Glomerular actions of ANG II during reduction of renal artery pressure: a morphometric analysis

Anderson, Warwick P.; Alcorn, Daine; Gilchrist, A.I.; Whiting, Jennifer M.; Ryan, Graeme B.

doi:10.1152/ajprenal.1989.256.6.f1021

Cited by 5 publications

(6 citation statements)

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“…The conductance then remained near this level for the remainder of the experiment (for example, it averaged 20.1 ±5.4% below mean prestenosis values on days 21-25 [ Figure l];/?<0.01). In the sham-stenosis group, total peripheral conductance did not change significantly (+1.3±13.5%, NS from pre-sham-stenosis values on days [21][22][23][24][25].…”

Section: Responses To Left Renal Artery Stenosismentioning

confidence: 94%

Development of hypertension from unilateral renal artery stenosis in conscious dogs.

1990

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The renal and systemic changes after stenosis of the left renal artery (n=S) or sham stenosis (n=6) in conscious dogs were studied sequentially over 25 days. Stenosis produced a prompt rise in arterial pressure, which was at all times due to reduced peripheral vascular conductance, with no increase in cardiac output despite initial evidence of mild fluid retention. The decrease in peripheral conductance was attributable to 1) the stenotic kidney (25% of the total and due to the mechanical effect of the stenosis itself), 2) the nonstenotic kidney (about 15% of the total and not caused by angiotensin II), and 3) the nonrenal vasculature (60%). The decrease in conductance in the nonrenal vasculature was due partly to angiotensin II, but there was also a gradually developing non-angiotensin II component Acute administration of captopril caused significantly greater changes in arterial pressure and peripheral conductance throughout the period of stenosis than before stenosis (and greater than in sham-stenosis dogs), indicating that angiotensin II was constricting the peripheral vasculature even when plasma renin levels were no longer elevated. In the stenotic kidneys, captopril produced a fall in renal vascular resistance, but renal blood flow did not rise because there was an approximately equal rise in the resistance of the stenosis. There was no evidence for a role for the autonomic nervous system in the hypertension, as ganglion blockade (pentolinium) had similar hemodynamic effects before and after stenosis. Thus, the hypertension was due at all times to reduced peripheral conductance, with the two kidneys responsible for 40% of this reduced conductance. (Hypertension 1990;16:441-451) U nilateral renal artery stenosis produces hypertension in humans and in experimental animals, including rats (see Reference 1), sheep, 2 and dogs, 3 " 5 provided that the stenosis is severe enough. 4 Evidence from previous experiments suggests that both the renin-angiotensin system and the autonomic nervous system are involved in the development of this two-kidney, one clip (2K 1C) form of hypertension. 8 However, gaining a complete understanding of the early stages of the hypertension has been complicated by the fact that stenosis has, with very few exceptions, been induced during surgery in anesthetized animals. Surgery itself disturbs the renin-angiotensin system, autonomic reflexes, and body fluid homeostasis, 9 the very factors thought to be involved in the initiation and development of hypertension.We recently published a comprehensive analysis of the hemodynamic events involved in the first hour of Received October 11, 1989; accepted in revised form May 25, 1990. this form of renal hypertension in conscious dogs. 10This showed that the initial rise in arterial pressure was due entirely to decreased peripheral vascular conductance (increased resistance) and, remarkably, that the kidneys themselves were responsible for almost half of this fall in conductance. In the case of the stenotic kidney, its conductance was reduced...

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Section: Responses To Left Renal Artery Stenosismentioning

confidence: 94%

Development of hypertension from unilateral renal artery stenosis in conscious dogs.

