Impaired renal blood flow and cortical pressure autoregulation in contralateral kidneys of Goldblatt hypertensive rats.

Ploth, David W.; Roy, Rabindra; Huang, Weimin; Navar, L. Gabriel

doi:10.1161/01.hyp.3.1.67

Cited by 65 publications

(29 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Because of the fall in systemic blood pressure in the absence of renal vasodilatation, there was a fall in glomerular capillary hydraulic pressure, plasma flow rates, and single nephron GFR in the nonclipped kidney. This is in keeping with the impaired autoregulatory control of nonclipped kidneys shown by Ploth et al 57 This suggests that AVP is at least partly responsible for maintenance of high glomerular pressures and flow rates in the nonclipped kidney of Goldblatt animals. Despite this strong evidence, the role of AVP in the regulation of systemic blood pressure in Goldblatt animals remains controversial.…”

Section: Reno-renal Reflex In Goldblatt Hypertensionsupporting

confidence: 82%

Pathophysiology of renovascular hypertension.

1991

View full text Add to dashboard Cite

Renovascular hypertension has its experimental counterpart in the two-kidney, one clip model (Goldblatt hypertension). From the study of this model, a general pathophysiological scheme has evolved suggesting that temporal stages in the development and maintenance of hypertension are regulated by complicated hormonal and neural interrelations. The central roles played by the renin-angiotensin system and the renal nerves is discussed as they relate to other hormones. In addition, the possible contribution of converting enzyme inhibitors to understanding the pathophysiology of this condition is discussed. (Hypertension 1991

show abstract

Section: Reno-renal Reflex In Goldblatt Hypertensionsupporting

confidence: 82%

Pathophysiology of renovascular hypertension.

1991

View full text Add to dashboard Cite

show abstract

“…Sham-operated control rats were prepared and handled identically except for the placement of the silver clip. 5 During the 5-6-week period between clipping and the experimental procedure, rats were fed a commercial rat chow and allowed tap water ad libitum. Systolic pressure was measured in conscious rats by the tail-cuff technique (Harvard Apparatus, South Natick, Massachusetts) two to three times each week.…”

Section: Methodsmentioning

confidence: 99%

Afferent arteriolar responsiveness to altered perfusion pressure in renal hypertension.

et al. 1990

Self Cite

View full text Add to dashboard Cite

The present study was performed to determine the role of afferent arterioles in the impaired autoregulatory response shown to occur in the contralateral kidney of Goldblatt hypertensive rats. The responsiveness of juxtamedullary afferent arterioles to alterations in perfusion pressure was studied in the nonclipped kidney of two-kidney, one clip hypertensive and sham-operated rats. Systolic pressure, 5-6 weeks after clipping, averaged 184±6 mm Hg in the hypertensive rats (n=16) and 121±3 mm Hg in the sham-operated control rats (n=7). By using the in vitro blood-perfused juxtamedullary nephron technique, afferent arterioles were directly visualized, and their inside diameters were measured by videomicroscopic methods. In sham-operated kidneys perfused with blood from normotensive rats, afferent arteriolar diameter averaged 22.8 ±1.8 fim at a renal arterial perfusion pressure of 151±1 mm Hg and increased to 24.8±1.8 fim when perfusion pressure was reduced to 110±2 mm Hg. Conversely, in hypertensive kidneys perfused with blood from either hypertensive or normotensive rats, the afferent arterioles failed to vasodilate and actually exhibited a slight decrease in diameter from 24.6 ±1.3 to 23.0 ±2.3 fim in response to the same reduction in perfusion pressure. Vasodilator capability, however, could be demonstrated in response to verapamil and sodium nitroprusside, which increased afferent diameter in both the sham-operated and hypertensive groups of rats. Thus, unlike arterioles from normotensive rats, juxtamedullary afferent arterioles from two-kidney, one clip Goldblatt hypertensive rats fail to vasodilate after a reduction in perfusion pressure. This impaired autoregulatory ability might result from an intrinsic functional defect in the vasculature of the high pressure contralateral kidney. (Hypertension 1990;15:748-752)

show abstract

“…27 Control animals (sham) were submitted to the same surgical procedure without partial renal artery occlusion. Anesthesia was reversed with atipamezole (1 mg/kg).…”

