The role of the kidney in canine blood pressure control: direct assessment of the closed‐loop gain.

Persson, Pontus B.; Ehmke, Heimo; Kirchheim, H. R.; Lempinen, Marko; Nafz, B.

doi:10.1113/jphysiol.1993.sp019626

Cited by 6 publications

(8 citation statements)

References 22 publications

(20 reference statements)

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“…The answer is both "yes" and "no." It is "no" because of its slow time constant relative to other systems that control sodium balance and blood pressure (36,40,43,72). Thus, even though any change in blood pressure certainly can begin changing urine output within minutes, quicker-acting systems normally are able to match sodium excretion to intake before there is a significant change in blood pressure.…”

Section: Using Sodium Balance As the Framework For Long-term Blood Prmentioning

confidence: 97%

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Chronic Blood Pressure Control

Brands

2012

Comprehensive Physiology

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Chronic blood pressure is maintained within very narrow limits around an average value. However, the multitude of physiologic processes that participate in blood pressure control present a bewildering array of possibilities to explain how such tight control of arterial pressure is achieved. Guyton and Coleman and colleagues addressed this challenge by creating a mathematical model that integrated the short- and long-term control systems for overall regulation of the circulation. The hub is the renal-body fluid feedback control system, which links cardiac function and vascular resistance and capacitance with fluid volume homeostasis as the foundation for chronic blood pressure control. The cornerstone of that system is renal sodium excretory capability, which is defined by the direct effect of blood pressure on urinary sodium excretion, that is, "pressure natriuresis." Steady-state blood pressure is the pressure at which pressure natriuresis balances sodium intake over time; therefore, renal sodium excretory capability is the set point for chronic blood pressure. However, this often is misinterpreted as dismissing, or minimizing, the importance of nonrenal mechanisms in chronic blood pressure control. This article explains the renal basis for the blood pressure set point by focusing on the absolute dependence of our survival on the maintenance of sodium balance. Two principal threats to sodium balance are discussed: (1) a change in sodium intake or renal excretory capability and (2) a change in blood pressure. In both instances, circulatory homeostasis is maintained because the sodium balance blood pressure set point is reached.

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Section: Using Sodium Balance As the Framework For Long-term Blood Prmentioning

confidence: 97%

“…Other blood pressure control systems have measurable, finite feedback gains (6,14,43,72,78). This means they can correct a blood pressure disturbance only a certain proportion of the way back to normal.…”

Section: Integration Of Blood Pressure Control Systemsmentioning

confidence: 99%

Chronic Blood Pressure Control

Brands

2012

Comprehensive Physiology

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“…It has previously been shown that when RPP is reduced to 70 mmHg, it takes 5 min before renal venous plasma renin activity is maximal (25). After 20 min of reduced RPP to ϳ80 mmHg, a 400% increase in arterial plasma renin activity (PRA) was found (30).…”

Section: Discussionmentioning

confidence: 99%

ANG II-induced downregulation of RBF after a prolonged reduction of renal perfusion pressure is due to pre- and postglomerular constriction

Sørensen¹,

Leyssac²,

Salomonsson³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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-Rathlou. ANG II-induced downregulation of RBF after a prolonged reduction of renal perfusion pressure is due to pre-and postglomerular constriction. Am J Physiol Regul Integr Comp Physiol 286: R865-R873, 2004. First published January 8, 2004 10.1152/ajpregu.00424.2003.-Previous experiments from our laboratory showed that longer-lasting reductions in renal perfusion pressure (RPP) are associated with a gradual decrease in renal blood flow (RBF) that can be abolished by clamping plasma ANG II concentration ([ANG II]). The aim of the present study was to investigate the mechanisms behind the RBF downregulation in halothane-anesthetized Sprague-Dawley rats during a 30-min reduction in RPP to 88 mmHg. During the 30 min of reduced RPP we also measured glomerular filtration rate (GFR), proximal tubular pressure (P prox), and proximal tubular flow rate (QLP). Early distal tubular fluid conductivity was measured as an estimate of early distal [NaCl] ([NaCl] ED), and changes in plasma renin concentration (PRC) over time were measured. During 30 min of reduced RPP, RBF decreased gradually from 6.5 Ϯ 0.3 to 6.0 Ϯ 0.3 ml/min after 5 min (NS) to 5.2 Ϯ 0.2 ml/min after 30 min (P Ͻ 0.05). This decrease occurred in parallel with a gradual increase in PRC from 38.2 Ϯ 11.0 ϫ 10 Ϫ5 to 87.1 Ϯ 25.1 ϫ 10 Ϫ5 Goldblatt units (GU)/ml after 5 min (P Ͻ 0.05) to 158.5 Ϯ 42.9 ϫ 10 Ϫ5 GU/ml after 30 min (P Ͻ 0.01). GFR, P prox, and [NaCl]ED all decreased significantly after 5 min and remained low. Estimates of pre-and postglomerular resistances showed that the autoregulatory mechanisms initially dilated preglomerular vessels to maintain RBF and GFR. However, after 30 min of reduced RPP, both pre-and postglomerular resistance had increased. We conclude that the decrease in RBF over time is caused by increases in both pre-and postglomerular resistance due to rising plasma renin and ANG II concentrations. renal vascular resistance; autoregulation; glomerular filtration rate THE MYOGENIC RESPONSE and the tubuloglomerular feedback (TGF) mechanism autoregulate renal blood flow (RBF) and glomerular filtration rate (GFR) when acute changes in renal perfusion pressure (RPP) occur (26,36). Autoregulation ensures that the kidney accurately can control salt and water excretion and thereby maintain the extracellular fluid volume by separating kidney function from acute fluctuations in blood pressure.A previous study from our laboratory showed that a longerlasting decrease in RPP is associated with a decrease in RBF that gradually develops a few minutes after the pressure reduction (38). This is also the case when the decrease in RPP is within the limits of autoregulation. This we refer to as regulation of RBF. Because this downregulation of RBF could be completely abolished by clamping the plasma ANG II concentration ([ANG II]), we hypothesized that the decrease in RBF was dependent on an increase in local and plasma [ANG II].The mechanism behind this downregulation of RBF is not clear. A direct effect of ANG II on the renal vessels is possible. As RPP ...

