Why the study?
Does short-term experimental diabetes alter blood pressure and heart rate responses to norepinephrine and angiotensin II in conscious rats?
Does short-term experimental diabetes alter blood pressure and heart rate responses to norepinephrine and angiotensin II in conscious rats?
Short-term experimental diabetes in rats leads to hypotension, bradycardia, and depressed vascular responsiveness to norepinephrine and angiotensin II.
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Hypothesis-generating for early autonomic and vascular changes in diabetes; does not support changes in clinical practice.
Hypertension, atherosclerosis, arteriosclerosis, and cardiomyopathy account for 80% of all diabetic deaths. A paucity of data exists concerning reactivity of the diabetic vasculature to vasopressor substances. The purpose of this investigation was to determine the influence of short-term (4-5 weeks) diabetes on the responsiveness of the cardiovascular system to vasopressor substances in the intact conscious rat. Diabetes was chemically induced with streptozotocin (65 mg/kg i.v.) in 42-43-days-old, nonfasted, male Sprague-Dawley--derived rats. Direct blood pressure and heart rate were recorded, and responses to the vasopressor agonists norepinephrine and angiotensin II were obtained. Short-term diabetic rats were hypotensive and had lower heart rates when compared with control rats. Blood pressure responses to norepinephrine and angiotensin II were depressed in the short-term diabetic rat; however, the baroreceptor reflexes in these rats were more sensitive to increases in blood pressure. Therefore, it appears that there is some type of nonspecific alteration in the responsiveness of the cardiovascular system to the vasopressor agonists in the short-term diabetic rat.
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Jackson et al. (1983) studied this question.
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