Tail-cuff blood pressure measurement without external preheating in awake rats.

Buñag, Ruben D.; Butterfield, James L.

doi:10.1161/01.hyp.4.6.898

Cited by 212 publications

(93 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Systolic arterial BP was monitored by a tail cuff sphygmomanometer using an automated system with a photoelectric sensor (IITC; Life Sciences, Woodland Hills, CA) that has been shown to closely correlate with intraarterial measurement of BP (15). All rats were preconditioned for this machine at least two times before the actual measurement of BP.…”

Section: Systolic Bp Uric Acid Proteinuria and Renal Functionmentioning

confidence: 99%

A Role for Uric Acid in the Progression of Renal Disease

Kang

Nakagawa²,

Li³

et al. 2002

Journal of the American Society of Nephrology

1,177

770

View full text Add to dashboard Cite

Abstract. Hyperuricemia is associated with renal disease, but it is usually considered a marker of renal dysfunction rather than a risk factor for progression. Recent studies have reported that mild hyperuricemia in normal rats induced by the uricase inhibitor, oxonic acid (OA), results in hypertension, intrarenal vascular disease, and renal injury. This led to the hypothesis that uric acid may contribute to progressive renal disease. To examine the effect of hyperuricemia on renal disease progression, rats were fed 2% OA for 6 wk after 5/6 remnant kidney (RK) surgery with or without the xanthine oxidase inhibitor, allopurinol, or the uricosuric agent, benziodarone. Renal function and histologic studies were performed at 6 wk. Given observations that uric acid induces vascular disease, the effect of uric acid on vascular smooth muscle cells in culture was also examined. RK rats developed transient hyperuricemia (2.7 mg/dl at week 2), but then levels returned to baseline by week 6 (1.4 mg/dl). In contrast, RKϩOA rats developed higher and more persistent hyperuricemia (6 wk, 3.2 mg/dl). Hyperuricemic rats demonstrated higher BP, greater proteinuria, and higher serum creatinine than RK rats. Hyperuricemic RK rats had more renal hypertrophy and greater glomerulosclerosis (24.2 Ϯ 2.5 versus 17.5 Ϯ 3.4%; P Ͻ 0.05) and interstitial fibrosis (1.89 Ϯ 0.45 versus 1.52 Ϯ 0.47; P Ͻ 0.05). Hyperuricemic rats developed vascular disease consisting of thickening of the preglomerular arteries with smooth muscle cell proliferation; these changes were significantly more severe than a historical RK group with similar BP. Allopurinol significantly reduced uric acid levels and blocked the renal functional and histologic changes. Benziodarone reduced uric acid levels less effectively and only partially improved BP and renal function, with minimal effect on the vascular changes. To better understand the mechanism for the vascular disease, the expression of COX-2 and renin were examined. Hyperuricemic rats showed increased renal renin and COX-2 expression, the latter especially in preglomerular arterial vessels. In in vitro studies, cultured vascular smooth muscle cells incubated with uric acid also generated COX-2 with time-dependent proliferation, which was prevented by either a COX-2 or TXA-2 receptor inhihbitor. Hyperuricemia accelerates renal progression in the RK model via a mechanism linked to high systemic BP and COX-2-mediated, thromboxane-induced vascular disease. These studies provide direct evidence that uric acid may be a true mediator of renal disease and progression.

show abstract

Section: Systolic Bp Uric Acid Proteinuria and Renal Functionmentioning

confidence: 99%

A Role for Uric Acid in the Progression of Renal Disease

Kang

Nakagawa²,

Li³

et al. 2002

Journal of the American Society of Nephrology

1,177

770

View full text Add to dashboard Cite

show abstract

“…The tail-cuff method, without external preheating, was used to measure the systolic blood pressure. 12 Ambient temperature was kept at 30° C. The equipment used included magnetic animal holders connected with manual scanner (model 65-12, IITC, Inc., Woodland Hills, California), pulse amplifier (model 59, IITC, Inc.), and dual-channel recorder (model 1202, Linear Instrs. Corp., Reno, Nevada).…”

Section: Blood Pressure Measurementmentioning

confidence: 99%

Somatostatin inhibition of fructose-induced hypertension.

