Effect of Increased Renal Venous Pressure on Circulatory "Autoregulation" of Isolated Dog Kidneys

Semple, S. J. G.; Wardener, H. E. de

doi:10.1161/01.res.7.4.643

Cited by 107 publications

(61 citation statements)

References 11 publications

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“…At least the two faster responses are in perfect congruence with previous observations of the responses to a step rise in RAP (40,43,45,51,53), although in one of these studies (24) response 1 and thus the plateau were not overtly discernible.…”

Section: Time Coursesupporting

confidence: 90%

“…Therefore, it is possible to dissociate both mechanisms by their distinct temporal characteristics. This has been done successfully already by studying the transfer function (2,12,14,21,30) and by analyzing the autoregulatory response to a step increase in perfusion pressure (24,40,43,45,51,53). Transfer function studies have shown that although active under physiological conditions (2,12,14,21,30), the TGF is not required to explain the limited autoregulatory strength, which is observed under these conditions (2,14,30).…”

mentioning

confidence: 99%

“…However, the transfer function does not allow for assessment of the actual contribution of the TGF under resting conditions. Although to some extent this would be possible by a step function analysis, the available studies have not directly made use of this feature and were limited to anesthetized animals (24,43,45,49,53) and the artificially perfused kidney (40,51).…”

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confidence: 99%

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Dynamic characteristics and underlying mechanisms of renal blood flow autoregulation in the conscious dog

Just

Ehmke

Toktomambetova

et al. 2001

American Journal of Physiology-Renal Physiology

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The time course of the autoregulatory response of renal blood flow (RBF) to a step increase in renal arterial pressure (RAP) was studied in conscious dogs. After RAP was reduced to 50 mmHg for 60 s, renal vascular resistance (RVR) decreased by 50%. When RAP was suddenly increased again, RVR returned to baseline with a characteristic time course (control; n = 15): within the first 10 s, it rose rapidly to 70% of baseline ( response 1), thus already comprising 40% of the total RVR response. Thereafter, it increased at a much slower rate until it started to rise rapidly again at 20–30 s after the pressure step ( response 2). After passing an overshoot of 117% at 43 s, RVR returned to baseline values. Similar responses were observed after RAP reduction for 5 min or after complete occlusions for 60 s. When tubuloglomerular feedback (TGF) was inhibited by furosemide (40 mg iv, n = 12), response 1 was enhanced, providing 60% of the total response, whereas response 2 was completely abolished. Instead, RVR slowly rose to reach the baseline at 60 s ( response 3). The same pattern was observed when furosemide was given at a much higher dose (>600 mg iv; n = 6) or in combination with clamping of the plasma levels of nitric oxide ( n = 6). In contrast to RVR, vascular resistance in the external iliac artery after a 60-s complete occlusion started to rise with a delay of 4 s and returned to baseline within 30 s. It is concluded that, in addition to the myogenic response and the TGF, a third regulatory mechanism significantly contributes to RBF autoregulation, independently of nitric oxide. The three mechanisms contribute about equally to resting RVR. The myogenic response is faster in the kidney than in the hindlimb.

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Section: Time Coursesupporting

confidence: 90%

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confidence: 99%

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confidence: 99%

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Dynamic characteristics and underlying mechanisms of renal blood flow autoregulation in the conscious dog

Just

Ehmke

Toktomambetova

et al. 2001

American Journal of Physiology-Renal Physiology

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“…The contribution of the metabolic response to autoregulation has not been previously evaluated. Including the metabolic response with both the myogenic and shear-dependent responses produces a level of autoregulation close to that which is observed in cerebral (7,12,21), mesenteric (14), and renal (30,31) tissue. The current model shows that the combined effects of the myogenic and metabolic responses are necessary and sufficient to generate autoregulatory behavior, despite the contrary effect of the shear-dependent response.…”

