Measurement of sympathetic nerve activity in the unanesthetized rat

Flückiger, Jean-Pierre; Gremaud, G.; Waeber, Bernard; Kulik, Alexander; Ichino, A.; Nussberger, Jürg; Brunner, H R

doi:10.1152/jappl.1989.67.1.250

Cited by 20 publications

(10 citation statements)

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“…The skin incision was closed, and mice were allowed to recover for 3 hr. After placing them in Plexiglas tubes for 30 min to partially restrict their movements, the arterial line was connected to a pressure transducer, and mean arterial blood pressure was recorded with a computerized data-acquisition system as described (17). Phenylephrine (Sigma) and norepinephrine (Sigma) were dissolved in saline, and increasing doses were administered in a volume of 100 l at 15-20 min intervals to allow blood pressure and heart rate to return to baseline values.…”

Section: Methodsmentioning

confidence: 99%

Decreased blood pressure response in mice deficient of the α _1b -adrenergic receptor

Lattion

Hummler

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

276

222

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To investigate the functional role of different ␣ 1 -adrenergic receptor (␣ 1 -AR) subtypes in vivo, we have applied a gene targeting approach to create a mouse model lacking the ␣ 1b -AR (␣ 1b ؊͞؊). Reverse transcription-PCR and ligand binding studies were combined to elucidate the expression of the ␣ 1 -AR subtypes in various tissues of ␣ 1b ؉͞؉ and ؊͞؊ mice. Total ␣ 1 -AR sites were decreased by 98% in liver, 74% in heart, and 42% in cerebral cortex of the ␣ 1b ؊͞؊ as compared with ؉͞؉ mice. Because of the large decrease of ␣ 1 -AR in the heart and the loss of the ␣ 1b -AR mRNA in the aorta of the ␣ 1b ؊͞؊ mice, the in vivo blood pressure and in vitro aorta contractile responses to ␣ 1 -agonists were investigated in ␣ 1b ؉͞؉ and ؊͞؊ mice. Our findings provide strong evidence that the ␣ 1b -AR is a mediator of the blood pressure and the aorta contractile responses induced by ␣ 1 agonists. This was demonstrated by the finding that the mean arterial blood pressure response to phenylephrine was decreased by 45% in ␣ 1b ؊͞؊ as compared with ؉͞؉ mice. In addition, phenylephrine-induced contractions of aortic rings also were decreased by 25% in ␣ 1b ؊͞؊ mice. The ␣ 1b -AR knockout mouse model provides a potentially useful tool to elucidate the functional specificity of different ␣ 1 -AR subtypes, to better understand the effects of adrenergic drugs, and to investigate the multiple mechanisms involved in the control of blood pressure.

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Section: Methodsmentioning

confidence: 99%

Decreased blood pressure response in mice deficient of the α _1b -adrenergic receptor

Lattion

Hummler

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

276

222

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“…Intra-arterial pressure and heart rate were monitored as described previously by using a computerized data acquisition system. 16 The internal diameter (ID) of the left common carotid artery was measured simultaneously by using an A-mode ultrasonic echo-tracking device (Diarad, Asulab). This device, which has a precision close to 1 fim, has been used in humans and animals.…”

Section: Methodsmentioning

confidence: 99%

Long-term nitric oxide synthase inhibition and distensibility of carotid artery in intact rats.

et al. 1994

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The goal of the present study was to evaluate the effect of long-term nitric oxide synthase inhibition by Af G -nitro-L-arginine-methyl ester (L-NAME) on the morphology and viscoelastic properties of the carotid arteries in rats. Twelveweek-old Wistar-Kyoto rats were treated for 6 weeks with either the nitric oxide synthase inhibitor L-NAME (0.4 g/L in drinking water; L-NAME rats, n=13) or tap water (control rats, n=13). Age-matched spontaneously hypertensive rats (SHR, n=14) received tap water for the same period. The internal diameter of the common carotid artery was measured continuously with an echo-tracking device with the rats under anesthesia with halothane. Intra-arterial pressure was monitored on the contralateral side. L-NAME rats exhibited arterial pressures similar to those of SHR. The distensibility pressure-curve determined in L-NAME rats was a direct T he close correlation between vascular structure and blood pressure is well known, 1 and there is strong evidence that blood pressure plays a major role in vascular remodeling, 2 but growth factors might also be involved.3 At the level of conductance arteries, a striking increase in arterial distensibility and compliance has been reported in hypertensive animals 46 and humans 5 ' 7 -10 compared with normotensive counterparts. In the presence of increased wall thickness, increased distensibility can be achieved only through concurrent changes in composition or organization of the arterial wall.11 Recently the endothelium has been recognized to play a pivotal role in the regulation of vascular tone, 12 but it is still unknown whether it also has an impact on the mechanical properties of the arterial wall.The aim of the present study was to investigate whether the production of nitric oxide (NO) by the endothelium has an influence on the viscoelastic properties of the arteries. For this purpose we treated Wistar-Kyoto (WKY) rats for 6 weeks with the NO synthase inhibitor N -nitro-L-arginine-methyl ester (L-NAME), which produced sustained hypertension. These animals were compared not only with normotensive WKY rats (controls) but also with age-matched spontaneously hypertensive rats (SHR) displaying the same degree of hypertension as L-NAME-treated rats (L-NAME rats). The distensibility-pressure curve of the common carotid artery was established in intact Correspondence to Dr Bernard Waeber, Division of Hypertension, CHUV, CH-1011 Lausanne, Switzerland.continuation of that obtained in control rats. In contrast the distensibility in SHR was increased (P<.01, SHR versus L-NAME rats). Carotid artery cross-sectional area and left ventricular weight index were increased similarly in SHR and L-NAME rats compared with control rats. Thus the hypertension caused by long-term nitric oxide synthesis inhibition was not associated with the increased arterial distensibility observed in SHR despite similar blood pressure elevations, similar arterial hypertrophy, and consequently similar wall stress. This suggests a role for nitric oxide in regulating the mech...

