Control of renal hemodynamics in hyperglycemia: possible role of tubuloglomerular feedback

Woods, L. L.; Mizelle, H. L.; Hall, John E.

doi:10.1152/ajprenal.1987.252.1.f65

Cited by 61 publications

(62 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The maximal decrease in bp was seen with combination treatment. The increase in systolic bp in diabetes mellitus could be related to the stimulatory effect of hyperglycaemia on the RAS [36,37,38] or generation of oxygen radical species reducing the availability of nitric oxide [39]. A normalisation of systemic bp in nonselective ET-1 blockade in diabetic rats is described [40].…”

Section: Discussionmentioning

confidence: 99%

ACE-inhibition is superior to endothelin A receptor blockade in preventing abnormal capillary supply and fibrosis of the heart in experimental diabetes

et al. 2004

View full text Add to dashboard Cite

Aims/hypothesis. There is little information whether cardiac capillary supply is deranged in diabetes. Hyperglycaemia is a potent stimulus for endothelin-1 (ET-1) production. We therefore hypothesised that increased ET-1 production in Streptozotocin-induced Type 1 diabetes causes abnormalities of cardiac capillaries and the aorta. To this end we compared the effects of an ET receptor A blocker (ET A -RB) with that of an ACE-inhibitor (ACE-i) or their combination in rats with Streptozotocin (STZ) diabetes. Methods. Sprague Dawley rats were injected with 65 mg STZ i.v. and subsequently developed diabetes. Rats were left untreated or received daily either the ACE-i Trandolapril, the ET A -RB Darusentan or a combination of both. After 6 months the experiment was terminated and the heart and the aorta were investigated using quantitative morphological techniques. Results. ACE-i but not ET A -RB lowered blood pressure in STZ Type 1 diabetic rats. Capillary length density was lower in untreated STZ diabetic rats (2932±128 mm/mm 3 ) compared to non-diabetic control rats (3410±252 mm/mm 3 ). Treatment with ACE-i (3568±431 mm/mm 3 ), but not with ET A -RB (2893±192 mm/mm 3 ), prevented the decrease in capillary supply. Volume density of the myocardial interstitium was higher in untreated STZ diabetic rats (0.86±0.04%) compared to non-diabetic control rats (0.36±0.06%). In all three intervention groups the values were lower (ACE-i: 0.53±0.05%, ET A -RB: 0.7±0.08% and combination: 0.69±0.1). Conclusion/interpretation. Our study identifies a capillary defect of the heart in STZ diabetes, i.e. decreased capillary supply. This abnormality was reversed by ACE-i, but not by ET A -R blockade. A similar trend, although not complete normalisation, was seen in cardiac fibrosis. [Diabetologia (2004) 47:316-324]

show abstract

Section: Discussionmentioning

confidence: 99%

ACE-inhibition is superior to endothelin A receptor blockade in preventing abnormal capillary supply and fibrosis of the heart in experimental diabetes

et al. 2004

View full text Add to dashboard Cite

show abstract

“…In fact, it is highly likely that other mechanisms are operative to at least some extent. For example, acute intrarenal hyperglycemia has been shown to increase renin secretion due to stimulation of proximal tubular sodium reabsorption (46). Thus the sympathetic nervous system was required for the progressive increase in PRA, and that action seemed to account for most of the blood pressure effect of adrenergic blockade.…”

Section: Discussionmentioning

confidence: 99%

Hypertension inl-NAME-treated diabetic rats depends on an intact sympathetic nervous system

