Renal sympathetic nerve activity in mice: comparison between mice and rats and between normal and endothelin-1 deficient mice

Ling, Guoyu; Cao, Weihua; Onodera, Makoto; Ju, Kihwan; Kurihara, Hiroki; Kurihara, Yukiko; Yazaki, Yoshio; Kumada, Mamoru; Fukuda, Yasuichiro; Kuwaki, Tomoyuki

doi:10.1016/s0006-8993(98)00848-8

Cited by 48 publications

(46 citation statements)

References 34 publications

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“…For example, changes in arterial blood pressure evoke powerful baroreflex-mediated changes in renal sympathetic nerve activity in mice, as has also been observed in rats and other species (Ling et al, 1998;Ma et al, 2001).…”

Section: Discussionmentioning

confidence: 63%

“…Such studies commonly involve direct recording of neural activity in fibers traveling in the extrinsic renal nerves (Judy et al, 1976Judy and Farrel, 1979;Ricksten and Thorén, 1981;Lundin et al, 1984;DiBona and Kopp, 1997;Ling et al 1998;Ma et al, 2001). The absolute level of activity recorded is dependent not only on the activity in single nerve fibers but also on the number of nerve fibers near the recording electrode and the recording conditions.…”

Section: Discussionmentioning

confidence: 99%

“…The absolute level of activity recorded is dependent not only on the activity in single nerve fibers but also on the number of nerve fibers near the recording electrode and the recording conditions. Ling et al (1998) recently reported that the absolute levels of resting and maximal renal sympathetic nerve activity, and the range of baroreflex control of sympathetic activity are less in mice than in rats. The authors acknowledged that the lack of information on the number of fibers and fiber diameter in the renal nerves of mice prevented evaluation of the underlying cause of the lower nerve activity in mice.…”

Section: Discussionmentioning

confidence: 99%

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Qualitative and quantitative morphology of renal nerves in C57BL/6J mice

Fazan

Chapleau

et al. 2002

Anat. Rec.

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The detailed morphology of the renal nerves in mice has not been reported previously. The aims of this study were to describe the general morphology of the extrinsic renal nerve in C57BL/6 mice, and determine its morphometric parameters. The major renal nerve innervating the left kidney was isolated in five mice. Thin sections of the nerve segments were then examined by transmission electron microscopy. The renal nerve averaged 35.4 Ϯ 3.6 (S.E.M.) m in diameter and 741 Ϯ 104 m in area. The renal nerve contained an average of 830 Ϯ 169 unmyelinated fibers and only 4.6 Ϯ 1.7 myelinated fibers. The axon diameter of myelinated and unmyelinated fibers averaged 2.2 Ϯ 0.3 m and 0.76 Ϯ 0.02 m, respectively. The diameter of the unmyelinated fibers ranged from 0.3 to 2.0 m, and the distribution histogram was unimodal. The majority of fibers (85%) had diameters of 0.6 -1.0 m. These results are similar to those obtained for renal nerves of rats with respect to the predominance of unmyelinated fibers. However, the diameter of unmyelinated fibers is larger in rats and the distribution histogram of rat unmyelinated fibers is bimodal, in contrast to the unimodal distribution in mice. The morphological description of the renal nerves in mice provides baseline data for further investigations of the structural basis of altered autonomic reflexes. The results will be useful in analyses of genes that influence the development and structure of sympathetic and sensory innervation of the kidney in genetically manipulated mice. Anat Key words: mice; renal nerve; morphology; morphometry; electron microscopyThe renal nerves contain efferent sympathetic nerve fibers that are important in regulating renal function, and afferent fibers that transmit sensory information from the kidneys to the central nervous system. Changes in multiple sensory inputs and central nervous system activity influence efferent renal sympathetic nerve activity, thereby altering kidney function through changes in renal vascular resistance, renin release, and tubular sodium reabsorption. The innervation within mammalian kidneys (intrinsic innervation) has been extensively described in the literature, particularly for rats (Barajas and Muller,

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Section: Discussionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Qualitative and quantitative morphology of renal nerves in C57BL/6J mice

Fazan

Chapleau

et al. 2002

Anat. Rec.

