Blood pressure and heart rate can be determined in conscious mice by one of three methods. These methods include the determination of blood pressure and heart rate in conscious freely roving mice (radiotelemetry via a chronic indwelling arterial catheter, Data Sciences International, Inc), chronic indwelling carotid catheters that require tethering the mice, (17, 18, 19) or by tail cuff (Visitech tail cuff set ups are available). Each approach provides unique advantages and problems. Telemetry is the most accurate, but it requires an operative procedure, whereas tail cuff determination is non-invasive. In contrast the tail cuff is more dependent on mouse training and only provides systolic blood pressure accurately. The tethered approach is particularly useful if chronic intravenous infusions need to be performed.
Blood pressure measurements > Literature Section
Publications for Blood pressure measurements (3)
Ichihara S, Senbonmatsu T, Price E Jr, Ichiki T, Gaffney FA, Inagami T. Angiotensin II type 2 receptor is essential for left ventricular
hypertrophy and cardiac fibrosis in chronic angiotensin II-induced
hypertension. Circulation (2001) 104:346-51
View abstract View in PubMed
BACKGROUND: The roles of angiotensin II (Ang II) in the regulation of heart function under normal and pathological conditions have been well documented. Although 2 types of Ang II receptor (AT(1) and AT(2)) are found in various proportions, most studies have focused on AT(1)-coupled events. In the present study, we examined the hypothesis that signaling by AT(2) is important to the development of left ventricular hypertrophy and cardiac fibrosis by Ang II infusion in mice lacking the AT(2) gene (Agtr2-/Y). METHODS AND RESULTS: Male Agtr2-/Y and age-matched wild-type (WT) mice were treated long-term with Ang II, infused at a rate of 4.2 ng. kg(-1). min(-1) for 3 weeks. Ang II elevated systolic blood pressure to comparable levels in Agtr2-/Y and WT mice. WT mice developed prominent concentric cardiac hypertrophy, prominent fibrosis, and impaired diastolic relaxation after Ang II infusion. In contrast, there was no cardiac hypertrophy in Agtr2-/Y mice. Agtr2-/Y mice, however, did not show signs of heart failure or impairment of ventricular relaxation and only negligible fibrosis after Ang II infusion. The absence of fibrosis may be a clue to the absence of impairment in ventricular relaxation and account for the normal left ventricular systolic and diastolic performances in Agtr2-/Y mice. CONCLUSIONS: Chronic loss of AT(2) by gene targeting abolished left ventricular hypertrophy and cardiac fibrosis in mice with Ang II-induced hypertension.
Senbonmatsu T, Ichihara S, Price E Jr, Gaffney FA, Inagami T. Evidence for angiotensin II type 2 receptor-mediated cardiac myocyte
enlargement during in vivo pressure overload. J Clin Invest (2000) 106:R25-9
View abstract View in PubMed
The pathophysiological roles of the angiotensin II type 2 receptor (AT(2)) in cardiac hypertrophy remain unclear. By the targeted deletion of mouse AT(2) we were able to prevent the left ventricular hypertrophy resulting from pressure overload, while cardiac contractile functions remained normal. This implies that AT(2) is a mediator of cardiac hypertrophy in response to increased blood pressure. The effects of AT(2) deletion were independent of activation of embryonic genes for cardiac hypertrophy. However, p70(S6k), one of the key factors in cardiac hypertrophy, was markedly and specifically reduced in the ventricles of Agtr2(-)/Y mice. We propose that p70(S6k) plays a major role in AT(2)-mediated ventricular hypertrophy. This article may have been published online in advance of the print edition. The date of publication is available from the JCI website, http://www.jci.org.
This study describes a technique for the direct daily measurement of arterial blood pressure, sampling of arterial blood, and continuous intravenous infusion in free-moving, conscious, Swiss-Webster mice. Catheters were chronically implanted in the femoral artery and vein, tunneled subcutaneously, exteriorized at the back of the neck in a lightweight tethering spring, and attached to a swivel device at the top of the cage. Time-control experiments (n = 8) demonstrated stable values of mean arterial pressure (MAP, 116 +/1 mmHg) and heart rate (HR, 627 +/21 beats/min) for up to 35 days after catheter implantation. It was further observed that restraining mice (n = 7) increased MAP by 10 +/3 mmHg and HR by 78 +/8 beats/min from the values observed under free-moving conditions. To demonstrate the chronic use of the venous catheter, intravenous infusion of NG-nitro-L-arginine methyl ester (L-NAME, 8.6 mg.kg-1.day-1, n = 6) for 5 days significantly increased MAP from 117 +/4 to 131 +/4 mmHg without altering HR. In a final group of mice (n = 5), oral L-arginine (2% in drinking water) increased plasma arginine concentration from 90 +/7 to 131 +/17 microM and prevented L-NAME hypertension. These experiments illustrate the feasibility of long-term intravenous infusion, direct arterial blood pressure measurements, and arterial blood sampling in conscious mice.
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Last updated on 2007-02-06 Moderated by Jimmy Hao