1989

View full text Add to dashboard Cite

The role of insulin resistance and byperinsulinemia in the etiology of fructose-induced hypertension was studied in male Sprague-Dawley rats. Rats consumed a fructose-enriched diet (containing 66% of total calories as fructose) for 11 days and were infused continuously during the last 7 days with either a somatostatin analogue or vehicle. At the end of this period, rats receiving the somatostatin analogue had a lower plasma insulin concentration (52±4 vs. 70±6 /iunits/ml, /><0.01) and a lower blood pressure (133±2 vs. 150±2 mm Hg) than did the rats infused with the control solution. In addition, the increase in plasma triglyceride concentration in response to the fructose-enriched diet was significantly attenuated (p<0.001) in the rats infused with somatostatin. These data provide further support that the increase in blood pressure that occurs when normal rats are fed a high fructose diet is dependent on the ability of this intervention to cause insulin resistance and hyperinsulinemia. and the hyperinsulinemia appears to be associated with resistance to insulin-stimulated glucose uptake.5 ' 6 Sprague-Dawley rats become insulin resistant, hyperinsulinemic, and hypertrigryceridemic when fed a fructose-enriched diet, 7 -8 and the fact that this dietary manipulation also leads to an increase in blood pressure 8 lends further support to the possibility that insulin resistance and hyperinsulinemia may play a role in the genesis of high blood pressure. Furthermore, we have shown that exercise training of rats, which enhances insulin sensitivity 9 and reduces fructose-induced hyperinsulinemia, 10 also attenuates the increase in blood pressure seen in fructose-fed rats. 11The present experiments were initiated to further study the relation between insulin-resistance, hyperinsulinemia, and hypertension in fructosefed rats and were based on the use of somatostatin Received September 1, 1988; accepted February 14, 1989. to suppress insulin secretion by /3 cells in pancreatic islets. We reasoned that the infusion of somatostatin would suppress the hyperinsulinemia that normally results when rats are fed a fructoseenriched diet, 7 -8 -10 ' 11 and if elevated plasma insulin concentrations play a role in fructose-induced hypertension, this intervention would also ameliorate the rise in blood pressure that occurs when rats eat a high fructose diet. The results indicated that this prediction was borne out, providing further support for the view that insulin plays a role in the regulation of blood pressure in rats with fructose-induced hypertension. Materials and Methods General ProtocolMale Sprague-Dawley rats (Simonsen Laboratories, Gilroy, California), initially weighing 160-180 g, were used for all experiments. Before dietary manipulation, all rats were fed standard rat chow (Wayne Lab Blox, Allied Mills, Chicago, Illinois) containing 60% vegetable starch, 11% fat, and 29% protein and were maintained on a 12-hour light/dark (6:00 AM-6:00 PM) cycle. In addition, rats were acclimated to the procedure of blood pressure measure...

show abstract

“…The tail-cuff method, without external preheating, was used to measure the systolic blood pressure. 10 Ambient temperature was kept at 30 °C. The equipment used included magnetic animal holders, connected with manual scanner (Model 65-12, IITC, Woodland Hills, CA, USA), pulse amplifier (Model 59, IITC), and dual-channel recorder (Model 1202, Linear Instruments, Reno, NV, USA).…”

Section: Blood Pressure Measurementmentioning

confidence: 99%

Attenuation of fructose-induced hypertension in rats by exercise training.

Reaven¹,

Ho²,

Hoffman³

1988

Hypertension

141

View full text Add to dashboard Cite

SUMMARY This study was initiated to see if the insulin resistance, hyperinsulinemia, and hypertension that follow feeding nonnotensive Sprague-Dawley rats a fructose-rich diet could be prevented by letting rats run spontaneously in exercise wheel cages. Blood pressure in sedentary rats increased from (mean ± SEM) 125 ± 2 to 148 ± 3 mm Hg in response to 2 weeks of a high fructose diet, and this increment was significantly (p < 0.001) attenuated in exercising rats (from 121 ± 1 to 131 ± 2 mm Hg). In addition, mean (±SEM) plasma insulin concentration was lower in fructose-fed rats allowed to run spontaneously (44 ± 2 vs 62 ± 5 /xU/ml; p < 0.01). Finally, resistance to insulin-stimulated glucose uptake was assessed by determining the steady state plasma glucose response to a continuous glucose and exogenous Insulin infusion during a period in which endogenous insulin secretion was suppressed. The results of these studies indicated that the mean ( ± SEM) steady state plasma glucose concentration was significantly lower in the exercise-trained rats (127 ± 5 vs 168 ± 6 mg/dl; p < 0.001), despite tbe fact that the steady state plasma insulin levels were also lower in rats allowed to run spontaneously (75 ± 4 vs 90 ± 5 ftU/ml; p < 0.05). Thus, the ability of exercise-trained rats to stimulate glucose disposal was enhanced as compared with that of sedentary rats fed the same fructose-rich diet. These data demonstrate that the insulin resistance, hyperinsulinemia, and hypertension produced hi nonnotensive rats by feeding them a high fructose diet can be attenuated if rats are allowed to run spontaneously. I N a previous report we found that hypertension can be produced by feeding a high fructose diet to normal rats.1 Fructose-fed rats also develop resistance to insulin-stimulated glucose uptake and hyperinsulinemia, 1 -3 phenomena that have recently been identified as occurring in patients with hypertension.4 -7 Based on these findings, we raised the possibility that the changes in insulin action and concentration noted in fructose-fed rats with hypertension may play a role in the pathogenesis of the elevated blood pressure seen in this situation. In this context, we have previously demonstrated that insulin-stimulated glucose uptake is enhanced in exercise-trained rats 8 and that the hyperinsulinemia associated with feeding rats a high fructose diet is attenuated if rats are allowed to run spontaneously. 9Thus, in the present report, we tested the hypothesis that insulin resistance and hyperinsulinemia are involved in the development of hypertension in fructose-fed rats by comparing the effects of fructoserich diets on both insulin metabolism and blood pressure in sedentary rats with those seen in rats allowed to exercise spontaneously in running wheels. Materials and Methods General ProtocolMale Sprague-Dawley rats (Harlan, Indianapolis, IN, USA) were used for all experiments. The rats were approximately 6 weeks old and weighed approximately 150 g when the study was started. Prior to any manipulation of diet or level of ...

show abstract

Tail-cuff blood pressure measurement without external preheating in awake rats.

Cited by 212 publications

References 18 publications

A Role for Uric Acid in the Progression of Renal Disease

A Role for Uric Acid in the Progression of Renal Disease

Somatostatin inhibition of fructose-induced hypertension.

Attenuation of fructose-induced hypertension in rats by exercise training.

Contact Info

Product

Resources

About