Autoregulation of renal blood flow in two-kidney, one-clip hypertensive rats

Iversen, Bjarne M.; Heyeraas, Karin J.; Sekse, Ingegjerd; Andersen, Knut-Jan; Ofstad, J.

doi:10.1152/ajprenal.1986.251.2.f245

Cited by 22 publications

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“…In agreement with previous findings, 12 weeks after clipping, the clipped kidney contained a higher level of renin mRNA than the nonclipped kidney, as shown previously. 14 In addition, TTA treatment had no effect on the renin mRNA level in the nonclipped kidney, but markedly reduced this level in the clipped kidney. This was accompanied by reduced plasma renin activity and a strong tendency to decrease the plasma angiotensin II level by TTA.…”

Section: Discussionmentioning

confidence: 96%

Prevention of Hypertension and Organ Damage in 2-Kidney, 1-Clip Rats by Tetradecylthioacetic Acid

et al. 2006

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Abstract-Dietary lipids are reported to affect the blood pressure in both humans and experimental animal models with hypertension. In the present study, 2-kidney, 1-clip (2K1C) hypertensive rats were treated with the modified fatty acid tetradecylthioacetic acid (TTA) from the time of clipping or after hypertension was established. TTA treatment attenuated the development of hypertension and reduced established 2K1C hypertension. The mRNA level of renin in the clipped kidney and the plasma renin activity were markedly reduced, and the plasma angiotensin II level tended to decrease after TTA treatment. In addition, TTA reduced the mRNA level of angiotensinogen in white adipose tissue.Prevention of organ damage was demonstrated by normal urinary excretion of protein, maintained serum albumin, lower heart weight, and clearly reduced vascular, glomerular, and tubulointerstitial damage in the nonclipped kidney. Renal function was not affected as estimated by unchanged plasma creatinine. Furthermore, the serum levels of triacylglycerol and cholesterol were reduced by TTA. The serum fatty acid composition was changed, resulting in a favorable increase of oleic acid. However, the levels of all of the omega-3 fatty acids and of linoleic acid were reduced, and no change was seen in the level of arachidonic acid, but the urinary excretion of 8-iso-prostaglandin F2␣ was declined. In conclusion, TTA attenuated the development of hypertension, reduced established hypertension, and prevented the development of organ damage in 2K1C rats, possibly by reducing the amounts of the vasoconstrictors angiotensin II and 8-iso-prostaglandin F2␣ and by inducing a favorable increase of oleic acid in serum. Key Words: renin-angiotensin system Ⅲ renal disease Ⅲ fatty acids E levated blood pressure is closely related to increase in cardiovascular death from events like stroke, myocardial infarction, and chronic renal failure 1 and is defined as one of the risk factors for the metabolic syndrome. 2,3 Other risk factors include insulin resistance, hyperglycemia, and elevated serum triacylglycerol, which are conditions that are improved in rats after treatment with the modified fatty acid tetradecylthioacetic acid (TTA). 4 The pleiotropic effects of TTA seem to be mediated through both peroxisome proliferator-activated receptor (PPAR)-dependent and PPAR-independent mechanism 4 and include changes in the fatty acid composition of both liver and serum in rats. [5][6][7] Based on these potential possibilities to change composition of the metabolic system, and because the fatty acid composition of cholesteryl ester and phospholipids in serum has been related to the blood pressure level in humans, 8 -10 we examined the effect of TTA on hypertension in the present study.An inducible model of high blood pressure is the 2-kidney, 1-clip (2K1C) hypertension model, where the increased blood pressure is induced after clipping of one renal artery. This is an angiotensin II-dependent model of hypertension with increased level of plasma renin and angioten...

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Section: Discussionmentioning

confidence: 96%

Prevention of Hypertension and Organ Damage in 2-Kidney, 1-Clip Rats by Tetradecylthioacetic Acid

et al. 2006

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“…Ang II-mediated (see References 1,[28][29][30]. Increased vascular reactivity to other vasoconstrictors or increased levels of an unidentified vasoconstrictor are possible reasons for this decrease in conductance.…”

Section: Figure 5 Bar Graphs Showing Mean Effects Of Captopril Adminmentioning

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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“…TWO-KIDNEY, ONE-CLIP (2K1C) hypertension is an angiotensin II (ANG II)-dependent model of hypertension, and plasma as well as intrarenal ANG II concentrations are increased (14,15). Removal of the clip is followed by rapid reversal of high blood pressure with normalization of renin values (14,15).…”

