Effect of carotid occlusion and of perfusion pressure on renal function in conscious dogs.

Gross, R; Kirchheim, H. R.; Ruffmann, K

doi:10.1161/01.res.48.6.777

Cited by 25 publications

(24 citation statements)

References 25 publications

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“…Our own previous studies show that carotid occlusion in the conscious dog does not change kidney blood flow (Gross, Ruffmann & Kirchheim, 1979;Gross & Kirchheim, 1980) although it increases sympathetic outflow to the kidney under comparable conditions (Gross & Kirchheim, 1980); furthermore there are no changes in glomerular filtration rate and sodium reabsorption when kidney perfusion pressure is controlled (Gross & Kirchheim, 1978). Thus this experimental model seems to be suitable to investigate the influence of sympathetic nerves independent of other factors affecting renin release.…”

Section: Introductionmentioning

confidence: 78%

Interaction between perfusion pressure and sympathetic nerves in renin release by carotid baroreflex in conscious dogs.

Gross¹,

Hackenberg²,

Hackenthal³

et al. 1981

The Journal of Physiology

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SUMMARY1. The effect of bilateral carotid occlusion on carotid sinus pressure, systemic blood pressure, heart rate, renal blood flow, renal-venous and arterial plasma renin activity was studied in twelve trained conscious foxhounds on a normal sodium diet (4 7 mmol/kg per day).2. When renal perfusion pressure was allowed to rise with systemic pressure by 51-0 + 63 mmHg during carotid occlusion, renin release decreased by 72-3 ± 22-2 ng/min (78 % of control; P < 0 05) while renal blood flow remained at its resting level of 232-7+201 ml/min (n = 8 dogs).3. When renal perfusion pressure was maintained constant at 93-0 + 3-6 mmHg during carotid occlusion (suprarenal aortic cuff), renin release increased by 154-6 + 60-4 ng/min (73 % of control; P < 0 05), again there was no significant change of renal blood flow (n = 7 dogs).4. After fi-adrenergic blockade carotid occlusion increased systemic blood pressure by 47-7 + 7-8 mmHg, decreased renin release by 34-6 ± 9-9 ng/min (67 % of control; P < 0-05) and had no effect on renal blood flow (n = 4 dogs).5. When renal perfusion pressure was controlled at its resting level, no significant change of renin release and renal blood flow was observed during carotid occlusion in the surgically denervated kidney (n = 3 dogs) or in the intact kidney after /3-adrenergic blockade (n = 4 dogs).6. It is concluded that a reduction of carotid sinus pressure in the conscious dog increases renin release by a directf,-adrenergic stimulation without exerting vasomotor effects provided renal perfusion pressure is maintained at control level. The vascular receptor mechanism can effectively counteract the stimulating influence of the renal sympathetic nerves when perfusion pressure is allowed to rise.

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Section: Introductionmentioning

confidence: 78%

Interaction between perfusion pressure and sympathetic nerves in renin release by carotid baroreflex in conscious dogs.

Gross¹,

Hackenberg²,

Hackenthal³

et al. 1981

The Journal of Physiology

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“…Under short-term steady-state conditions (stepwise pressure reduction), a pronounced influence of RPP on renin release has been detected only below Ϸ90 mm Hg. 30 Thus, the minima of the RPP oscillations should lead to a pressuredependent stimulation in renin release, whereas maxima in RPP should not reduce renin release to the same degree. Therefore, if one assumes that possible hysteresis effects can be neglected, one would expect higher PRA during Osc than during P85.…”

Section: Discussionmentioning

confidence: 99%

Antihypertensive Effect of 0.1-Hz Blood Pressure Oscillations to the Kidney

et al. 2000

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Background-Physiological blood pressure (BP) fluctuations with frequencies Ͼ0.1 Hz can override renal blood flow autoregulation. The influence of such immediate changes in renal perfusion pressure (RPP) on daily BP regulation, eg, via shear stress-stimulated liberation of renal endothelial NO, however, is unknown. Thus, we studied the effects of such RPP oscillations on renal function and on systemic BP during the onset of renal hypertension. Methods and Results-Seven beagles (randomly assigned to each of the following protocols) were chronically instrumented for the measurement of systemic BP, RPP, and renal excretory function. An inflatable cuff was used to reduce and to oscillate RPP over 24 hours in the freely moving dog. Reducing RPP to 87Ϯ2 mm Hg diminished excretion of sodium and water and doubled plasma renin activity (PRA, nϭ7, PϽ0.01) but had no significant effect on urinary nitrate excretion (nϭ6), a marker of NO generation. Superimposing 0.1-Hz oscillations (Ϯ10 mm Hg) onto the reduced RPP blunted hypertension, returned fluid excretion almost to control levels, and doubled renal sodium elimination. Nitrate excretion peaked at 8 hours, only to return to control values shortly thereafter. PRA, conversely, was significantly reduced during the last third of the experimental protocols. Conclusions-BP fluctuations transiently stimulate NO liberation and induce a reduction in PRA, which enhances 24-hour sodium and water excretion and markedly attenuates the acute development of renovascular hypertension. (Circulation.

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“…A polyurethane renal artery catheter was placed with its tip located downstream of the occluder in order to allow the servocontrolling of RAP. The renal artery catheter and the constricting cuff were connected to an external electropneumatic pressure control system, which allowed us to reduce RAP and keep it constant at a pre-set level (control precision of < + 1 mmHg) (Gross et al 1981). A silastic catheter was implanted into the left renal vein after ligation of the spermatic or ovarian vein.…”

Section: Renal Haemodynamicsmentioning

confidence: 99%

Autoregulation and non‐homeostatic behaviour of renal blood flow in conscious dogs.

Persson

Ehmke

Kirchheim

et al. 1993

The Journal of Physiology

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SUMMARY1. Spontaneously occurring haemodynamic variations within 4 h affecting renal blood flow (RBF) were compared with externally induced short changes of renal artery pressure (RAP) in conscious resting dogs.2. In all animals in which RAP was servo-controlled (n = 6), perfect autoregulation of RBF was observed.3. In all 4 h recordings of spontaneous renal blood flow (n = 9), certain combinations of blood pressure and blood flow occurred remarkably frequently as indicated by three-dimensional frequency distributions.4. Cluster analysis demonstrated significant differences between these areas of accumulation (P < 0-001). The average number of 'set points' per 4 h session was 3-1+03.5. The shift from one set point to another is probably mediated by multiple control systems impinging on renal haemodynamics as suggested by 1/f fluctuations.6. In seven dogs, an additional renal venous catheter allowed measurements of the arterial-venous (A-V) oxygen partial pressure (Po2) difference as an indicator of the renal metabolic demand. An inverse relationship between A-V Po2 difference and RBF (Y = X( -0034) + 409, r = -0O9, P < 0.00 1) was found, indicating that the metabolic demands vary little (if at all) between the different set points. 7. The presented data suggest a modified view of renal homeostasis. There exist distinct combinations between RBF and RAP, which are very stable. Autoregulation merely buffers the fluctuations around these set points.

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Effect of carotid occlusion and of perfusion pressure on renal function in conscious dogs.

Cited by 25 publications

References 25 publications

Interaction between perfusion pressure and sympathetic nerves in renin release by carotid baroreflex in conscious dogs.

Interaction between perfusion pressure and sympathetic nerves in renin release by carotid baroreflex in conscious dogs.

Antihypertensive Effect of 0.1-Hz Blood Pressure Oscillations to the Kidney

Autoregulation and non‐homeostatic behaviour of renal blood flow in conscious dogs.

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