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“…10,11,20 In a recent study, Ling et al demonstrated that MAP and RSNA in ET-1 deficient mice were significantly higher than in wild-type mice in basal conditions. 21 Although the site of this effect of ET is unknown, tissue autoradiographic studies have shown the presence of specific binding sites for ET-1 in the rat and human brain stem involved in cardiovascular regulation, such as the nucleus tracts solitarius and ventrolateral medulla, basal ganglia, and cerebellum. [22][23][24] Furthermore, immunoreactive ET-1 and ET-3, as well as their mRNAs, are present in the central nervous system of the rat.…”

Section: Discussionmentioning

confidence: 99%

Acute Effect of Endothelin AB Antagonist on Sympathetic Outflow in Conscious Rats With Heart Failure.

Tsuchiyama

Kasamatsu

Hano

et al. 2002

Circ J

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ndothelin (ET) is a vasoconstrictor peptide thatgreatly increases the contractility of vascular smooth muscle in pathological and physiological states. 1,2 Recent studies have shown that myocardial and plasma ET concentrations are elevated in congestive heart failure (HF), and increased endogenous ET plays a role in the progression of HF by induction of hypertrophy in cardiomyocytes and left ventricular dilatation. 3 Furthermore, long-term inhibition by the administration of ET A and AB receptor antagonist improves the survival, hemodynamic parameters, and ventricular remodeling in animals with HF. [4][5][6] However, the role of this peptide acting on the autonomic nervous system in HF remains unknown. Sympathoexcitation is well documented in both clinical and experimental HF, and plasma norepinephrine is an entirely independent predictor of mortality in patients with HF. 7-9 It has been reported that exogenous ET promotes sympathetic activation at several loci, including the central nervous system, in the normal animal. 10,11 Thus, it is possible that increased endogenous ET also contributes to this abnormality in HF, and sympathoexcitation via increased ET may be associated with the harmful effect in the progression of HF. However, only 2 studies to our knowledge have shown this phenomenon in the HF state. 12,13 In a recent study, Liu et al Circulation Journal Vol.66, September 2002 showed that the chronic dual ET-1 blockade, L-754, 142, reduced sympathetic activity and normalized the desensitized arterial baroreflex function in another model of experimental HF induced by pacing in rabbits. 14 We hypothesized that ET blockade also reduces the sympathoexcitation in the HF associated with myocardial infarction (MI) and observed the effects of the ET AB dual antagonist, TAK044, on sympathetic outflow and arterial baroreflex sensitivity (BRS) in a conscious rat model of this condition. Methods SubjectsAll procedures were in accordance with institutional guidelines for animal research. Male Wistar rats (n=14, 8 weeks old) were used as the experimental subjects. MI rats were produced by left coronary artery ligation, using techniques similar to those described previously, under intraperitoneal sodium pentobarbital anesthesia. 5 Rats with autopsy-proven transmural MI of the left ventricle were designated as MI rats. The rats were allowed access to their respective drinking water and standard rat chow ad libitum. We used 7 rats with MI at autopsy and elevated left ventricular (LV) end-diastolic pressure (EDP) ≥10 mmHg as models of HF (n=7). We also prepared 7 sham-operated rats (Sham) to compare all data with the HF group. Shams received left side open chest surgery without coronary ligation. All experiments were carried out 6 weeks after ligation. Although ET-1 antagonists have been beneficial in the treatment of heart failure (HF), their involvement in the effect on the sympathetic nervous system in HF remains unknown. The present study investigated the role of endogenous endothelin (ET) in the sympathetic nervou...

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“…7 This hypertensive state may be caused by the adaptation of the ET-1 (ϩ/Ϫ) KO mouse through enhanced central and/or peripheral sympathetic influences on the cardiovascular function. 8 Whether the same hypertensive state as in ET-1 (ϩ/Ϫ) KO occurs after heterozygous knock-out of ET A or ET B receptors remains to be reported.In the present study, we have therefore explored whether a partial defect in endothelin receptors, as in heterozygous ET A or ET B KO mice, would be sufficient to induce significant phenotypic alterations in the cardiovascular pharmacology of exogenous and endogenous ET-1. However, it was first required to fully identify the respective contribution of the ET A and/or ET B receptors in the vasoactive effects of endothelins in the WT littermates.…”