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“…The contribution of the renin‐angiotensin system (RAS) to the maintenance of mean arterial blood pressure (MABP) becomes apparent when it is strongly stimulated by sodium deprivation (Johnson & Davis, 1973; Fray et al 1977; Kopelman et al 1983) or during pathophysiological conditions which provoke major circulatory disturbances such as haemorrhage (Brough et al 1975; Kopelman et al 1983). More recently, a continuous tonic influence, as evidenced by a fall in MABP after angiotensin converting enzyme (ACE) inhibition (MacGregor et al 1981; Kopelman et al 1983; Ehmke et al 1987; Hasser & Bishop, 1988; Persson et al 1993), has also been observed under physiological conditions. This tonic effect of the RAS on the level of MABP appears to be controlled, at least in part, by the pressure‐dependent mechanism of renin release, for the following reasons.…”

mentioning

confidence: 99%

“…(2) In conscious dogs, the level of arterial plasma renin activity (PRA) was found to be strongly dependent on the actual difference between MABP and threshold pressure, with higher PRA values being present when MABP was closer to the threshold pressure (Ehmke et al 1987). (3) When MABP was artificially reduced to below the threshold pressure by inducing a constant pressure reduction between the suprarenal aortic and the renal arterial blood pressure (RABP) in conscious dogs, both aortic and renal arterial pressure rose within 2 h until RABP was almost completely restored (Persson et al 1993). Therefore, the pressure‐dependent mechanism of renin release might very well participate in the buffering of the spontaneous blood pressure variability.…”

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confidence: 99%

Buffering of blood pressure variability by the renin‐angiotensin system in the conscious dog

Just

Kirchheim

Ehmke

1998

The Journal of Physiology

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The renin‐angiotensin system (RAS) participates in the compensation of major blood pressure disturbances such as haemorrhage and is involved in the tonic long‐term (> 1 day) maintenance of mean arterial blood pressure (MABP). Since its contribution to the short‐term (< 1 h) buffering of normal blood pressure variability is not known, this was investigated in resting conscious dogs. The regulatory efficiency and the response time of the RAS were studied by an acute step reduction of renal artery pressure to 70 mmHg for 1 h using a suprarenal aortic cuff. After a delay of at least 100 s, MABP rose exponentially by 22 ± 5 mmHg in normal dogs (n= 4), by 6 ± 3 mmHg after angiotensin converting enzyme (ACE) inhibition (n= 4), and by 25 ± 5 mmHg after ganglionic blockade (n= 4). MABP returned to control after release of the cuff with similar time courses. The time constants of the MABP responses were in the range of 20 min. Thus, possible feedback oscillations of the RAS would be expected around 0.0025 Hz (1/(4 × 100 s)); a buffering effect would be possible below this frequency. Blood pressure variability was investigated by spectral analysis of MABP from 3.75 h recordings in the frequency ranges of 0.002–0.003 Hz (feedback oscillations) and below 0.002 Hz (buffering effect). ACE inhibition (n= 7) decreased MABP by 11 ± 2 mmHg (P < 0.05), but in both frequency ranges integrated spectral density was not affected. ACE inhibition also failed to significantly change spectral density in either of the two frequency ranges under the following conditions: (1) during ganglionic blockade (n= 7), (2) during a low‐sodium diet (except for a very slight elevation below 0.002 Hz) (n= 7), and (3) when the fall of MABP induced by ACE inhibition was compensated by an angiotensin II infusion (n= 7). It is concluded that in spite of its high regulatory efficiency with an adequate response time the RAS does not directly contribute to the short‐term buffering of blood pressure variability, nor does it give rise to feedback oscillations under normal resting conditions. Even if the RAS is stimulated by sodium restriction its contribution to short‐term blood pressure buffering is only marginal.

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The role of the kidney in canine blood pressure control: direct assessment of the closed‐loop gain.

Cited by 6 publications

References 22 publications

Chronic Blood Pressure Control

Chronic Blood Pressure Control

ANG II-induced downregulation of RBF after a prolonged reduction of renal perfusion pressure is due to pre- and postglomerular constriction

Buffering of blood pressure variability by the renin‐angiotensin system in the conscious dog

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