Separate renal function studies in conscious dogs with renovascular hypertension

DeForrest, Jack M.; Davis, James O.; Freeman, R. H.; Watkins, Barry E.; Stephens, Gregory A.

doi:10.1152/ajprenal.1978.235.4.f310

Cited by 15 publications

(13 citation statements)

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“…In mildly hypertensive conscious dogs, the rise in GFR of the undipped kidney usually takes 2-3 weeks. 72 In this species, the rise in RPF never achieves statistical significance. Nevertheless, RPF and GFR tend to normalize in both kidneys by 3-4 weeks, although at 4 weeks in anesthetized rats, reduced GFR results from a fall in the clipped kidney and no rise in the undipped kidney.…”

Section: Reno-renal Reflex In Goldblatt Hypertensionmentioning

confidence: 93%

Pathophysiology of renovascular hypertension.

1991

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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

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Section: Reno-renal Reflex In Goldblatt Hypertensionmentioning

confidence: 93%

Pathophysiology of renovascular hypertension.

1991

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“…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.…”

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confidence: 99%

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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“…An increased urinary flow from the contralateral kidney was observed over a short period after renal artery stenosis by Galvez et al [15]. Also, DeForrest and co-workers studied separate renal functions in the two-kidney, one-clip hypertension model in dogs [16]. The renal plasma flow, glomerular filtration rate, and sodium and water excretion decreased in the kidney with the stenosed renal artery, whereas these parameters of renal functions increased in the contralateral kidney.…”

Section: Resultsmentioning

confidence: 96%

Time Course Study of Body Fluid Volumes in Two-Kidney, One-Clip and One-Kidney, One-Clip Hypertension in Rats

Yagi

Ichikawa

Sakamaki

et al. 1987

J. Clin. Biochem. Nutr.

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SummaryTime related changes in distributions of body fluid volumes were studied in rats with either of two types of Goldblatt hypertension; two-kidney, one-clip (2K1C) and one-kidney, one-clip (1K1C) models. Plasma volume (PV), extracellular fluid volume (ECF), and total body water (TBW) were measured on days 1, 7, and 28 after renal artery stenosis. Mean arterial pressure (MAP) and plasma renin activity (PRA) were also determined in conscious rats.In the 2K1C rats each fluid compartment on any experimental day did not differ from the sham controls except for a decrease in PV of the clipped rats on day 1. MAP in the 2K1C increased significantly (p<0.05) only on day 28 as compared with the controls. In the 1 K1 C rats the tendency toward an increase in PV and ECF on early days was followed by a significant (p <0.05) elevation in ECF on day 28. MAP was higher in the clipped rats than in the controls on days 7 and 28. There were no differences in PRA between the clipped rats and the controls either in 2K1C or 1K1C throughout the study.These results suggest that alterations of body fluid volumes might be involved in the development and maintenance of hypertension in the 1K1C rats, but not in the 2K1C ones. In contrast, the role of the reninangiotensin system was rather negligible in these two models, as judged from the PRA levels.

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Separate renal function studies in conscious dogs with renovascular hypertension

Cited by 15 publications

References 0 publications

Pathophysiology of renovascular hypertension.

Pathophysiology of renovascular hypertension.

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

Time Course Study of Body Fluid Volumes in Two-Kidney, One-Clip and One-Kidney, One-Clip Hypertension in Rats

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