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  • Author or Editor: Chollada Buranakarl x
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Abstract

Objective—To determine norepinephrine (NE) kinetics in dogs with experimentally induced renal vascular hypertension.

Animals—4 mixed-breed dogs.

Procedure—The study comprised a control and hypertensive period. The hypertensive period followed induction of renal vascular hypertension achieved by surgical placement of clips on both renal arteries to reduce diameter by approximately 80%. Arterial blood pressure, renal clearance, and NE kinetics were measured during each period while dogs were receiving a low-sodium diet. Measurements of NE kinetics and renal clearance during the hypertensive period were made 5 days after induction of hypertension.

Results—Five days after induction of hypertension, arterial blood pressure increased by 15 to 20 mm Hg. Mean (± SEM) plasma NE concentration and NE spillover rate increased significantly from 151.5 ± 14.1 pg/ml and 8.03 ± 0.62 ng/kg/min, respectively, during the control period to 631.4 ± 30.5 pg/ml and 54.0 ± 5.2 ng/kg/min, respectively, during the hypertensive period. Norepinephrine clearance rate also increased (54.0 ± 2.4 vs 86.0 ± 9.3 ml/kg/min). Positive associations between mean arterial pressure (MAP) and NE concentration and spillover rate were detected. However, MAP and NE clearance rate were not associated.

Conclusions and Clinical Relevance—Increased blood pressure during the hypertensive period was likely attributable to increased NE spillover rate, which resulted in a significant increase in plasma NE concentration. Analysis of these results suggests that central sympathetic outflow was increased and may be responsible for the pathogenesis of high blood pressure during the acute phase of renal vascular hypertension in dogs. (Am J Vet Res 2000;61: 1534–1541)

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in American Journal of Veterinary Research

Abstract

Objective—To determine effects of variations in dietary intake of sodium chloride (NaCl) on systemic arterial blood pressure (ABP) in cats with normal and reduced renal function.

Animals—21 adult cats (7 with intact kidneys [control cats; group C], 7 with unilateral renal infarction with contralateral nephrectomy [remnant-kidney model; group RK], and 7 with unilateral renal infarction and contralateral renal wrapping and concurrent oral administration of amlodipine [remnant-wrap model; group WA]).

Procedure—All cats were sequentially fed 3 diets that differed only in NaCl content (50, 100, or 200 mg of Na/kg); each diet was fed for 7 days. The ABP was recorded continuously by radiotelemetry, and renal function (glomerular filtration rate [GFR]) was determined on the sixth day of each feeding period.

Results—Dietary supplementation with NaCl did not affect ABP, but it increased GFR in groups C and WA. The renin-angiotensin-aldosterone axis was activated in groups RK and WA at the lowest NaCl intake, but supplementation with NaCl suppressed this activation in group WA. The lowest NaCl intake was associated with hypokalemia and a high fractional excretion of potassium that decreased in response to supplementation with NaCl. Arterial baroreceptor resetting was evident after chronic hypertension but was not modified by dietary supplementation with NaCl.

Conclusions and Clinical Relevance—Low NaCl intake was associated with inappropriate kaliuresis, reduced GFR, and activation of the renin-angiotensinaldosterone axis without evidence of a beneficial effect on ABP. Therefore, this common dietary maneuver could contribute to hypokalemic nephropathy and progressive renal injury in cats. ( Am J Vet Res 2004;65:620–627)

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in American Journal of Veterinary Research