A new method for measurement of blood pressure, heart  rate, and activity in the mouse by radiotelemetry

Mills, Perry; Huetteman, Daniel A.; Brockway, Brian; Zwiers, Lynn M.; Gelsema, A. J.; Schwartz, Robert S.; Krämer, K.

doi:10.1152/jappl.2000.88.5.1537

Cited by 145 publications

(124 citation statements)

References 10 publications

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“…The components of the radiotelemetry system (Transoma Medical, St. Paul, MN), includ-ing the mouse blood pressure telemetry device (TA11PA-C20), are described in ref. 62. Six to 8 days after the kidney transplantation procedure, the pressure catheter was implanted in the left carotid artery as described in ref.…”

Section: Methodsmentioning

confidence: 99%

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Angiotensin II causes hypertension and cardiac hypertrophy through its receptors in the kidney

Crowley

Gurley

Herrera

et al. 2006

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

624

542

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Essential hypertension is a common disease, yet its pathogenesis is not well understood. Altered control of sodium excretion in the kidney may be a key causative feature, but this has been difficult to test experimentally, and recent studies have challenged this hypothesis. Based on the critical role of the renin-angiotensin system (RAS) and the type I (AT 1) angiotensin receptor in essential hypertension, we developed an experimental model to separate AT 1 receptor pools in the kidney from those in all other tissues. Although actions of the RAS in a variety of target organs have the potential to promote high blood pressure and end-organ damage, we show here that angiotensin II causes hypertension primarily through effects on AT 1 receptors in the kidney. We find that renal AT1 receptors are absolutely required for the development of angiotensin II-dependent hypertension and cardiac hypertrophy. When AT 1 receptors are eliminated from the kidney, the residual repertoire of systemic, extrarenal AT1 receptors is not sufficient to induce hypertension or cardiac hypertrophy. Our findings demonstrate the critical role of the kidney in the pathogenesis of hypertension and its cardiovascular complications. Further, they suggest that the major mechanism of action of RAS inhibitors in hypertension is attenuation of angiotensin II effects in the kidney. transgenic mice ͉ kidney transplantation ͉ blood pressure H igh blood pressure (BP) is a highly prevalent disorder, and its complications (including heart disease, stroke, and kidney disease) are a major public health problem (1). Despite decades of scrutiny, the precise pathogenesis of essential hypertension has been difficult to delineate. Guyton and his associates suggested that defective handling of sodium by the kidney and consequent dysregulation of body fluid volumes is a requisite, final common pathway in hypertension pathogenesis (2). The powerful capacity of this pathway to modulate blood pressure is illustrated by the elegant studies of Lifton and associates showing that virtually all of the Mendelian disorders with major impact on blood pressure homeostasis are caused by genetic variants affecting salt and water reabsorption by the distal nephron (3). On the other hand, several recent studies have suggested that primary vascular defects may cause hypertension by impacting peripheral resistance without direct involvement of renal excretory functions (4-7).Among the various regulatory systems that impact blood pressure, the RAS has a key role. Inappropriate activation of the RAS, as in renal artery stenosis, leads to profound hypertension and cardiovascular morbidity (8). Moreover, in patients with essential hypertension who typically lack overt signs of RAS activation, ACE inhibitors and angiotensin receptor blockers (ARBs) effectively reduce blood pressure and ameliorate cardiovascular complications (9-11), suggesting that dysregulation of the RAS contributes to their elevated blood pressure.

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Section: Methodsmentioning

confidence: 99%

“…Blood pressures were measured on unanesthetized, unrestrained animals beginning 7 days after the catheter implantation when the mice had reestablished normal circadian rhythms (63). Telemetry data were collected continuously with sampling every 6 min for 10-s intervals (62).…”

Section: Methodsmentioning

confidence: 99%

Angiotensin II causes hypertension and cardiac hypertrophy through its receptors in the kidney

Crowley

Gurley

Herrera

et al. 2006

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

624

542

View full text Add to dashboard Cite

show abstract

“…Implantable mouse BP transmitters (TA11PA-C20; Data Sciences International, St Paul, MN, USA) were used to directly measure arterial pressure in individual conscious and freely moving mice [28,29]. The mice were anaesthetised and the left carotid artery was isolated.…”

