous adenosine, and decreased CS flow to 89 (58–119), 120 (79–161) and 190 (162–218) mL min‐1at normoxic rest, hypoxic rest and hypoxic exercise, respectively. The overall decrease amounted to 23% (P<0.05). The calculated coronary vascular conductance also decreased by 23% (P<0.05) and (A‐CS)O2D increased by 15% (P<0.001). In conclusion, the data support the hypothesis that endogenous adenosine is involv

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09978.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Previous studies have demonstrated numerous immunobiological changes in conection with exercise. A decrease in peripheral blood mononuclear white cells (PBMC) 2 h after intense exercise has been shown. This lymphocytopenia in humans after exercise is thought to be of great importance regarding the morbidity to viral infection. We constructed an animal experimental set‐up, previously published, to investigate the exercise‐induced lymphocyte redistribution. The experimental set‐up allowed us to draw blood from catheters implanted in the right carotid artery in rats. PBMC were isolated and labelled with Ins111and reinfused before the exercise run on a treadmill to exhaustion. The runner and control rats were killed and dissection performed 1 h after the exercise. Tissue samples were weighed and measured in a gamma counter. Furthermore, blind microscopic examinations of selected tissues were performed to study a hypothesized accumulation of blood mononuclear cells in relation to muscle fibre lesions. We found that the total number of PBMC in the running rats was decreased (P = 0.018) and granulocytes increased, 1 h after the exercise (P = 0.028). Similar findings in humans in connection with physical activity have been observed. The percentage of total injected counts per minute per gram tissue (% c.p.m. g‐1) showed significantly lower values in the liver and kidney from runners than from controls (P = 0.032 and P = 0.028). These findings might be the result of a visceral hypoflowin connection with exercise. Furthermore, a tendency to decreased % c.p.m. g‐1in the lungs was seen in the exercised rats (P = 0.083) indicating a possible redistribution from the lungs during the run. Light microscopy demonstrated an accumulation of PBMC around muscle fibre lesions, but there was no significant difference between runners and controls. Furthermore, no significant difference in % c.p.m: g‐1was found between working muscle groups in runner and control rats. In conclusion, the demonstration of the redistribution of PBMC from the liver and kidney in the exercised rats and the absence of any significant accumulation of PBMC in working muscles or other organs, do not explain the lymphocytopenia demons

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1995.tb09979.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY