Autoregulation of blood flow in the rat kidney

Arendshorst, WJ; Finn, WF; Cw, Gottschalk

doi:10.1152/ajplegacy.1975.228.1.127

Cited by 109 publications

(50 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the relationship was not linear, and the threshold pressure was 96 mmHg. Meanwhile, it was demonstrated that the lowest RAP at which renal blood flow was autoregulated was approximately 100 mmHg in the anaesthetized rat (11). Thus, the threshold pressure demonstrated in the present study is very close to the lowest perfusion pressure of the renal autoregulatory range, although there are some differences between the anaesthetized and unanaesthetized condition, so that some relationship between renal autoregulatory range and threshold pressure may be considered.…”

supporting

confidence: 65%

Direct Relationship between Renal Arterial Pressure and Plasma Ren n Activity in Conscious Rats

Imagawa

Miyauchi

Satoh

1984

Japanese Journal of Pharmacology

View full text Add to dashboard Cite

supporting

confidence: 65%

Direct Relationship between Renal Arterial Pressure and Plasma Ren n Activity in Conscious Rats

Imagawa

Miyauchi

Satoh

1984

Japanese Journal of Pharmacology

View full text Add to dashboard Cite

“…A blood flow sensor with an inner diameter of 0.6 to 0.8 mm was placed on the renal artery, allowing continuous RBF monitoring by an electromagnetic square wave flow meter (Skalar Medical, Delft, The Netherlands) [18]. Calibration of the flow probe was conducted as described previously [19].…”

Section: Methodsmentioning

confidence: 99%

The impaired renal vasodilator response attributed to endothelium-derived hyperpolarizing factor in streptozotocin - induced diabetic rats is restored by 5-methyltetrahydrofolate

et al. 2000

View full text Add to dashboard Cite

Dysfunction of the endothelium is an early and key event in the development of microvascular and macrovascular complications [1], which account for most of the morbidity and mortality of diabetes. Endothelial integrity is generally assessed by evaluating the vasodilator response of a blood vessel or a vascular bed to an endothelium-dependent agonist [2]. Endothelial cells relax the tone of the underlying vascular smooth muscle cells by releasing a number of vasodi- Diabetologia (2000) Abstract Aims/hypothesis. Endothelial dysfunction contributes to the development of diabetic vascular complications. A better understanding of the pathophysiology of endothelial dysfunction in diabetes could lead to new approaches to prevent microvascular disease. Methods. Endothelium-dependent and endotheliumindependent vasodilator responses were investigated in the renal microcirculation of streptozotocin-induced diabetic rats. We measured renal blood flow changes with an electromagnetic flow probe. In addition, the responses of the different segments of the renal microcirculation were evaluated with videomicroscopy using the hydronephrotic kidney technique. Because endothelial cells release different relaxing factors (nitric oxide, prostacyclin and an unidentified endothelium-derived hyperpolarizing factor), responses to acetylcholine were measured before and after treatment with the nitric oxide synthase inhibitor l-N G -nitroarginine methylester HCI (l-NAME) and the cyclooxygenase inhibitor indomethacin. We evaluated with the effect of 5-methyltetrahydrofolate, the active form of folate, on the responses. Results. The l-NAME-and indomethacin-resistant vasodilation to intra-renal acetylcholine was significantly reduced in the diabetic compared with control rats, suggesting impaired endothelium-derived hyperpolarizing factor-mediated vasodilation. The responses to the nitric oxide donor (Z)-1-[-2-(aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NONOate) and to the K + -channel opener pinacidil were similar in diabetics and controls, indicating intact endothelium-independent vasodilator mechanisms. The contribution of endothelium-derived hyperpolarizing factor to vasodilation induced by acetylcholine was greatest in the smallest arterioles. In diabetic rats, the response to acetylcholine was increasingly impared as vessel size decreased. Defective vasodilation in diabetic kidneys was rapidly normalized by 5-methyltetrahydrofolate. Conclusion-interpretation. Endothelium-derived hyperpolarizing factor-mediated vasodilation is impaired in the renal microcirculation of diabetic rats, in particular in the smallest arteries. Treatment with folate restores the impaired endothelial function in diabetes. [Diabetologia (2000

show abstract

“…The flow probe size was chosen that circumferentially fit closely about the arterial wall by low-power microscopic observation but did not alter urine flow rate. Calibration was conducted according to the method of Arendshorst et al (16 Responses to L-NAME and AG. In separate anesthetized NE-and sham-ARF rats, after baseline RBF measurements were determined, L-NAME (10 mg/kg) was given intravenously over 5 min.…”

Section: Methodsmentioning

confidence: 99%

Increased nitric oxide synthase activity despite lack of response to endothelium-dependent vasodilators in postischemic acute renal failure in rats.

Conger

Robinette²,

Villar³

et al. 1995

J. Clin. Invest.

113

View full text Add to dashboard Cite

Lack of response to endothelium-dependent vasodilators generally has been considered to be evidence for decreased nitric oxide synthase (NOS) activity and NO generation after ischemic or hypoxic injury to vital organs including the kidney. In this study, renal blood flow (RBF) responses to endothelium-dependent vasodilators acetylcholine and bradykinin and the endothelium-independent vasodilator prostacyclin, the nonselective NOS inhibitor L-NAME (without and with L-arginine), the inducible NOS inhibitor aminoguanidine, and the NO-donor sodium nitroprusside were examined in 1-wk norepinephrine-induced (NE) and sham-induced acute renal failure (ARF) rats. Compared with sham-ARF, there was no increase in RBF to intrarenal acetylcholine and bradykinin, but a comparable RBF increase to prostacyclin in NE-ARF kidneys. However, there was a signiflcantiy greater decline in RBF to intravenous L-NAME in NE-than sham-ARF rats (-65±8 vs. -37±5%, P < 0.001) which was completely blocked by prior L-arginine infusion. There was no change in RBF to the inducible NOS specific inhibitor aminoguanidine. Unlike sham-ARF, there was no increase in RBF to intrarenal sodium nitroprusside in NE-ARF. Immunohistochemistry and immunofluorescence detection of constitutive (c) NOS using mouse monoclonal antibody were carried out to positively determine the presence of cNOS in NE-ARF. 90% of renal resistance vessels showed evidence of endothelial cNOS in both sham-and NE-ARF. Taken together, results of these experiments are consistent with the conclusion that NOS/NO activity is, in fact, maximal at baseline in 1-wk NE-ARF and cannot be increased further by exogenous stimuli of NOS activity. The increased NOS is likely of the constitutive form and of endothelial origin. It is suggested that the increased NOS activity Clin. Invest. 1995. 96:631-638.)

show abstract

Autoregulation of blood flow in the rat kidney

Cited by 109 publications

References 0 publications

Direct Relationship between Renal Arterial Pressure and Plasma Ren n Activity in Conscious Rats

Direct Relationship between Renal Arterial Pressure and Plasma Ren n Activity in Conscious Rats

The impaired renal vasodilator response attributed to endothelium-derived hyperpolarizing factor in streptozotocin - induced diabetic rats is restored by 5-methyltetrahydrofolate

Increased nitric oxide synthase activity despite lack of response to endothelium-dependent vasodilators in postischemic acute renal failure in rats.

Contact Info

Product

Resources

About