Fitzgerald

Brands

2002

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Fitzgerald, Sharyn M., and Michael W. Brands. Hypertension in L-NAME-treated diabetic rats depends on an intact sympathetic nervous system. Am J Physiol Regulatory Integrative Comp Physiol 282: R1070-R1076, 2002. First published November 23, 2001 10.1152/ajpregu.00468. 2001.-We demonstrated previously that induction of diabetes in rats that were treated chronically with the nitric oxide synthase inhibitor N G -nitro-L-arginine methyl ester (L-NAME) causes a severe, progressive increase in mean arterial pressure. This study tested the role of the sympathetic nervous system in that response. Rats were instrumented with chronic artery and vein catheters and assigned randomly to four diabetic groups pretreated with vehicle (D), L-NAME (DϩL), the ␣1-and ␤-adrenergic receptor antagonists terazosin and propranolol (DϩB), or L-NAME, terazosin, and propranolol (DϩLB). After baseline measurements were taken, rats were pretreated; 6 days later, streptozotocin was administered and 3 wk of diabetes ensued. DϩL rats had a marked, progressive increase in arterial pressure that by day 20 was ϳ60 mmHg greater than in D rats. The pressor response to L-NAME was significantly attenuated in diabetic rats cotreated with adrenergic blockers. During week 1 of diabetes, plasma renin activity (PRA) increased and then returned to control levels in D rats. PRA increased progressively in DϩL rats, and chronic adrenergic receptor blockade restored the biphasic renin response in DϩLB rats. These results suggest that the sympathetic nervous system may be involved in the hypertensive response to onset of diabetes in L-NAME-treated rats, possibly through control of renin secretion. nitric oxide; mean arterial pressure; glucose; angiotensin II; glomerular filtration rate; N G -nitro-L-arginine methyl ester DIABETES GENERALLY IS ASSOCIATED with an impairment in endothelial function (10,34,35,37,43). The long-term consequences of this impairment have not been well established, but it may play an important role in the accelerated atherosclerosis and increased prevalence of cardiovascular disease that is observed in diabetic populations (45a). Also unclear is what role the endothelium and its vasoactive hormones play in circulatory homeostasis early in diabetes before significant impairment develops (4,20,34,44). We demonstrated recently (15) that the induction of diabetes in the absence of a functional nitric oxide (NO) system causes a severe, progressive increase in mean arterial pressure (MAP). This finding suggests that there may be increased dependence on NO in the early stages of diabetes such that NO is essential to prevent hypertension from developing. This is consistent with reports (10, 31) that NO production is increased during the early stages of diabetes.The mechanism for this potentiating interaction on blood pressure between induction of diabetes and chronic NO synthesis inhibition is not known, but a role for the renin-angiotensin system was implicated by the finding of increased plasma renin activity (PRA) in the rats in our study ...

show abstract

“…It has been suggested that tubuloglomerular feedback may be altered by hyperglycemia (23)(24)(25). The (26).…”

Section: Discussionmentioning

confidence: 99%

Control of glomerular hypertension by insulin administration in diabetic rats.

Scholey¹,

Meyer²

1989

J. Clin. Invest.

View full text Add to dashboard Cite

Micropuncture studies were performed in Munich Wistar rats made diabetic with streptozotocin and in normal control rats. Diabetic rats received daily ultralente insulin to maintain moderate hyperglycemia (-300 mg/dl). Group 1 diabetic rats studied after routine micropuncture preparation exhibited elevation of the single nephron glomerular filtration rate (SNGFR) due to increases in the glomerular transcapillary hydraulic pressure difference and glomerular plasma flow rate. In group 2 diabetic rats infusion of insulin to achieve acute blood glucose control normalized the glomerular transcapillary pressure gradient while increasing the glomerular ultrafiltration coefficient, so that SNGFR remained elevated. Persistent elevation of SNGFR despite normalization of the transcapillary pressure gradient was also observed in group 3 diabetic rats infused with insulin plus sufficient dextrose to maintain hyperglycemia. These studies indicate that glomerular capillary hypertension in diabetes is an acutely reversible consequence of insulin deficiency and not the result of renal hypertrophy.

show abstract

Control of renal hemodynamics in hyperglycemia: possible role of tubuloglomerular feedback

Cited by 61 publications

References 0 publications

ACE-inhibition is superior to endothelin A receptor blockade in preventing abnormal capillary supply and fibrosis of the heart in experimental diabetes

ACE-inhibition is superior to endothelin A receptor blockade in preventing abnormal capillary supply and fibrosis of the heart in experimental diabetes

Hypertension inl-NAME-treated diabetic rats depends on an intact sympathetic nervous system

Control of glomerular hypertension by insulin administration in diabetic rats.

Contact Info

Product

Resources

About