Abstract
Impaired baroreflex sensitivity in diabetes is well described and has been attributed to autonomic diabetic neuropathy. In the present study conducted on acute (10-20 days) streptozotocin (STZ)-induced diabetic rats we examined: 1) cardiac baroreflex sensitivity, assessed by the slope of the linear regression between phenylephrine- or sodium nitroprusside-induced changes in arterial pressure and reflex changes in heart rate (HR) in conscious rats; 2) aortic baroreceptor function by means of the relationship between systolic arterial pressure and aortic depressor nerve (ADN) activity, in anesthetized rats, and 3) bradycardia produced by electrical stimulation of the vagus nerve or by the iv injection of methacholine in anesthetized animals. Reflex bradycardia (-1.4 +/- 0.1 vs -1.7 +/- 0.1 bpm/mmHg) and tachycardia (-2.1 +/- 0.3 vs -3.0 +/- 0.2 bpm/mmHg) were reduced in the diabetic group. The gain of the ADN activity relationship was similar in control (1.7 +/- 0.1% max/mmHg) and diabetic (1.5 +/- 0.1% max/mmHg) animals. The HR response to vagal nerve stimulation with 16, 32 and 64 Hz was 13, 16 and 14% higher, respectively, than the response of STZ-treated rats. The HR response to increasing doses of methacholine was also higher in the diabetic group compared to control animals. Our results confirm the baroreflex dysfunction detected in previous studies on short-term diabetic rats. Moreover, the normal baroreceptor function and the altered HR responses to vagal stimulation or methacholine injection suggest that the efferent limb of the baroreflex is mainly responsible for baroreflex dysfunction in this model of diabetes.
Highlights
Autonomic neuropathy is the most serious complication of diabetes in terms of morbidity and mortality [1]
In the present investigation we examined the baroreflex control of heart rate (HR) in rats with short-term diabetes induced by STZ, as well as the aortic baroreceptor function and the HR response to vagal stimulation or muscarinic agonist injections
The reflex bradycardia elicited by phenylephrine (-1.4 ± 0.1 vs -1.7 ± 0.1 bpm/ mmHg; P = 0.03) as well as the reflex tachycardia elicited by sodium nitroprusside (-2.1 ± 0.3 vs -3.0 ± 0.2 bpm/mmHg; P = 0.02) were significantly reduced in the diabetic group as indicated by the slope of the linear regression relating changes in HR to changes in mean arterial pressure (MAP) (Figure 1)
Summary
Autonomic neuropathy is the most serious complication of diabetes in terms of morbidity and mortality [1]. It has been frequently reported that diabetes can affect both somatic (mainly sensitive) and autonomic nerves. The arterial baroreceptors are an important system that acts against wide oscillations in arterial pressure (AP), acting on both the sympathetic and parasympathetic limbs of the autonomic nervous system [2,3]. A number of studies have dealt with cardiac baroreflex function in humans [4], as well as in experimental diabetes [5,6]. Most studies point to baroreflex dysfunction, it is
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
