Regional distribution of vascular resistance in two models of experimental renovascular hypertension

Flohr, H.; Breull, W.; Dahners, H. W.; Redel, D. A.; Conradi, Henk Jan; Stoepel, K.

doi:10.1007/bf00583642

Cited by 21 publications

(17 citation statements)

References 22 publications

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“…PAGE, 1965;LEDINGHAM and PELLING, 1967;FERRARIO and PAGE, 1974;TERANISHI and IRIUCHIJIMA, 1983). Elevation of vascular resistance is not uniformly distributed over the whole body, but it is especially marked at the superior mesenteric area in two-kidney hypertensive rats (FLOHR et al, 1976;TERANISHI and IRIUCHIJIMA, 1985) and in the renal area in one-kidney hypertenslve rats (TERANISHI and IRIUCHIJIMA, 1988). As shown in Table 3, a similar finding was again observed in the present study.…”

Section: Discussionsupporting

confidence: 90%

Acute effects of captopril on blood pressure and regional blood flows in two types of renovascular hypertensive rats in conscious state.

1988

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Mean arterial pressure and three regional blood flows-renal, superior mesenteric, and hindquarter flows-were monitored in conscious normotensive control rats (NCR), in two-kidney, one-clip (two-kidney), and in one-kidney, one-clip (one-kidney) hypertensive rats. After administering captopril, an angiotensin-converting enzyme inhibitor, mean arterial pressure decreased in all three groups. However, lowering of arterial pressure was not statistically significant in any of the groups. Renal flow increased significantly in the intact artery of two-kidney hypertensive rats, whereas it did not significantly increase in the clipped artery of one-kidney hypertensive rats and in the intact artery of NCR. Superior mesenteric flow increased significantly only in one-kidney hypertensive rats. Hindquarter flow did not significantly change in the three groups. Regional resistance reduced significantly in not only renal but also in superior mesenteric vascular area in two-kidney hypertensive rats, whereas it did not reduce significantly in these two vascular areas in one-kidney hypertensive rats and in NCR. The present findings show that the reninangiotensin-mediated vasoconstriction plays a role in not only renal but also in superior mesenteric vascular area in two-kidney hypertensive rats, whereas it hardly plays a role in these three vascular beds in one-kidney hypertensive rats.

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Section: Discussionsupporting

confidence: 90%

Acute effects of captopril on blood pressure and regional blood flows in two types of renovascular hypertensive rats in conscious state.

1988

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“…In rats with one-clip, one-kidney renovascular hypertension, by a radioactive particle distribution technique under light ether anesthesia, FLOHR et al (1976) have observed an increase in vascular resistance in skeletal muscle to be higher than that of total peripheral resistance, as we did in SHR. However, such a special involvement of skeletal muscle blood vessels was not observed by BRALET et al (1973) in conscious two-clip renovascular and collodion hypertensive rats by the 86Rb distribution method .…”

Section: Discussionsupporting

confidence: 70%

Regional blood flow in conscious spontaneously hypertensive rats.

Iriuchijima

1983

Jpn.J.Physiol

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In spontaneously hypertensive and normal control rats in the conscious state, blood flow was observed in the carotid artery, superior mesenteric artery, renal artery, and terminal aorta with a chronically implanted electromagnetic flow probe. At rest, flow per body weight was not different between the two groups except at the terminal aorta where it was significantly smaller in hypertensive rats (P<0.05).Regional peripheral resistance was higher in hypertensive rats than in normal rats in all the four arteries, but its elevation in the former was not uniform but most marked in the hindquarter area supplied by the terminal aorta. Quantitatively, this area was estimated to contribute about 40% of the total conductance decrease in hypertensive rats in comparison with the control. This suggests the importance of elevation of resistance in muscle blood vessels in hypertension. The contributions from the superior mesenteric area and the bilateral kidneys were estimated to be about 15 % each. In the transposition response induced by transposing rats from their home cage to a new cage, the increase in hindquarter flow was significantly greater in hypertensive rats than in normal rats (P<0.01).The sum of the mean flows of the four arteries, a measure of cardiac output, was not different between hypertensive and normal rats at rest but greater in the former during transposition response. Elevation of arterial pressure in the response in hypertensive rats but not in the normal rats was ascribable largely to a greater increase in cardiac output in the former than the latter.

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“…The technique for calibration of the flow meter has been described previously. 18 Mechanical zero flow was checked by momentarily occluding the renal artery in every experiment. The kidney surface was superfused continuously with warm (38° C) isotonic saline from the tip of a quartz rod light conductor.…”

Section: Control Ratsmentioning

confidence: 99%

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

Ploth¹,

Roy²,

Huang³

et al. 1981

Hypertension

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SUMMARY Experiments were conducted on two-kidney, one clip renal vascular hypertensive rats to assess the ability of the kidney contralateral to renal vascular stenosis to autoregulate renal blood flow (RBF), glomerular filtration rate (GFR), and hydrostatic pressures in cortical structures during conditions of acutely reduced renal arterial blood pressure (BP). When observed at their respective, spontaneous BPs, RBF and GFR were not different in the contralateral kidneys of the hypertensive rats (n = 11) compared to normal animals (n = 7). However, the contralateral kidneys exhibited a significantly higher renal vascular resistance (RVR), 28.9 ± 2.8 mm Hg • min/ml than the control animals, 23.1 ± 1.5 mm Hg • min/ml. At spontaneous BP (169 ± 5 mm Hg), urine flow, absolute and fractional sodium excretion, and absolute and fractional potassium excretion were all significantly greater in the contralateral kidneys of hypertensive rats than in kidneys of normal rats. Hydrostatic pressures in cortical structures were similar in the two groups. When BP was reduced acutely, the kidney comralateral to the renal artery stenosis achieved only small decreases in RVR that failed to allow RBF, GFR, or cortical pressures to be maintained. In contrast, normal rats efficiently autoregulated RBF and GFR. In addition, hydrostatic pressures in proximal tubules, distal tubules, and first order peritubular capillaries were maintained during reductions in BP to as low as 100 mm Hg. Urine flow and electrolyte excretion decreased to a greater extent in the hypertensive kidneys, such that at comparable BP these indices of excretory function were not different in the two groups. These observations indicate that the capacity of the contralateral kidney to maintain hemodynamic and glomerular function at reduced BP is compromised severely and suggest the possibility that the impaired autoregulatory capability may contribute to the maintenance of hypertension observed in this model.

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Regional distribution of vascular resistance in two models of experimental renovascular hypertension

Cited by 21 publications

References 22 publications

Acute effects of captopril on blood pressure and regional blood flows in two types of renovascular hypertensive rats in conscious state.

Acute effects of captopril on blood pressure and regional blood flows in two types of renovascular hypertensive rats in conscious state.

Regional blood flow in conscious spontaneously hypertensive rats.

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

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