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confidence: 99%

“…Removal of the clip is followed by rapid reversal of high blood pressure with normalization of renin values (14,15). ANG II mediates its effect in the renal vasculature through two main G-coupled receptors, the AT 1 (AT 1 R) and AT 2 receptors, where AT 1 R mediates the vascular constrictor effects of ANG II (2).…”

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confidence: 99%

The renal vascular response to ANG II injection is reduced in the nonclipped kidney of two-kidney, one-clip hypertension

Bivol¹,

Vågnes²,

Iversen³

2005

American Journal of Physiology-Renal Physiology

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1R) level in the nonclipped kidney of twokidney, one-clip hypertension (2K1C) has shown to be unchanged despite a high circulating angiotensin (ANG) II level. To examine the vasoreactive response to ANG II in this kidney, injections of ANG II into renal artery were performed 6 wk after clipping of the kidney and compared with normotensive controls. The renal blood flow (RBF) response to 2.5 ng ANG II was measured by a Transonic transit-time flowmeter, before and after indomethacin and candesartan treatment, and analyzed by a computer program. The RBF response to 5 ng arginine-vasopressin (AVP) was examined for comparison with ANG II. The mRNA for AT 1A and AT1B as well as Western blotting for AT 1R in renal resistance vessels were determined, and plasma renin activity (PRA) was measured. Systolic blood pressure was 183 Ϯ 4 mmHg in 2K1C rats compared with 113 Ϯ 1 mmHg in controls (P Ͻ 0.001). PRA was significantly increased in 2K1C animals (P Ͻ 0.05). Injection of ANG II reduced RBF with 10 Ϯ 2% in the nonclipped kidney and 24 Ϯ 3% in controls (P Ͻ 0.001). After indomethacin, the RBF response increased from 10 Ϯ 2 to 20 Ϯ 3% (P Ͻ 0.02) in 2K1C rats and from 24 Ϯ 3 to 34 Ϯ 6% in controls (P Ͻ 0.01). The doses of candesartan needed to completely inhibit RBF response to ANG II were 30 g/kg in the nonclipped kidney and 100 g/kg in controls (P Ͻ 0.001). Western blotting and mRNA for AT 1A and AT1B in the nonclipped kidney were similar to the controls. The results indicate that despite no difference in total AT 1R levels, functional AT1R is downregulated in the nonclipped kidney of 2K1C rats. plasma renin activity; AT 1 receptor; renal blood flow; blood pressure TWO-KIDNEY, ONE-CLIP (2K1C) hypertension is an angiotensin II (ANG II)-dependent model of hypertension, and plasma as well as intrarenal ANG II concentrations are increased (14, 15). Removal of the clip is followed by rapid reversal of high blood pressure with normalization of renin values (14, 15). ANG II mediates its effect in the renal vasculature through two main G-coupled receptors, the AT 1 (AT 1 R) and AT 2 receptors, where AT 1 R mediates the vascular constrictor effects of ANG II (2). The rat has two types of AT 1 receptors, the AT 1A and AT 1B receptors (AT 1A and AT 1B ), which have 95% homology in their receptor amino acid sequences (16). The AT 2 receptor has only 34% homology with the AT 1 R and is expressed at a low level, particularly in the renal vasculature (7).The AT 1A receptor plays an essential role in the development of 2K1C hypertension, as knockout mice lacking this receptor do not develop hypertension (3). Usually AT 1A is downregulated when the ANG II levels are high, as during a low-salt diet, and upregulated when ANG II levels are low, as in high salt intake (25). In the nonclipped kidney, reports indicate that the modulation of the AT 1 R is different from controls and this seems also to be the case during long-term infusion of ANG II (13). The data concerning regulation of the AT 1 R in the nonclipped kidney are, however, contro...

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Autoregulation of renal blood flow in two-kidney, one-clip hypertensive rats

Cited by 22 publications

References 0 publications

Prevention of Hypertension and Organ Damage in 2-Kidney, 1-Clip Rats by Tetradecylthioacetic Acid

Prevention of Hypertension and Organ Damage in 2-Kidney, 1-Clip Rats by Tetradecylthioacetic Acid

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

The renal vascular response to ANG II injection is reduced in the nonclipped kidney of two-kidney, one-clip hypertension

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