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“…On the day of the experiment, the rats were placed in a Plexiglas tube to continuously record intra-arterial pressure and heart rate with the use of a data acquisition system. 24 After an initial 1-hour period in which hemodynamic parameters reached baseline values, blood pressure was measured for 10 minutes. The animals were then killed with an overdose of methohexital sodium.…”

Section: Measurement Of Blood Pressurementioning

confidence: 99%

Aortic Connexin43 Is Decreased During Hypertension Induced by Inhibition of Nitric Oxide Synthase

Haefliger

Meda

Formenton

et al. 1999

ATVB

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Abstract-Connexin43 (Cx43), the predominant gap junction protein in vessels and heart, is involved in the control of cell-to-cell communication and is thought to modulate the contractility of the vascular wall and the electrical coupling of cardiac myocytes. We have investigated the effects of arterial hypertension induced by inhibition of nitric oxide synthase on the expression of Cx43 in aorta and heart as well as on the distensibility of the carotid artery. Administration of 0.4 g/L N G -nitro-L-arginine methyl ester (L-NAME) to rats in their drinking water for 4 weeks increased intra-arterial mean blood pressure, wall thickness of aorta and carotid artery (25%), and heart weight (17%). Analysis of heart mRNA demonstrated increased expression of the fetal skeletal ␣-actin and of atrial natriuretic peptide but not of Cx43. In contrast, Cx43 mRNA and protein were decreased by 50% in the aortas of L-NAME-treated rats that did not show increased carotid distensibility. Because these data contrasted with those obtained in the 2-kidney, 1 clip model of rat hypertension, which is characterized by increased arterial distensibility and Cx43 expression in aorta, we investigated by Western blot analysis the posttranslational modifications of Cx43. We found that Cx43 was more phosphorylated in the aorta of 2-kidney, 1 clip rats than in that of L-NAME or control rats, which indicated a differential regulation of Cx43 in different models of hypertension. The data suggest that the cell-to-cell communication mediated by Cx43 channels may help regulate the elasticity of the vascular wall. Key Words: connexin Ⅲ aorta Ⅲ heart Ⅲ elasticity Ⅲ hypertension Ⅲ nitric oxide G ap junctions comprise specialized channels that represent 1 pathway by which vertebrate cells communicate 1 and ensure the electrical and mechanical coupling of different types of muscle cells. 2,3 In vessels, gap junctions provide a pathway to modulate the contractile activity of smooth muscle cells. 4 -9 In the myocardium, junctional coupling ensures the same function and is also implicated in the propagation and synchronization of electrical activity. 10 Characterization of the proteins that form gap junctions is expected to provide insights on the possible involvement of junctional channels during cardiac and arterial hypertrophy associated with hypertension. [11][12][13] We have recently shown that in 2 hypertensive rat models that feature a comparable degree of hypertension, as a result of either the clipping of 1 renal artery or of a DOCA-salt treatment, increased levels of Cx43 were associated with a marked hypertrophy of smooth muscle cells in the aortic wall. 11,12 Under these conditions, the isobaric distensibility of the carotid has been shown to increase because of a reduced elastic modulus that corresponds to a reduction of wall material stiffness. 14,15 These biomechanical changes are not observed in another rat model in which a degree of hypertension similar to that observed in the 2-kidney, 1 clip (2K-1C) and the DOCA-salt models can be induced...

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Measurement of sympathetic nerve activity in the unanesthetized rat

Cited by 20 publications

References 0 publications

Decreased blood pressure response in mice deficient of the α _1b -adrenergic receptor

Decreased blood pressure response in mice deficient of the α _1b -adrenergic receptor

Long-term nitric oxide synthase inhibition and distensibility of carotid artery in intact rats.

Aortic Connexin43 Is Decreased During Hypertension Induced by Inhibition of Nitric Oxide Synthase

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Measurement of sympathetic nerve activity in the unanesthetized rat

Cited by 20 publications

References 0 publications

Decreased blood pressure response in mice deficient of the α 1b -adrenergic receptor

Decreased blood pressure response in mice deficient of the α 1b -adrenergic receptor

Long-term nitric oxide synthase inhibition and distensibility of carotid artery in intact rats.

Aortic Connexin43 Is Decreased During Hypertension Induced by Inhibition of Nitric Oxide Synthase

Contact Info

Product

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Decreased blood pressure response in mice deficient of the α _1b -adrenergic receptor

Decreased blood pressure response in mice deficient of the α _1b -adrenergic receptor