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confidence: 97%

Heterozygous Knock-Out of ET _B Receptors Induces BQ-123–Sensitive Hypertension in the Mouse

et al. 2000

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Abstract-Homozygous knock-out of ET A or ET B receptor genes results in lethal developmental phenotypes in the mouse. Such deleterious phenotypes do not occur in heterozygous littermates. However, it remains to be determined whether mice partially defective in ET A or ET B receptors display significant alterations in their responses to exogenous or endogenous endothelin-1 (ET-1). Furthermore, the anesthetized ET B (ϩ/Ϫ) knock-out mice showed a significantly higher mean arterial blood pressure than the ET A (ϩ/Ϫ) knock-out or their wild-type littermates. The pressor response to ET-1 but not to a selective ET B agonist, IRL-1620, was significantly reduced in the ET A (ϩ/Ϫ) knock-out mice. In ET B (ϩ/Ϫ) knock-out mice, the pressor effect of IRL-1620 was more markedly altered than those induced by ET- Unlike endothelin receptors, the total deletion of the B 2 receptor for bradykinin or AT-1 receptor subtypes for angiotensin II does not induce short-term lethal effects in these genetically modified animals, 3,4 albeit the former is sensitive to high salt diets. 5 Furthermore, heterozygous knock-out of the B 2 or AT-1 receptor does not significantly affect the vasoactive response to bradykinin or angiotensin II (Ang II), respectively, 5,6 in the murine model. Unexpectedly, the heterozygous knock-out of endothelin-1 (ET-1) induced a paradoxical mild yet significant elevation of basal mean arterial blood pressure (MAP) in these animals when compared with wild-type (WT) congeners. 7 This hypertensive state may be caused by the adaptation of the ET-1 (ϩ/Ϫ) KO mouse through enhanced central and/or peripheral sympathetic influences on the cardiovascular function. 8 Whether the same hypertensive state as in ET-1 (ϩ/Ϫ) KO occurs after heterozygous knock-out of ET A or ET B receptors remains to be reported.In the present study, we have therefore explored whether a partial defect in endothelin receptors, as in heterozygous ET A or ET B KO mice, would be sufficient to induce significant phenotypic alterations in the cardiovascular pharmacology of exogenous and endogenous ET-1. However, it was first required to fully identify the respective contribution of the ET A and/or ET B receptors in the vasoactive effects of endothelins in the WT littermates. We have therefore attempted in this study to characterize the pharmacodynamic characteristics of endothelin in the systemic circulation of the WT mouse by the use of the selective ET A antagonist, BQ-123, 9 the selective ET B agonist, IRL-1620, 10 and antagonist, BQ-788, 11 as well as the mixed ET A /ET B antagonist, SB 209670. 12 We have also attempted to demonstrate the respective contribution of ET A or ET B receptor types as well as that of endogenous ET-1 in the regulation of blood pressure in both strains of anesthetized KO mice.Finally, ET B receptors have been reported to be involved in the clearance of endogenous endothelin. 13 The effect of heterozygous knock-out of the ET B receptor on the clearance of radiolabeled ET-1 has been analyzed in this report. Methods Animals Use...

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Renal sympathetic nerve activity in mice: comparison between mice and rats and between normal and endothelin-1 deficient mice

Cited by 48 publications

References 34 publications

Qualitative and quantitative morphology of renal nerves in C57BL/6J mice

Qualitative and quantitative morphology of renal nerves in C57BL/6J mice

Acute Effect of Endothelin AB Antagonist on Sympathetic Outflow in Conscious Rats With Heart Failure.

Heterozygous Knock-Out of ET _B Receptors Induces BQ-123–Sensitive Hypertension in the Mouse

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Renal sympathetic nerve activity in mice: comparison between mice and rats and between normal and endothelin-1 deficient mice

Cited by 48 publications

References 34 publications

Qualitative and quantitative morphology of renal nerves in C57BL/6J mice

Qualitative and quantitative morphology of renal nerves in C57BL/6J mice

Acute Effect of Endothelin AB Antagonist on Sympathetic Outflow in Conscious Rats With Heart Failure.

Heterozygous Knock-Out of ET B Receptors Induces BQ-123–Sensitive Hypertension in the Mouse

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Heterozygous Knock-Out of ET _B Receptors Induces BQ-123–Sensitive Hypertension in the Mouse