1990

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“…, 2001). In dogs with reduced kidney perfusion following renal artery stenosis, angiotensin II caused the contraction of mesangial cells, but did not change the glomerular ultrafiltration surface area (Anderson et al. , 1989).…”

Section: Role Of Raas In the Progression Of Renal Diseasesmentioning

confidence: 99%

“…Renal proteases are indeed inactivated by plasminogen activator inhibitor type 1, the production of which is increased by angiotensin II (Wolf, 1998;Mezzano et al, 2001). In dogs with reduced kidney perfusion following renal artery stenosis, angiotensin II caused the contraction of mesangial cells, but did not change the glomerular ultrafiltration surface area (Anderson et al, 1989). The glomeruli nevertheless were examined morphometrically after renal ablation, which may explain that glomerular structures may not have retained their in vivo dimensions.…”

Section: Role Of Raas In the Progression Of Renal Diseasesmentioning

confidence: 99%

Angiotensin‐converting enzyme inhibitors in the therapy of renal diseases

Lefebvre

Toutain

2004

Vet Pharm & Therapeutics

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Renal diseases, especially chronic renal failure (CRF), are common in canine and feline medicine. The renin-angiotensin-aldosterone system (RAAS) plays a pivotal role in these conditions in the development of renal lesions and the progression of kidney dysfunction. Angiotensin-converting enzyme inhibitors (ACEI) are currently considered as the most efficient agents in therapeutic strategies. The benefit of an ACEI treatment can be explained by at least three mechanisms: ACEI limit systemic and glomerular capillary hypertension, have an antiproteinuric effect, and retard the development of glomerulosclerosis and tubulointerstitial lesions. These effects have been studied in dogs and cats, and there is now some evidence to support the recommendation of ACEI therapy in dogs and cats with CRF. Nevertheless the prescription of ACEI in such patients should take into account the potential influence of renal impairment on ACEI disposition, and adverse effects on the renal function itself (especially hypotension and acute reductions in glomerular filtration rate). The risk of drug interaction with diuretics, nonsteroidal anti-inflammatory drugs and anesthetics, should not be overestimated. Furthermore, hypotension may occur in patients on a low sodium diet.

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“…P values for differences between cortical regions (P Region ) and for the effects of increasing dose of ANG II (P Dose ) were derived from F(45,2) and the interaction between cortical region and increasing dose of ANG II (P Region‫ء‬Dose ) was derived from F (30,1). P values for differences between arteriole (P Arteriole ) and for the effects of increasing dose of ANG II (P Dose ) were derived from F (30,2) and the interaction between arteriole and increasing dose of ANG II (P Arteriole‫ء‬Dose ) was derived from F (30,2). than their efferent counterparts (P Ͻ 0.001), but for juxtamedullary glomeruli, efferent and afferent arterioles were similar in size (P ϭ 0.62).…”

Section: Vessel Luminal Diameters and Calculated Relative Resistancesmentioning

confidence: 99%

Effects of angiotensin II on regional afferent and efferent arteriole dimensions and the glomerular pole

Denton

Anderson

Sinniah

2000

American Journal of Physiology-Regulatory, Integrative and Comp

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The diversity of renal arteriole diameters in different cortical regions has important consequences for control of glomerular capillary pressure. We examined whether intrarenal angiotensin II (ANG II; 0.1, 1, or 5 ng. kg(-1). min(-1)) in anesthetized rabbits acts preferentially on pre- or postglomerular vessels using vascular casting. ANG II produced dose-related reductions in afferent and efferent diameters in the outer, mid, and inner cortex, without effecting arterial pressure. Afferent diameter decreased more than efferent in the outer and mid cortex (P < 0.05) but by a similar extent in juxtamedullary nephrons (P = 0.58). Calculated efferent resistance increased more than afferent, especially in the outer cortex (127 vs. 24 units; 5 ng. kg(-1). min(-1) ANG II). ANG II produced significant dose-related increases in the distance between the arterioles at the entrance to the glomerular pole in all regions. Thus afferent diameter decreased more in response to ANG II, but efferent resistance rose more due to smaller resting luminal dimensions. The results also indicate that glomerular pole dimensions change in response to ANG II.

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Glomerular actions of ANG II during reduction of renal artery pressure: a morphometric analysis

Cited by 5 publications

References 0 publications

Development of hypertension from unilateral renal artery stenosis in conscious dogs.

Development of hypertension from unilateral renal artery stenosis in conscious dogs.

Angiotensin‐converting enzyme inhibitors in the therapy of renal diseases

Effects of angiotensin II on regional afferent and efferent arteriole dimensions and the glomerular pole

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