Section: Methodsmentioning

confidence: 99%

Glycogen synthase kinase 3 inhibition improves insulin-stimulated glucose metabolism but not hypertension in high-fat-fed C57BL/6J mice

et al. 2006

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Aims/hypothesis In the current study, the effect of a highly specific peptide inhibitor of glycogen synthase kinase 3 (GSK3) (L803-mts) on glucose metabolism and BP was examined in a high-fat (HF) fed mouse model of diabetes. Methods C57/BL6J mice were placed on an HF diet for 3 months and treated with L803-mts for 20 days, following which glucose metabolism was examined by euglycaemichyperinsulinaemic clamp studies. BP and heart rate were measured by radio-telemetry. Results The HF mice were obese, with impaired glucose tolerance and high plasma insulin and leptin levels. L803-mts treatment significantly reduced the insulin levels and doubled the glucose infusion rate required to maintain a euglycaemic condition in the HF+L803-mts group compared with the HF group. Insulin failed to suppress the endogenous glucose production rate in the HF group while decreasing it by 75% in the HF+L803-mts group, accompanied by increased liver glycogen synthase activity and net hepatic glycogen synthesis. GSK3 inhibition also reduced peripheral insulin resistance. Plasma glucose disappearance rate increased by 60% in the HF+L803-mts group compared with the HF group. In addition, glucose uptake in heart and gastrocnemius muscle was markedly improved. Although mean arterial pressure increased following the HF diet, it did not change significantly during the 12 days of L803-mts treatment. Conclusions/interpretation These studies demonstrate that GSK3 inhibition improved hepatic and peripheral insulin resistance in a mouse model of HF-induced diabetes, but it failed to have an effect on BP. GSK3 may represent an important therapeutic target for insulin resistance.

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“…23 Briefly, mice were anesthetized with 2% to 3% isoflurane, and body temperature was maintained at 36°C to 37°C with an isothermal pad (Braintree Scientific, Inc). After antiseptic preparation, the left carotid artery was isolated, and the lumen was cut to allow insertion of the transmitter catheter to the point of bifurcation.…”

Section: Surgerymentioning

confidence: 99%

Norepinephrine Transporter–Deficient Mice Exhibit Excessive Tachycardia and Elevated Blood Pressure With Wakefulness and Activity

et al. 2004

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Background-Norepinephrine (NE) is a primary neurotransmitter of central autonomic regulation and sympathetic nerve conduction, and the norepinephrine transporter (NET) is crucial in limiting catecholaminergic signaling. NET is sensitive to antidepressants, cocaine, and amphetamine. NET blockade often is associated with cardiovascular side effects, and NET deficiency is linked to tachycardia in familial orthostatic intolerance. Methods and Results-We telemetrically monitored NET-deficient (NET Ϫ/Ϫ ) mice to determine the cardiovascular effects of reduced NE reuptake. Mean arterial pressure was elevated in resting NET Ϫ/Ϫ mice compared with NET ϩ/ϩ controls (103Ϯ0.6 versus 99Ϯ0.4 mm Hg; PϽ0.01), and corresponding pressures increased to 122Ϯ0.3 and 116Ϯ0.3 mm Hg (PϽ0.0001) with activity. Heart rate was also greater in resting NET Ϫ/Ϫ mice (565Ϯ5 versus 551Ϯ3 bpm; PϽ0.05), and genotypic differences were highly significant during the active phase (640Ϯ5 versus 607Ϯ3 bpm; PϽ0.0001). Conversely, the respiratory rate of resting NET Ϫ/Ϫ mice was dramatically reduced, whereas increases after the day/night shift surpassed those of controls. Plasma catecholamines in NET Ϫ/Ϫ and NET ϩ/ϩ mice were as follows: NE, 69Ϯ8 and 32Ϯ7; dihydroxyphenylglycol, 2ϩ0.4 and 17Ϯ3; epinephrine, 15Ϯ3 and 4Ϯ0.6; and dopamine, 13Ϯ4 and 4Ϯ1 pmol/mL. Catechols in urine, brain, and heart also were determined. Conclusions-Resting mean arterial pressure and heart rate are maintained at nearly normal levels in NET-deficient mice, most likely as a result of increased central sympathoinhibition. However, sympathetic activation with wakefulness and activity apparently overwhelms central modulation, amplifying peripheral catecholaminergic signaling, particularly in the heart.

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A new method for measurement of blood pressure, heart rate, and activity in the mouse by radiotelemetry

Cited by 145 publications

References 10 publications

Angiotensin II causes hypertension and cardiac hypertrophy through its receptors in the kidney

Angiotensin II causes hypertension and cardiac hypertrophy through its receptors in the kidney

Glycogen synthase kinase 3 inhibition improves insulin-stimulated glucose metabolism but not hypertension in high-fat-fed C57BL/6J mice

Norepinephrine Transporter–Deficient Mice Exhibit Excessive Tachycardia and Elevated Blood Pressure With Wakefulness and Activity

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