Section: Discussionmentioning

confidence: 57%

Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses

Carlson¹,

Arciero²,

Secomb³

2008

American Journal of Physiology-Heart and Circulatory Physiology

153

160

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Carlson BE, Arciero JC, Secomb TW. Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses. Am J Physiol Heart Circ Physiol 295: H1572-H1579, 2008. First published August 22, 2008; doi:10.1152/ajpheart.00262.2008The autoregulation of blood flow, the maintenance of almost constant blood flow in the face of variations in arterial pressure, is characteristic of many tissue types. Here, contributions to the autoregulation of pressure-dependent, shear stress-dependent, and metabolic vasoactive responses are analyzed using a theoretical model. Seven segments, connected in series, represent classes of vessels: arteries, large arterioles, small arterioles, capillaries, small venules, large venules, and veins. The large and small arterioles respond actively to local changes in pressure and wall shear stress and to the downstream metabolic state communicated via conducted responses. All other segments are considered fixed resistances. The myogenic, shear-dependent, and metabolic responses of the arteriolar segments are represented by a theoretical model based on experimental data from isolated vessels. To assess autoregulation, the predicted flow at an arterial pressure of 130 mmHg is compared with that at 80 mmHg. If the degree of vascular smooth muscle activation is held constant at 0.5, there is a fivefold increase in blood flow. When myogenic variation of tone is included, flow increases by a factor of 1.66 over the same pressure range, indicating weak autoregulation. The inclusion of both myogenic and shear-dependent responses results in an increase in flow by a factor of 2.43. A further addition of the metabolic response produces strong autoregulation with flow increasing by a factor of 1.18 and gives results consistent with experimental observation. The model results indicate that the combined effects of myogenic and metabolic regulation overcome the vasodilatory effect of the shear response and lead to the autoregulation of blood flow. conducted response; microcirculation; blood flow regulation; vascular smooth muscle; vascular tone THE ABILITY OF VASCULAR BEDS to maintain a relatively constant blood flow over a large range of arterial pressures is known as vascular autoregulation. With increasing arterial pressure, the degree of vascular smooth muscle (VSM) activation, VSM tone, increases in arterioles, resulting in decreased vessel diameter and increased flow resistance. Several mechanisms contribute to changes in vascular tone, including responses to intraluminal pressure (myogenic response), shear stress on the endothelial lining of vessels (shear-dependent response), metabolite concentrations in vessels and/or tissue (metabolic response), and neural stimuli. The cerebral and renal vasculature show the most stable flow over a wide range of arterial pressures (2, 25), whereas in other beds, such as those in the mesentery, autoregulation is less effective.Several theoretical models for the autoregulation of blood flow have been developed using a multicompartmen...

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“…An index of the autoregulatory abilities of the animals was calculated by the following equation 18 : auto-…”

Section: Discussionmentioning

confidence: 99%

The antihypertensive mechanism of verapamil. Alteration of glomerular filtration rate regulation.

Lin

Young

1988

Hypertension

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SUMMARY The renal hemodynamic and renin release responses to verapamil were analyzed to determine if the antihypertensive action of the calcium entry blocker could be due to its renal effects. Hemodynamic and renin release measurements were compared in a control group of nine anesthetized rabbits and in a group of 10 rabbits given verapamil (200 /ig/kg i.v. initially, 4 ^g/kg/min thereafter), starting 30 minutes before data collection. Measurements were made over a range of controlled renal perfusion pressure from 100 to 40 mm Hg. The renal blood flow at 100 mm Hg of the verapamiltreated group was 18% greater (p<0.02) than that of the control group, while the glomerular filtration rate was 51% greater (p<0.001) than that of the control group. Renal blood flow and glomerular filtration rate autoregulation were highly effective in the control group down to 80 mm Hg, but both variables were poorly regulated in the verapamil-treated group. The filtration fraction of the treated group was 36.9 ± 1.5% versus 28.5 ± 1.6% in the control group (p<0.003) at 100 mm Hg, and the filtration fraction of the treated group remained significantly greater down to 40 mm Hg. Renin release rates of the two groups were similar at the 100 mm Hg pressure level, but the increase in release due to the progressive reduction in perfusion pressure was significantly greater in the treated group than in the control group. At the 80 mm Hg pressure level, the mean release rate for the treated group was more than three times greater (p<0.05) than that of the control group. These findings demonstrate that verapamil is an effective renal vasodilator and that the effect is proportionally greater on the preglomenilar than on the postglomerular resistance. This action could be the basis for its antihypertensive efficacy. (Hypertension 11: 639-644, 1988) KEY WORDS • renal hemodynamics • renin * renal blood flow • vasodilation filtration fraction • hypertension • rabbit T HE primary effect of calcium entry blockers is to reduce the rate of entry of calcium into the cytoplasm of a wide range of cell types. In vascular smooth muscle this effect results in a decrease in cytosolic calcium concentration and a reduction in contractile activity, leading to vasodilation. A variety of calcium entry blockers have proved to be effective in the treatment of hypertension, and the general vasodilator action is believed by many to be the mechanism of the effect. However, many effective vasodilators do not reduce the steady state level of arterial pressure in hypertensive patients, and several maneuvers that drastically affect total peripheral resistance (e.g., pregnancy, amputation, closing an arteriovenous

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Effect of Increased Renal Venous Pressure on Circulatory "Autoregulation" of Isolated Dog Kidneys

Cited by 107 publications

References 11 publications

Dynamic characteristics and underlying mechanisms of renal blood flow autoregulation in the conscious dog

Dynamic characteristics and underlying mechanisms of renal blood flow autoregulation in the conscious dog

Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses

The antihypertensive mechanism of verapamil. Alteration of glomerular filtration rate regulation.

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