Section: Renovascular Hypertension Modelmentioning

confidence: 99%

Kidney-Induced Hypertension Depends on Superoxide Signaling in the Rostral Ventrolateral Medulla

et al. 2010

View full text Add to dashboard Cite

Abstract-Reactive oxygen species in peripheral cardiovascular tissues are implicated in the pathogenesis of 2 kidney-1 clip hypertension. We recently identified an imbalance between reactive oxygen species generation and oxidant scavenging in the rostral ventrolateral medulla (RVLM) of 2 kidney-1 clip in rats. We tested whether enhanced superoxide signaling in RVLM of 2 kidney-1 clip rats contributes to the chronic hypertension via sympathetic activation in conscious rats. We enhanced superoxide scavenging in RVLM by overexpressing cytoplasmically targeted superoxide dismutase using an adenoviral vector (Ad-CMV-CuZnSOD) in Wistar rats (male, 150 to 180 g) in which the left renal artery was occluded partially 3 weeks earlier. Hypertension was documented using radiotelemetry recording of arterial pressure in conscious rats for 6 weeks. Renovascular hypertension elevated both serine phosphorylation of p47phox subunit of NADPH and superoxide levels in RVLM. The elevated superoxide levels were normalized by expression of CuZnSOD in RVLM. Moreover, the hypertension produced in the 2 kidney-1 clip rats was reversed 1 week after viral-mediated expression of CuZnSOD. This antihypertensive effect was maintained and associated with a decrease in the low-frequency spectra of systolic blood pressure variability, suggesting reduced sympathetic vasomotor tone. The expression of CuZnSOD was localized to RVLM neurons, of which some contained tyrosine hydroxylase. None of the above variables changed in control rats receiving Ad-CMV-eGFP in RVLM. In Goldblatt hypertension, superoxide signaling in the RVLM plays a major role in the generation of sympathetic vasomotor tone and the chronic sustained hypertension in this animal model. (Hypertension. 2010;56:290-296.)Key Words: hypertension Ⅲ renal Ⅲ blood pressure Ⅲ heart rate Ⅲ brain Ⅲ free radicals I nvolvement of oxidative stress in the pathology of arterial hypertension was reported in various animal models, including the renovascular 2 kidney-1 clip (2K-1C), 1-3 the 1 kidney-1 clip, 4 angiotensin II (Ang II)-induced hypertension, [5][6][7] Dahl salt-sensitive (desoxycorticosterone acetate-salt) hypertension, 8 spontaneously hypertensive rats (SHRs), 9,10 and strokeprone SHRs. 11,12 In addition, oxidative stress also plays an important role in humans with renovascular hypertension 13 and essential hypertension. 14 From these studies it is clear that oxidative stress acts at the level of the vascular wall but also within the brain. The renin-angiotensin-aldosterone system plays a major role in the 2K-1C model. 15 Ang II stimulates superoxide (O 2 ⅐Ϫ ) radical generation by increasing the activity of NADPH oxidase within peripheral blood vessel walls. 16 -18 However, there is evidence that reactive oxygen species (ROS) in the brain are involved in neuronal signaling, contributing to sympathoexcitation and hypertension. 12,19 Intracerebroventricular infusion of an NADPH oxidase inhibitor antagonizes both the increase in renal sympathetic nerve activity and pressor response ind...

show abstract

Impaired renal blood flow and cortical pressure autoregulation in contralateral kidneys of Goldblatt hypertensive rats.

Cited by 65 publications

References 27 publications

Pathophysiology of renovascular hypertension.

Pathophysiology of renovascular hypertension.

Afferent arteriolar responsiveness to altered perfusion pressure in renal hypertension.

Kidney-Induced Hypertension Depends on Superoxide Signaling in the Rostral Ventrolateral Medulla

Contact Info

Product

Resources

About